STANFORD, Calif. — You're in the supermarket eyeing a basket of sweet, juicy plums. You reach for the conventionally grown stone fruit, then decide to spring the extra $1/pound for its organic cousin. You figure you've just made the healthier decision by choosing the organic product — but new findings from Stanford University cast some doubt on your thinking.
"There isn't much difference between organic and conventional foods, if you're an adult and making a decision based solely on your health," said Dena Bravata, MD, MS, the senior author of a paper comparing the nutrition of organic and non-organic foods, to be published in the Sept. 4 issue of Annals of Internal Medicine.
A team led by Bravata, a senior affiliate with Stanford's Center for Health Policy, and Crystal Smith-Spangler, MD, MS, an instructor in the school's Division of General Medical Disciplines and a physician-investigator at VA Palo Alto Health Care System, did the most comprehensive meta-analysis to date of existing studies comparing organic and conventional foods. They did not find strong evidence that organic foods are more nutritious or carry fewer health risks than conventional alternatives, though consumption of organic foods can reduce the risk of pesticide exposure.
My take: There's a real advantage to be gained from shifting away from eating cheaper less healthy non-organic foods toward more expensive and healthier non-organic foods. In particular, drop cheap grains in favor of more expensive fruits and vegetables. For fruits eat more berries, cherries, and dark grapes (darker have more good chemicals). Concentrations of polyphenols and other healthy compounds are higher in berries and cherries than in cheaper large fruits like bananas and peaches. Same for vegetables. Go for the ones with the richest colors (no worthless iceberg lettuce when you can go for arugula and radicchio instead) and smaller sizes.
So if you are limiting the quality of your food due to budget limits don't splurge on organic when you can splurge on strawberries, kiwis, and blackberries. Also, want to improve your root vegetable diet? Get some sweet potatoes. Lots of carotenoids and other beneficial chemicals.
Nobody dare be shocked by this finding. Fast food is toxic, even in low doses. Once a week does serious damage.
MINNEAPOLIS/ST. PAUL (JULY 2, 2012) – The dangers of fast food are well documented; the portions are often larger and the food is generally high in calories and low in nutrients. Now, University of Minnesota School of Public Health researchers have examined the eating habits of residents in Singapore and found new evidence that a diet heavy in fast food increases the risk of developing Type 2 diabetes and coronary heart disease.
The latest research, published online today by the American Heart Association's journal Circulation, found that people who consume fast food even once a week increase their risk of dying from coronary heart disease by 20 percent in comparison to people who avoid fast food. For people eating fast food two-three times each week, the risk increases by 50 percent, and the risk climbs to nearly 80 percent for people who consume fast food items four or more times each week.
Do some people eat fast food because they want to die but don't want to be seen to be trying to kill themselves?
Get yourself back to traditional foods. (and FuturePundit thinks dark chocolate is a traditional food - it is certainly a tradition for me)
To arrive at their results, School of Public Health researchers worked alongside researchers from the National University of Singapore. Together, they examined results of a study conducted over a period of 16 years beginning in 1993, which looked at the eating habits of 52,000 Chinese residents of Singapore who have experienced a recent and sudden transition from traditional foods to Western-style fast food.
Vegetables. Fruits. Unrefined foods. Go paleo.
Canola oil and olive oil,both high in monounsaturated fats, do a better job of enabling carotenoid absorption than polyunsaturated fats such as corn oil and soybean oil.
In a human trial, researchers fed subjects salads topped off with saturated, monounsaturated and polyunsaturated fat-based dressings and tested their blood for absorption of fat-soluble carotenoids – compounds such as lutein, lycopene, beta-carotene and zeaxanthin. Those carotenoids are associated with reduced risk of several chronic and degenerative diseases such as cancer, cardiovascular disease and macular degeneration.
The study, published early online in the journal Molecular Nutrition & Food Research, found that monounsaturated fat-rich dressings required the least amount of fat to get the most carotenoid absorption, while saturated fat and polyunsaturated fat dressings required higher amounts of fat to get the same benefit.
So to absorb the beneficial compounds out of vegetables eat them with small amounts of olive oil or canola oil.
Olive oil and canola oil are effective at lower doses.
Monounsaturated fat-rich dressings, such as canola and olive oil-based dressings, promoted the equivalent carotenoid absorption at 3 grams of fat as it did 20 grams, suggesting that this lipid source may be a good choice for those craving lower fat options but still wanting to optimize absorption of health-promoting carotenoids from fresh vegetables.
The study found that women who had the highest consumption of chocolate -- about two candy bars a week -- had a 20 percent reduced risk of stroke.
Another study finds in women several different vitamins taken as supplements are associated with higher risk of dying.
Multivitamins, folic acid, vitamin B6, magnesium, zinc, copper and iron in particular appeared to increase mortality risk.
Calcium might be protective. But the researchers aren't confident about that finding.
Conversely, calcium supplements appeared to reduce death risk.
More here. No mention of vitamin D.
CHICAGO -- In a trial that included about 35,000 men, those who were randomized to receive daily supplementation with vitamin E had a significantly increased risk of prostate cancer, according to a study in the October 12 issue of JAMA.
"Lifetime risk of prostate cancer in the United States is currently estimated to be 16 percent. Although most cases are found at an early, curable stage, treatment is costly and urinary, sexual, and bowel-related adverse effects are common," according to background information in the article. There has been considerable preclinical and epidemiological evidence that selenium and vitamin E may reduce prostate cancer risk. "The initial report [published December 2008] of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) found no reduction in risk of prostate cancer with either selenium or vitamin E supplements but a statistically nonsignificant increase in prostate cancer risk with vitamin E. Longer follow-up and more prostate cancer events provide further insight into the relationship of vitamin E and prostate cancer."
So what to eat aside from chocolate? Less cooked broccoli is better than taking phytochemicals from broccoli in a pill. Activity of an enzyme called myrosinase in the broccoli makes several times more of glucosinolates chemicals get absorbed. So eat raw vegetables. Really.
CORVALLIS, Ore. -- New research has found that if you want some of the many health benefits associated with eating broccoli or other cruciferous vegetables, you need to eat the real thing – a key phytochemical in these vegetables is poorly absorbed and of far less value if taken as a supplement.
The study, published by scientists in the Linus Pauling Institute at Oregon State University, is one of the first of its type to determine whether some of the healthy compounds found in cruciferous vegetables can be just as easily obtained through supplements.
The answer is no.
And not only do you need to eat the whole foods, you have to go easy on cooking them.
I'm a big cauliflower and a big chocolate eater. I do take vitamin D though and sometimes vitamin K.
Soy isoflavones block DNA repair mechanisms and help radiation kill cancer cells. But you might worry about what blocking the DNA repair mechanism does to your cells if you aren't undergoing treatment for cancer.
"To improve radiotherapy for lung cancer cells, we are studying the potential of natural non-toxic components of soybeans, called soy isoflavones, to augment the effect of radiation against the tumor cells and at the same time protect normal lung against radiation injury," said Dr. Gilda Hillman, an associate professor in the Department of Radiation Oncology at Wayne State University's School of Medicine and the Karmanos Cancer Institute in Detroit.
"These natural soy isoflavones can sensitize cancer cells to the effects of radiotherapy, by inhibiting survival mechanisms which cancer cells activate to protect themselves," Hillman said. "At the same time, soy isoflavones can also act as antioxidants in normal tissues, which protect them against unintended damage from the radiotherapy. In a recent study, published in the Journal of Thoracic Oncology, we demonstrated that soy isoflavones increase killing of cancer cells by radiation via blocking DNA repair mechanisms, which are turned on by the cancer cells to survive the damage caused by radiation."
Soy is very un-paleo. Soy is high in lectins (unless fermented) and for men the soy isoflavone genistein is only appropriate if you want to shrink your prostate and don't mind the feminization.
Soy might not be as harmful as poisonous sugar and high fructose corn syrup. We need to turn back the clock on our diets by about a century.
The Mediterranean diet has proven beneficial effects not only regarding metabolic syndrome, but also on its individual components including waist circumference, HDL-cholesterol levels, triglycerides levels, blood pressure levels and glucose metabolism, according to a new study published in the March 15, 2011, issue of the Journal of the American College of Cardiology. The study is a meta-analysis, including results of 50 studies on the Mediterranean diet, with an overall studied population of about half a million subjects.
Here's the diet in broad outline:
The Mediterranean diet is a dietary pattern characterized by high consumption of monounsaturated fatty acids, primarily from olives and olive oils; daily consumption of fruits, vegetables, whole grain cereals, and low-fat dairy products; weekly consumption of fish, poultry, tree nuts, and legumes; a relatively low consumption of red meat; and a moderate daily consumption of alcohol, normally with meals.
Out of that list what are the good foods versus the less bad foods? Are whole grains beneficial or less bad? Are low-fat dairy products beneficial or less bad? A previous study provides clues to these questions.
Curiously the admonitions against eating lots of red meat put the Mediterranean diet at odds with most versions of the Paleo Diet. I'd like to see the Mediterranean and Paleo diets compared by blood triglycerides and blood sugar.
Researchers at the University of California, San Diego School of Medicine and Creighton University School of Medicine in Omaha have reported that markedly higher intake of vitamin D is needed to reach blood levels that can prevent or markedly cut the incidence of breast cancer and several other major diseases than had been originally thought. The findings are published February 21 in the journal Anticancer Research
While these levels are higher than traditional intakes, they are largely in a range deemed safe for daily use in a December 2010 report from the National Academy of Sciences Institute of Medicine.
Among the diseases whose risks appear to be cut in half by higher D: breast cancer, colon cancer, multiple sclerosis, and type 1 diabetes.
"We found that daily intakes of vitamin D by adults in the range of 4000-8000 IU are needed to maintain blood levels of vitamin D metabolites in the range needed to reduce by about half the risk of several diseases - breast cancer, colon cancer, multiple sclerosis, and type 1 diabetes," said Cedric Garland, DrPH, professor of family and preventive medicine at UC San Diego Moores Cancer Center. "I was surprised to find that the intakes required to maintain vitamin D status for disease prevention were so high – much higher than the minimal intake of vitamin D of 400 IU/day that was needed to defeat rickets in the 20th century."
One could get one's blood tested for vitamin D and adjust upward on dose and get retested until one reaches the 40 to 60 ng/ml blood level this study suggests is needed for optimal benefit.
An article on the Harvard School of Public Health web site argues that the USDA's 2010 Dietary Guidelines for Americans still falls short of embracing all the recent research on ideal diet.
The USDA does advise eating more fish (though fisheries depletion means they'll have to be farmed). But Walter Willett thinks "Big Beef" and "Big Dairy" (that would be a Big Mac with Cheese) have too much influence at the USDA.
“I had hoped that the USDA would be able to give Americans the clear advice about diet that they deserve,” says Dr. Walter Willett, Fredrick John Stare Professor of Epidemiology and Nutrition, and chair of the Dept. of Nutrition at Harvard School of Public Health. “However, the continued failure to highlight the need to cut back on red meat and limit most dairy products suggests that ‘Big Beef’ and ‘Big Dairy’ retain their strong influence within this department. Might it be time for the USDA to recuse itself because of conflicts of interest and get out of the business of dietary advice?”
Willett believes fat is not the problem. It is simple sugars and refined grains we most need to avoid.
So what about red meat? Processed meat is clearly unhealthy. The harm caused by processed meat is basically clouding the signal about just how much red meat is optimal. Too many studies have looked at harm from meat without breaking it down enough between processed and unprocessed meat. I welcome links from readers to studies that more clearly show whether higher fat red meat cause net harm. The major Paleo Diet advocates appear to be split on the subject.
"Fat is not the problem," says Dr. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health. "If Americans could eliminate sugary beverages, potatoes, white bread, pasta, white rice and sugary snacks, we would wipe out almost all the problems we have with weight and diabetes and other metabolic diseases."
It's a confusing message. For years we've been fed the line that eating fat would make us fat and lead to chronic illnesses. "Dietary fat used to be public enemy No. 1," says Dr. Edward Saltzman, associate professor of nutrition and medicine at Tufts University. "Now a growing and convincing body of science is pointing the finger at carbs, especially those containing refined flour and sugar."
The old conventional wisdom is "precisely the opposite of what we now know to be true".
Since randomized trials of beta carotene supplementation did not appear to show a health benefit scientists have been trying to figure out what about vegetables make people healthier. One theory: alpha carotene might be a key beneficial substance in cancers.
High blood levels of the antioxidant alpha-carotene appear to be associated with a reduced risk of dying over a 14-year period, according to a report posted online today that will be published in the March 28 print issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Oxygen-related damage to DNA, proteins and fats may play a role in the development of chronic diseases like heart disease and cancer, according to background information in the article. Carotenoids—including beta-carotene, alpha-carotene and lycopene—are produced by plants and microorganisms and act as antioxidants, counteracting this damage. Carotenoids in the human body are obtained mainly through eating fruits and vegetables rich in the nutrients, or through antioxidant supplements.
Paleo Diet expert Loren Cordain says the lower acidity of vegetables balances higher acidic foods. Vegetables also contain assorted flavonoids and other compounds. So is alpha carotene a real benefit or just a marker for whatever else in veggies is good for you?
People with higher blood alpha carotene had lower all-cause mortality.
Over the course of the study, 3,810 participants died; the risk for dying was lower with higher levels of alpha-carotene in the blood. Compared with individuals with blood alpha-carotene levels between 0 and 1 micrograms per deciliter, the risk of death during the study period was 23 percent lower among who had concentrations between 2 and 3 micrograms per deciliter, 27 percent lower with levels between 4 and 5 micrograms per deciliter, 34 percent lower with levels between 6 and 8 micrograms per deciliter and 39 percent lower with levels of 9 micrograms per deciliter or higher.
Higher alpha-carotene concentration also appeared to be associated with lower risk of dying from cardiovascular disease or cancer individually, and of all other causes. "The association between serum alpha-carotene concentrations and risk of death from all causes was significant in most subgroups stratified by demographic characteristics, lifestyle habits and health risk factors," the authors write.
It seems likely the vegetables really are good for your health. You do not have to know how they deliver their health benefits. You can just eat them. Go for the yellow-orange vegetables and deep greens. About to buy food for Thanksgiving Day? Go for sweet potatoes, pumpkin pie, and dark greens.
Alpha-carotene is chemically similar to beta-carotene but may be more effective at inhibiting the growth of cancer cells in the brain, liver and skin, they note. "Moreover, results from a population-based case-control study of the association between the consumption of fruits and vegetables and risk of lung cancer suggest that consumption of yellow-orange (carrots, sweet potatoes or pumpkin and winter squash) and dark-green (broccoli, green beans, green peas, spinach, turnips greens, collards and leaf lettuce) vegetables, which have a high alpha-carotene content, was more strongly associated with a decreased risk of lung cancer than was consumption of all other types of vegetables," the authors write.
Count me in the ranks of those who would rather pass on broccoli. Better winter squash or sweet potatoes. Yams too.
BOSTON (October 20, 2010) - People who consume several servings of whole grains per day while limiting daily intake of refined grains appear to have less of a type of fat tissue thought to play a key role in triggering cardiovascular disease and type 2 diabetes, a new study suggests. Researchers at the Jean Mayer USDA Human Nutrition Researcher Center on Aging (USDA HNRCA) at Tufts University observed lower volumes of Visceral Adipose Tissue (VAT) in people who chose to eat mostly whole grains instead of refined grains.
“VAT volume was approximately 10 % lower in adults who reported eating three or more daily servings of whole grains and who limited their intake of refined grains to less than one serving per day,” says first author Nicola McKeown, PhD, a scientist with the Nutritional Epidemiology Program at the USDA HNRCA. “For example, a slice of 100% whole wheat bread or a half cup of oatmeal constituted one serving of whole grains and a slice of white bread or a half cup of white rice represented a serving of refined grains.”
The whole wheat wasn't protective for those study participants who also ate a lot of refined grains. So the whole grains aren't so much beneficial as just not harmful or perhaps less harmful than refined grains.
Paelo Diet advocate Loren Cordain says avoid grains. Stephan Guyenet says grain preparation techniques make a difference in determining whether grains are good or bad for us. Whole grains might even be harmful, but less harmful than white bread.
For those who fully embrace the the Paleo lifestyle this won't come as a shock: Credit and debit cards are so unnatural they cause us to make worse food buying choices as compared to buying with cash. Weird wild stuff.
People are more likely to buy unhealthy foods when they pay using credit or debit cards, according to a new study in the Journal of Consumer Research.
"Two factors contribute to this intriguing effect," write authors Manoj Thomas (Cornell University), Kalpesh Kaushik Desai (State University of New York, Binghamton), and Satheeshkumar Seenivasan (State University of New York, Buffalo). "First, there is a correlation between unhealthiness and impulsiveness of food items: Unhealthy food items also tend to elicit impulsive responses. Second, cash payments are psychologically more painful than card payments, and this pain of payment can curb the impulsive responses to buy unhealthy food items."
This serves as a reminder: Our technological advances have enabled us to create environments that our instincts are not well adapted for. We need to make choices that make our environments better suited to our natures.
If spending money hurts then using cash will be especially effective in encouraging better food-buying behavior.
The authors conducted an analysis of actual shopping behavior of 1,000 households over a period of six months. They found that shopping carts had a larger proportion of food items rated as impulsive and unhealthy when shoppers used credit or debit cards versus cash. In follow-up studies they found that the vice-regulation effect of cash payment is due to the "pain" of paying in cash, and that the effect is stronger in consumers who are chronically more sensitive to the pain of payment.
Though if you can manage to use credit to buy Paleo Diet food and eat like Loren Cordain then you have managed to insulate yourself from at least one of the damaging effects of our credit culture.
This report describes the results of that analysis, which indicated that, in 2009, an estimated 32.5% of adults consumed fruit two or more times per day and 26.3% consumed vegetables three or more times per day, far short of the national targets. Overall, the proportion of adults who met the fruit target declined slightly, but significantly, from 34.4% in 2000 to 32.5% in 2009; no significant change was observed in meeting the vegetable target.
People do not like vegetables and vegetables are inconvenient. Exhortations about eating better will not change this for the vast majority.
My modest proposal for solving this problem: hide vegetables inside of other foods. Imagine french fries that have some vegetable ground up into them. The vegetables could form the core inside the fry so as to keep the outside appearance unchanged. Or the vegetable could be mixed in with the fry but then a batter layer could be added to the outside of the fry. Could this be done in a way that is sellable at McDonald's? Or perhaps at a slightly more upscale fast food joint? Parenthetically, is there a good fast food hamburger? I haven't found it yet if it exists. One big problem: cheap buns. Hate em.
Meat can be used to boost consumption of berries and cherries. Cherries mixed in to ground beef even reduces carcinogen formation during cooking. So double bonus points. Stews are another way to use meat to deliver healthy foods.
Oklahomans are really bad about eating vegetables.
In 2009, an estimated 32.5% of U.S. adults consumed fruit two or more times per day (Table 1), with the highest percentage in DC (40.2%) and the lowest in Oklahoma (18.1%). The percentage of adults who consumed vegetables three or more times per day was 26.3%, with the highest percentage in Tennessee (33.0%) and the lowest in South Dakota (19.6%). Thus, no state met either of the Healthy People 2010 targets related to fruit and vegetable consumption among adults. Twelve states and DC had 35%--45% of adults who consumed fruit two or more times per day, compared with no states that had 35%--45% of adults who consumed vegetables three or more times per day (Figure).
The New York Times puts a human face on this report with New Yorkers who are embarrassed to admit how little they eat in the way of vegetables.
No one really wants to admit that they don’t eat vegetables. A nurse who works at the Hospital for Special Surgery on the Upper East Side openly acknowledges that vegetables make her gag. Still, she begged to not be publicly identified because she is in the health care field and knows that she should set a better example.
David Bernstein, who lives in Greenpoint, Brooklyn, is sheepish about the lack of vegetables in his diet. He waits tables at the hip M. Wells restaurant in Long Island City, Queens, and knows his way around the Union Square Greenmarket. But his diet consists largely of bacon, yogurt and frozen stuffed chicken breasts.
Embarrassed? Want a diet you can enjoy eating and still feel good about it? Some people have switched to advocating the Paleo Diet (and this has become a lifestyle) so they can make a virtue of their meat eating (plus, the Paleo Diet even makes sense). Stephan Guyenet covers that territory pretty well. See, for example his post on saturated fat, glycemic index, and insulin sensitivity. Also, his two part piece on coconut oil. After reading those posts read his brief take on dissolving away your bones with corn oil and corn oil and other high omega 6 fat sources as causes of cancer. Parenthetically, I see this as strengthening my argument for genetically engineering plant crops to boost omega 3 content. The very same genetic engineering will cause omega 3 to displace omega 6 in the oil as corn and other crops make omega 3 instead of omega 6. Bonus points.
They found that moderate drinkers tended to live longer across a 20-year follow-up compared to heavy drinkers and teetotalers. Mortality risk was 42% higher for heavy drinkers and 49% higher for abstainers than moderate drinkers.
A large prospective study of 5033 men and women in the Tromsø Study in northern Norway has reported that moderate wine consumption is independently associated with better performance on cognitive tests. The subjects (average age 58 and free of stroke) were followed over 7 years during which they were tested with a range of cognitive function tests. Among women, there was a lower risk of a poor testing score for those who consumed wine at least 4 or more times over two weeks in comparison with those who drink < 1 time during this period The expected associations between other risk factors for poor cognitive functioning were seen, i.e. lower testing scores among people who were older, less educated, smokers, and those with depression, diabetes, or hypertension.
It has long been known that "moderate people do moderate things." The authors state the same thing: "A positive effect of wine . . . could also be due to confounders such as socio-economic status and more favourable dietary and other lifestyle habits.
It could be that people who control their drinking also make other wise decisions on their health.
If alcohol really does deliver a health benefit then how? A few possibilities are mentioned.
Such effects could relate to the presence in wine of a number of polyphenols (antioxidants) and other micro elements that may help reduce the risk of cognitive decline with ageing. Mechanisms that have been suggested for alcohol itself being protective against cognitive decline include effects on atherosclerosis ( hardening of the arteries), coagulation ( thickening of the blood and clotting), and reducing inflammation ( of artery walls, improving blood flow).
My guess is that some subset benefits from alcohol while another subset is harmed. I'd like to see a prospective study where blood lipids, inflammation, stress hormones, and other indicators are looked at before and after starting moderate alcohol consumption. Perhaps some people experience a reduction in stress and inflammation as a result of consuming alcohol while others are harmed and still others already have low stress and low inflammation without using alcohol.
Here's another reason to kick the soda habit. New research published online in the FASEB Journal (http://www.fasebj.org) shows that high levels of phosphates may add more "pop" to sodas and processed foods than once thought. That's because researchers found that the high levels of phosphates accelerate signs of aging. High phosphate levels may also increase the prevalence and severity of age-related complications, such as chronic kidney disease and cardiovascular calcification, and can also induce severe muscle and skin atrophy.
"Humans need a healthy diet and keeping the balance of phosphate in the diet may be important for a healthy life and longevity," said M. Shawkat Razzaque, M.D., Ph.D., from the Department of Medicine, Infection and Immunity at the Harvard School of Dental Medicine. "Avoid phosphate toxicity and enjoy a healthy life."
This study does not indicate just how much phosphate is too much for humans. What's a reasonable amount of phosphate to consume per day?
Here are the details. Note how they used two different genetic modifications. The first group of mice only had the klotho knock-out which caused high phosphate in the bodies of the mice and shorter life. You might might that the klotho shortened life by some other mechanism. But a second group had both klotho and a second knock-out for the NaPi2a gene which lowered phosphate. Those mice lived longer. But then when mice with both knock-outs were fed a high phosphate diet they also lived only 15 weeks, just like the first group.
To make this discovery, Razzaque and colleague examined the effects of high phosphate levels in three groups of mice. The first group of mice was missing a gene (klotho), which when absent, causes mice to have toxic levels of phosphate in their bodies. These mice lived 8 to 15 weeks. The second group of mice was missing the klotho gene and a second gene (NaPi2a), which when absent at the same time, substantially lowered the amount of phosphate in their bodies. These mice lived to 20 weeks. The third group of mice was like the second group (missing both the klotho and NaPi2a genes), except they were fed a high-phosphate diet. All of these mice died by 15 weeks, like those in the first group. This suggests that phosphate has toxic effects in mice, and may have a similar effect in other mammals, including humans.
Here's a table of phosphate in common foods. That list doesn't have much in the way of processed foods though. Here's a table of phosphorus in dairy products. The recommended daily allowance of phosphorus for adults is 700 mg. Anyone know a link to a good list of phosphates in processed foods?
According a new study of over 3,000 adults aged 70-79, the apparent association between light-to-moderate alcohol consumption and reduced risk of functional decline over time did not hold up after adjustments were made for characteristics related to lifestyle, in particular physical activity, body weight, education, and income.
The authors of the study, publishing today in the Journal of the American Geriatrics Society, say this suggests that life-style related characteristics may be the real determinant of the reported beneficial effects of alcohol and functional decline.
“In recent years the relationship between alcohol intake and health outcomes has gained growing attention, but while there is now considerable consensus that consuming alcohol at moderate levels has a specific beneficial effect on the risk of cardiovascular disease, the benefit of alcohol intake on other health-related outcomes is less convincing,” said study author Cinzia Maraldi, M.D., of the University of Ferrara, Italy. “We wanted to evaluate this question over a long-term follow-up and with a prospective design, which most previous studies have not used.”
During a follow-up time of six and a half years, the researchers found that participants consuming moderate levels of alcohol had the lowest incidence of mobility limitation and disability. After adjusting for demographic characteristics, moderate alcohol intake was still associated with reduced risk compared to never or occasional consumption, but adjusting for life-style related variables substantially reduced the strength of the associations. Adjustment for diseases and health status indicators did not affect the strength of the associations, which led the authors to conclude that life-style is the most important factor in confounding this relationship.
I suspect that some people derive a net benefit from alcohol while obviously many others experience a net harm from drinking it. Similarly, when it comes to lots of different drugs and dietary practices I expect the evidence will eventually show that the trade-offs between costs and benefits will end up having a large variable genetic component. For example, we differ in liver metabolism that some people will process and excrete a given drug really fast and others much more slowly. Also, how well drugs bind to active sites differs between people.
The cost of genetic testing and genetic sequencing has fallen so far so fast that we are now at the point where the floodgates are just starting to open for a torrent of research results identifying functionally significant genetic differences and how they matter for food and drug metabolism. Some of us are probably going to learn that we should drink a glass of red wine or beer every day. Others will learn they should rarely if ever touch the stuff. Ditto for various diets and drugs. Should you eat saturated fats daily? Or eat lots of statins? We'll probably know in 5-10 years.
Okay, time for yet another post on the glories of vitamin D. If you are already taking vitamin D you can still use this post to feel good about your wisdom and sagacity. Maintain your strength and balance in your old age so you don't fall down and go boom.
A daily supplement of vitamin D at a dose of 700-1000 IU reduces the risk of falling among older people by 19% according to a study published on bmj.com today. But a dose of less than 700 IU per day has no effect.
Sounds like D3 works better than D2. I happen to take D3. So I got that going for me. Which is nice. (who am I quoting?)
Supplemental vitamin D2 and Vitamin D3 were investigated. 700-1000 IU supplemental vitamin D per day (vitamin D2 or vitamin D3) reduced falls by 19% and up to 26% with vitamin D3.
This effect was independent of age, type of dwelling or additional calcium supplementation. The effect was significant within two to five months of starting treatment and extended beyond 12 months.
Supplemental vitamin D did not reduce falls at a dose of less than 700 IU per day.
Now if you are 20 years old the odds are that by the time you turn 60 you'll be able to get stem cell treatments that'll restore your skin's youthful ability to synthesize vitamin D. Plus, stem cell therapies to restore muscle strength along with stem cell therapies to repair joints and connective tissue will have you out playing beach volleyball. So you'll synthesize lots of vitamin D in your skin in your old age.
Changes in medical policy and health care funding will not address the biggest causes of lower life expectancy in the United States as compared to some other industrialized countries. Poor diet choices and lack of exercise are more important than the health care system.
Two teams, one led by Pierre-Carl Michaud of the Rand Corporation in Santa Monica, California, the other by Samuel Preston of the University of Pennsylvania in Philadelphia, have dug into international health statistics to ask why US citizens can expect to die earlier than their counterparts in the richest European nations.
Michaud concludes that the blame lies largely with high rates of chronic disease caused by poor diet, lack of exercise and the lingering effects of tobacco use from a time when smoking was more prevalent in the US than in Europe.
Years of bad habits take their toll. The medical technologies of today can not reverse that damage. Once you get enough mutations to, say, trigger liver cancer you are checking out of the Life Hotel. Organ failures usually cause death because demand for donor organs far exceeds the number of donor organs available. Strokes kill because we can't repair brains and we lack the technology to repair blood vessels before they burst and kill lots of brain cells.
Now, you ought to look at your diet and habits and try to make at least small changes that'll tip the odds more in your favor. Close enough to a store to walk? Want to visit a friend who lives a mile away? How about walking? Choosing between vacations where one is more sedentary and the other provides greater potential for physical exercise? Choose the latter. Then there's food. Try this: Just eat a vegetable before you eat whatever you want to eat. If you do not want to deny yourself junk food at least preface it with something good for you.
Even if you eat the Mediterranean diet and jog 50 miles per week you can drop dead from a stroke or suddenly experience an auto-immune disease that rips apart some internal organs. Even if you become a vegan and swim laps every day you can suddenly experience kidney failure or get diagnosed with advanced stomach cancer. You could go for colonoscopy exams every year and still die from colon cancer. You could go for yearly physicals and go on preventative blood pressure drugs and still develop heart disease. The realm of the biotechnologically feasible today still falls far short of what we need to prevent death from our major killer diseases of today.
What matters for most of us today is not the size of our medical co-pays or deductibles. I know people who've gone without medical insurance for years without seeing a doctor (as compared to myself who goes for years with medical insurance and I still do not see a doctor). No, what matters most is the state of medical technology 10, 20, 30, or even 40 or 50 years from now. What matters is the rate of advance of biomedical science and biotechnology. Lots of factors play into that rate of advance. I am worried about how government policy changes might affect the incentives for new drug and new treatment development in the private sector.
But other things matter as well. Technologies from other industries play a big role in making biomedical advances possible. The rate of advance of computing technologies matters for multiple reasons (even printers can help make miniature microfluidic devices). Computers make CAT scans and other scans possible. Computers make the da Vinci Surgical System possible. Computers automate lots of medical testing lab work. Microfluidic devices are possible because of work in the computer industry to make computer chips. Microfluidic will enable home lab-on-a-chip testing as well as much more rapid and accurate testing in hospitals and clinics.
The regulatory environment is important too. Some economists believe the US Food and Drug Administration slows the development of new treatments and causes net harm. If this is true then for those of us who still have major health care problems only in our futures have an interest in lowering the barriers for introduction of new treatments.
After 20 years of waiting (hope you didn't get too impatient) the answer is finally in: This study increases the likelihood that calorie restriction will extend human life too.
MADISON — The bottom-line message from a decades-long study of monkeys on a restricted diet is simple: Consuming fewer calories leads to a longer, healthier life.
Writing today (July 10) in the journal Science, a team of researchers at the University of Wisconsin-Madison, the Wisconsin National Primate Research Center and the William S. Middleton Memorial Veterans Hospital reports that a nutritious but reduced-calorie diet blunts aging and significantly delays the onset of such age-related disorders as cancer, diabetes, cardiovascular disease and brain atrophy.
"We have been able to show that caloric restriction can slow the aging process in a primate species," says Richard Weindruch, a professor of medicine in the UW-Madison School of Medicine and Public Health who leads the National Institute on Aging-funded study. "We observed that caloric restriction reduced the risk of developing an age-related disease by a factor of three and increased survival."
During the 20-year course of the study, half of the animals permitted to eat freely have survived, while 80 percent of the monkeys given the same diet, but with 30 percent fewer calories, are still alive.
Begun in 1989 with a cohort of 30 monkeys to chart the health effects of the reduced-calorie diet, the study expanded in 1994 with the addition of 46 more rhesus macaques. All of the animals in the study were enrolled as adults at ages ranging from 7 to 14 years. Today, 33 animals remain in the study. Of those, 13 are given free rein at the dinner table, and 20 are on a calorie-restricted diet. Rhesus macaques have an average life span of about 27 years in captivity. The oldest animal currently in the study is 29 years.
Those on calorie restriction have a less debilitated old age too. They get less cancer, less insulin-resistant diabetes, less decay in motor control, less decline in motor functions.
What I want to know: Will resveratrol deliver these same benefits in humans without the need to live in perpetual hunger with a gaunt skinny look?
Calorie restriction may seem promising, but it has potential downsides, including constant hunger, sensitivity to cold, weakened immune function and sour mood, says Susan Roberts, professor of nutrition and psychiatry at Tufts University, where she is leading a study on calorie restriction diets.
My guess is that someone on CR will do worse in an accident because their body will have less reserves to draw on. Anyone know if that's the case?
Eating more vegetables, fruits, nuts, pulses and olive oil, and drinking moderate amounts of alcohol, while not consuming a lot of meat or excessive amounts of alcohol is linked to people living longer.
However, the study also claims, that following a Mediterranean diet high in fish, seafood and cereals and low in dairy products were not indicators of longevity.
While several studies have concluded that the Mediterranean diet improves chances of living longer, this is the first to investigate the importance of individual components of the diet.
Professor Dimitrios Trichopoulos at the Harvard School of Public Health explains that they have surveyed over 23,000 men and women who were participants in the Greek segment of the European Prospective Investigation into Cancer and Nutrition (EPIC).
So try harder to avoid red meat than dairy. Eat more fruits, nuts, and vegetables. I'm personally eating olives almost every day.
Update Here is the research paper.
The contributions of the individual components of the Mediterranean diet to this association were moderate ethanol consumption 23.5%, low consumption of meat and meat products 16.6%, high vegetable consumption 16.2%, high fruit and nut consumption 11.2%, high monounsaturated to saturated lipid ratio 10.6%, and high legume consumption 9.7%. The contributions of high cereal consumption and low dairy consumption were minimal, whereas high fish and seafood consumption was associated with a non-significant increase in mortality ratio.
We might have more allergy and autoimmune diseases due to an imbalance of too much omega 6 fatty acids as compared to omega 3 fatty acids. An increase in omega 3 fatty acids alters gene expression to lower inflammation-related genes.
For the past century, changes in the Western diet have altered the consumption of omega-6 fatty acids (w6, found in meat and vegetable oils) compared with omega-3 fatty acids (w3, found in flax and fish oil). Many studies seem to indicate this shift has brought about an increased risk of inflammation (associated with autoimmunity and allergy), and now using a controlled diet study with human volunteers, researchers may have teased out a biological basis for these reported changes.
Anthropological evidence suggests that human ancestors maintained a 2:1 w6/w3 ratio for much of history, but in Western countries today the ratio has spiked to as high as 10:1. Since these omega fatty acids can be converted into inflammatory molecules, this dietary change is believed to also disrupt the proper balance of pro- and anti- inflammatory agents, resulting in increased systemic inflammation and a higher incidence of problems including asthma, allergies, diabetes, and arthritis.
Floyd Chilton and colleagues wanted to examine whether theses fatty acids might have other effects, and developed a dietary intervention strategy in which 27 healthy humans were fed a controlled diet mimicking the w6/w3 ratios of early humans over 5 weeks. They then looked at the gene levels of immune signals and cytokines (protein immune messengers), that impact autoimmunity and allergy in blood cells and found that many key signaling genes that promote inflammation were markedly reduced compared to a normal diet, including a signaling gene for a protein called PI3K, a critical early step in autoimmune and allergic inflammation responses.
This study demonstrates, for the first time in humans, that large changes in gene expression are likely an important mechanism by which these omega fatty acids exert their potent clinical effects.
Omega 3 fatty acids are on a small list of nutrients I get from pills. Most nutritional improvements should come from better foods. But unless you are going to eat fish regularly you're probably going to need supplements to get enough omega 3 fatty acids.
Some vegetable cooking methods may be better than others when it comes to maintaining beneficial antioxidant levels, according to a new study in the Journal of Food Science, published by the Institute of Food Technologists. Results showed that, depending on the vegetable, cooking on a flat metal surface with no oil (griddling) and microwave cooking maintained the highest antioxidant levels.
Fruits and vegetables are considered to be the major contributors of nutritional antioxidants, which may prevent cancer and other diseases. Because of their high antioxidant levels and low-calorie content, consumers are encouraged to eat several servings of fruits and vegetables daily.
Researchers at the University of Murcia and the University of Complutense in Spain examined how various cooking methods affected antioxidant activity by analyzing six cooking methods with 20 vegetables. The six cooking methods were boiling, pressure-cooking, baking, microwaving, griddling and frying. Their findings showed the following:
• The highest antioxidant loss was observed in cauliflower after boiling and microwaving, peas after boiling, and zucchini after boiling and frying.
• Green beans, beets, and garlic were found to keep their antioxidant levels after most cooking treatments.
• The vegetables that increased their antioxidant levels after all cooking methods were green beans (except green beans after boiling), celery and carrots.
• Artichoke was the only vegetable that kept its high antioxidant level during all the cooking methods.
Griddle- and microwave-cooking helped maintain the highest levels of antioxidants, produced the lowest losses while “pressure-cooking and boiling [led] to the greatest losses,” says lead researcher A. M. Jiménez-Monreal. “In short, water is not the cook’s best friend when it comes to preparing vegetables.”
Eat more raw vegetables and you can avoid losses in all but a few vegetables. Cook grean beans, celery and carrots. Then eat all the rest raw.
You can also read a review of the beneficial compounds found in Brassica vegetables.
It's basically a given that diets loaded with fat can lead to considerable health problems. But a new study in the April issue of Cell Metabolism, a Cell Press publication, shows that in some cases diets that are high in both fat and protein can be even worse.
The researchers led by Christopher Newgard of Duke Medical Center report that rats fed high-fat (HF) diets supplemented with extra so-called branched chain amino acids (BCAA) don't have to eat as much or gain as much weight to develop insulin resistance as do chubbier animals fed a high-fat diet alone. Moreover, those ill effects of branched chain amino acids, which include 3 of the 20 amino acids that are the building blocks of proteins, occurred only in the context of a high-fat diet.
"We've all made a big deal out of the fact that people in the U.S. eat too much fat and sugar, but we've underestimated the protein component," Newgard said. And indeed, he said, surveys have shown that most people who overeat don't show any particular prejudice toward one food group or another.
By comparing the metabolic profiles of obese versus lean people in the new study, the researchers found that key among the many differences between the two groups were elevated levels of BCAA in those who were overweight. They also showed that BCAA tend to climb along with insulin resistance, a condition that is a precursor to diabetes. To further explore that correlation, they turned to studies of rats. Those controlled feeding studies revealed that, despite having reduced food intake and a low rate of weight gain equivalent to animals on standard chow, rats that consume more fat and BCAA were as insulin resistant as rats fed an HF diet. When added to a normal mouse diet, extra BCAA didn't result in insulin resistance.
I wonder if this is an artificial result. Does it apply to us eating real world diets? Would it happen with higher general protein diet and not just higher BCAA? Are there foods high in BCAA and low in the other amino acids?
Individuals who eat more red meat and processed meat appear to have a modestly increased risk of death from all causes and also from cancer or heart disease over a 10-year period, according to a report in the March 23 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. In contrast, a higher intake of white meat appeared to be associated with a slightly decreased risk for overall death and cancer death.
"Meat intake varies substantially around the world, but the impact of consuming higher levels of meat in relation to chronic disease mortality [death] is ambiguous," the authors write as background information in the article.
Rashmi Sinha, Ph.D., and colleagues at the National Cancer Institute, Rockville, Md., assessed the association between meat intake and risk of death among more than 500,000 individuals who were part of the National Institutes of Health-AARP Diet and Health Study. Participants, who were between 50 and 71 years old when the study began in 1995, provided demographic information and completed a food frequency questionnaire to estimate their intake of white, red and processed meats. They were then followed for 10 years through Social Security Administration Death Master File and National Death Index databases.
During the follow-up period, 47,976 men and 23,276 women died. The one-fifth of men and women who ate the most red meat (a median or midpoint of 62.5 grams per 1,000 calories per day) had a higher risk for overall death, death from heart disease and death from cancer than the one-fifth of men and women who ate the least red meat (a median of 9.8 grams per 1,000 calories per day), as did the one-fifth of men and women who ate the most vs. the least amount of processed meat (a median of 22.6 grams vs. 1.6 grams per 1,000 calories per day).
When comparing the one-fifth of participants who ate the most white meat to the one-fifth who ate the least white meat, those with high white meat intake had a slightly lower risk for total death, death from cancer and death from causes other than heart disease or cancer.
"For overall mortality, 11 percent of deaths in men and 16 percent of deaths in women could be prevented if people decreased their red meat consumption to the level of intake in the first quintile [one-fifth]. The impact on cardiovascular disease mortality was an 11 percent decrease in men and a 21 percent decrease in women if the red meat consumption was decreased to the amount consumed by individuals in the first quintile," the authors write. "For women eating processed meat at the first quintile level, the decrease in cardiovascular disease mortality was approximately 20 percent."
Processed meat appears to have a more potent effect as compared to red meat. So hot dogs and salami pose substantial risks. Why is that?
Among women, those who ate the most red meat were 36 percent more likely to die for any reason, 20 percent more likely to die of cancer and 50 percent more likely to die of heart disease. Men who ate the most meat were 31 percent more likely to die for any reason, 22 percent more likely to die of cancer and 27 percent more likely to die of heart disease.
In contrast, those who consumed the most white meat were about 8 percent less likely to die during the study period than those who ate the least, the researchers found. Poultry contains more unsaturated fat, which improves cholesterol levels, and fish contains omega-3 fatty acids, which are believed to help reduce the risk of heart disease.
I find the white meat result a little surprising. I wonder what the effect is of eating the dark meat in turkey. I also wonder whether consumption of more omega 3 fatty acids will reduce the harm from eating lots of red meat.
Eating just one more serving of green leafy vegetables or three more servings of fruit a day reduces the risk of developing Type II diabetes, according to results of data analysis performed by researchers in the Tulane School of Public Health and Tropical Medicine and the Harvard School of Public Health. The research team also found that one serving of fruit juice a day increased the risk of Type II diabetes in women.
Age and obesity both increase the risk of insulin resistant diabetes. That type of diabetes, just like the other type where the immune system attacks insulin-producing cells, accelerates the aging of the whole body. You really want to avoid this. Fortunately you can make dietary choices that'll cut your risk of insulin resistant diabetes. Familiar good foods are good for avoiding diabetes as well.
Tulane epidemiologist Dr. Lydia Bazzano says, “Based on the results of our study, people who have risk factors for diabetes may find it helpful to fill up on leafy greens like lettuces, kale and spinach and whole fruits, like apples, bananas, oranges and watermelon rather than drink fruit juices, which deliver a big sugar load in a liquid form that gets absorbed rapidly.”
Eat vegetables. Eat fruits. Then eat more vegetables and some more fruits.
Bazzano, an assistant professor of epidemiology, cautioned that since this is one of the first studies to separate fruit juice consumption from fruits as a whole, the association between juice and diabetes must be confirmed by additional research.
She and her team analyzed 18 years worth of diet and health data from 71,346 nurses who participated in the Nurses’ Health Study from 1984 to 2002. The women were all between 38 and 63 years old and diabetes-free when the study began. Approximately 7 percent of the participants developed diabetes over the course of the study.
According to a recent study published online in The FASEB Journal (http://www.fasebj.org), diets rich in omega-3 fatty acids protect the liver from damage caused by obesity and the insulin resistance it provokes. This research should give doctors and nutritionists valuable information when recommending and formulating weight-loss diets and help explain why some obese patients are more likely to suffer some complications associated with obesity. Omega-3 fatty acids can be found in canola oil and fish.
A reduction in the risk of insulin-resistant diabetes is a big win. Insulin resistance causes many things (higher heart attack risk, faster brain aging, and much more) to go wrong as we age.
"Our study shows for the first time that lipids called protectins and resolvins derived from omega-3 fatty acids can actually reduce the instance of liver complications, such as hepatic steatosis and insulin resistance, in obese people," stated Joan Claria, a professor from the University of Barcelona and one of the researchers involved in the work.
You need your protectins and resolvins.
The scientists found that two types of lipids in omega-3 fatty acids—protectins and resolvins—were the cause of the protective effect. To reach this conclusion, they studied four groups of mice with an altered gene making them obese and diabetic. One group was given an omega-3-enriched diet and the second group was given a control diet. The third group was given docosahexaenoic acid, and the fourth received only the lipid resolvin. After five weeks, blood serum and liver samples from the test mice were examined. The mice given the omega-3-rich diet exhibited less hepatic inflammation and improved insulin tolerance. This was due to the formation of protectins and resolvins from omega-3 fatty acids.
If you demand understanding of a molecular mechanism for why a nutrient will protect you before you will act then now you know the mechanism exists. Get omega 3 fatty acids into your diet.
In the study, published online by the Journal of Clinical Endocrinology and Metabolism, Teff and her collaborators studied 17 obese men and women. Each was admitted two times to the Clinical and Translational Research Center at the University of Pennsylvania. On each admission, the subjects were given identical meals and blood was collected from an intravenous catheter over a 24-hour period. The only difference was the sweetener used in the beverages that accompanied the meals; beverages were sweetened with glucose during one admission and with fructose during the other.
Blood triglyceride levels were higher when subjects drank fructose-sweetened beverages with their meals compared to when they drank glucose-sweetened beverages. The total amount of triglycerides over a 24-hour period was almost 200 percent higher when the subjects drank fructose-sweetened beverages.
Although fructose increased triglyceride levels in all of the subjects, this effect was especially pronounced in insulin-resistant subjects, who already had increased triglyceride levels. Insulin resistance is a pre-diabetic condition often associated with obesity.
What I would like to know: Can eating fruits cause the same effect?
A traditional Mediterranean diet with an additional daily serving of mixed nuts appears to be useful for managing some metabolic abnormalities in older adults at high risk for heart disease, according to a report in the December 8/22 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Avoid insulin resistant diabetes and some other bad changes in your metabolism by eating this diet.
At the beginning of the study, 61.4 percent of the participants met criteria for the metabolic syndrome. After one year, 409 participants in the Mediterranean diet plus olive oil group, 411 in the Mediterranean diet plus nuts group and 404 in the control group of low-fat diet advice were available for evaluation. The prevalence of metabolic syndrome decreased by 13.7 percent among those in the nut group, 6.7 percent in the olive oil group and 2 percent in the control group.
Participants' weight did not change over the one-year period. However, the number of individuals with large waist circumference, high triglycerides or high blood pressure significantly decreased in the Mediterranean diet plus nuts group compared with the control group. This suggests that components of the diet, principally the nuts, may have beneficial effects on pathophysiological characteristics of metabolic syndrome, such as oxygen-related cell damage, resistance to the effects of insulin or chronic inflammation. The Mediterranean diet is high in unsaturated fatty acids; in addition, nuts also contain beneficial nutrients such as fiber, arginine, potassium, calcium and magnesium.
Anybody follow this diet?
Vitamin K slowed the development of insulin resistance in elderly men in a study of 355 non-diabetic men and women ages 60 to 80 who completed a three-year clinical trial at the Jean Mayer Human Nutrition Research Center on Aging at Tufts University (USDA HNRCA).
“Men who received vitamin K supplementation had less progression in their insulin resistance by the end of the clinical trial,” said Sarah Booth, PhD, senior author and director of the Vitamin K Laboratory at the USDA HNRCA. “Conversely, we saw progression in insulin resistance in women who received vitamin K supplementation, and in the men or women who were not given vitamin K supplements.”
Among those given vitamin K, both men and women took daily multivitamins containing 500 micrograms of vitamin K, five times the Adequate Intake (AI) recommended by the Institute of Medicine’s Food and Nutrition Board, with instructions to maintain normal diets without any additional supplementation. They also received a calcium and vitamin D supplement. Men and women in the control group received no vitamin K supplementation but did receive the multivitamin and the calcium and vitamin D supplement. For the present study, insulin resistance was assessed by the homeostasis model (HOMA-IR). Additionally, participants’ blood glucose and blood insulin levels were measured following a minimum 10-hour fast. In addition to improved insulin resistance, the supplemented men had lower blood insulin levels compared to the unsupplemented men at the conclusion of the study.
Insulin resistance will accelerate your aging. Definitely worth avoiding.
The women might have needed a larger vitamin K dose to derive a benefit. Though cutting back on excess weight definitely would have helped.
Writing in the November issue of Diabetes Care, the authors speculate that weight might explain why only the vitamin K supplemented men improved their insulin resistance. “In our study, there was a higher prevalence of obese or overweight women in the vitamin K supplementation group compared to the male supplementation group,” Booth said. “Vitamin K is stored in fat tissue. If there is excess fat, vitamin K may not be readily available to cells that require it to process glucose.”
If you want to max out your dietary vitamin K then eat a cup a day of kale, collards, or spinach. Each will give you over 1000 mcg vitamin K or more than double the amount used in this study. See a longer list of good vitamin K food sources at that link.
Why have Americans been more overweight than other Westerners? We were ahead of them in a trend. Europeans are porking out. This porking trend has extended down into the part of Europe which has been celebrated for the success of its diet: the Mediterranean. Greeks, Italians, and Spaniards are abandoning the Mediterranean diet with unhealthful consequences.
Small towns like this one in western Crete, considered the birthplace of the famously healthful Mediterranean diet — emphasizing olive oil, fresh produce and fish — are now overflowing with chocolate shops, pizza places, ice cream parlors, soda machines and fast-food joints.
The fact is that the Mediterranean diet, which has been associated with longer life spans and lower rates of heart disease and cancer, is in retreat in its home region. Today it is more likely to be found in the upscale restaurants of London and New York than among the young generation in places like Greece, where two-thirds of children are now overweight and the health effects are mounting, health officials say.
We are not designed to handle the fast food diet. Better that the Greeks return to their traditional dishes. Greece now has the worst obesity rate in Europe. Wow.
This spring, a majority of children who were tested at the elementary school of this sleepy port town of 3,000, also known as Kissamos, were found to have high cholesterol. “It was the talk of the school,” said Stella Kazazakou, 44. “Instead of grades, the moms were comparing cholesterol levels.”
In Greece, three-quarters of the adult population is overweight or obese, the worst rate in Europe “by far,” according to the United Nations. The rates of overweight 12-year-old boys rose more than 200 percent from 1982 to 2002 and have been rising even faster since.
Italy and Spain are not far behind, with more than 50 percent of adults overweight. That compares with about 45 percent in France and the Netherlands.
Fresh produce and olive oil can't compete with hamburgers and fries. We need to either genetically engineer ourselves to dislike junk food or we need to genetically engineer our metabolisms to handle junk food without harmful effects.
A scientist at Washington University in St. Louis worked with Calorie Restriction Society members (known as CRONies - Calorie Restriction with Optimal Nutrition) to see whether calorie restriction (CR) would extend life as well in humans as it does in rats and mice. Well, among the CRONies calorie restriction did not lower the level of a growth factor called IGF-1 as well as CR does in mice. This suggests that human calorie restriction might not extend life as much as it does in mice.
St. Louis, Sept. 24, 2008 — Calorie restriction, a diet that is low in calories and high in nutrition, may not be as effective at extending life in people as it is in rodents, according to scientists at Washington University School of Medicine in St. Louis.
Previous research had shown that laboratory animals given 30 percent to 50 percent less food can live up to 50 percent longer. Because of those findings, some people have adopted calorie restriction in the hope that they can lengthen their lives. But the new research suggests the diet may not have the desired effect unless people on calorie restriction also pay attention to their protein intake.
Biogerontology theorist Aubrey de Grey already does not expect CR to extend human life by double digit percentages like it does in rodents. Aubrey argues that CR might extend human life by a year or two as a way to help people live longer to reproduce after a couple of bad growing seasons. The selective pressure on humans about how their metabolism should respond to CR probably didn't produce a capacity for human metabolism to reduce the rate of aging by such a large amount. Besides, we already have many life-extending mutations that mice do not have as we live much longer than they do.
In an article published online this month in the journal Aging Cell, investigators point to a discrepancy between humans and animals on calorie restriction. In the majority of the animal models of longevity, extended lifespan involves pathways related to a growth factor called IGF-1 (insulin-like growth factor-1), which is produced primarily in the liver. Production is stimulated by growth hormone and can be reduced by fasting or by insensitivity to growth hormone. In calorie-restricted animals, levels of circulating IGF-1 decline between 30 percent and 40 percent.
"We looked at IGF-1 in humans doing calorie restriction," says first author Luigi Fontana, M.D., Ph.D., assistant professor of medicine at Washington University and an investigator at the Istituto Superiore di Sanità in Rome, Italy. "For years, we have been following a cohort of people from the CR Society who have been on long-term calorie restriction. We found no difference in IGF-1 levels between people on calorie restriction and those who are not."
Fontana decided that since vegans have much lower IGF-1 levels that perhaps lowering protein intake in CRONies would work to lower IGF-1. Well, yes, it did. So here's the bottom line: maybe reducing protein consumption will allow us to live longer.
Again, Fontana had a ready-made study group. His team has been following a population of strict vegans for several years. They tend to eat less protein than the CRONies from the CR Society, so he compared IGF-1 levels between the two groups.
"The vegans had significantly less circulating IGF-1, even if they were heavier and had more body fat than CRONies," he says. "Protein in the diet seemed to correlate with the lower levels of IGF-1. The strict vegans took in about 10 percent of their total calories from protein, whereas those on calorie restriction tended to get about 23 or 24 percent of calories from protein."
The investigators wanted to take one more look at the relationship between dietary protein and IGF-1, so Fontana asked a group of CRONies to eat less protein for a few weeks. He says it was not easy to cut protein because those on calorie restriction have to do a lot of calculating and juggling to ensure they take in very few calories and still get adequate nutrition. Increasing dietary protein is one way many CRONies guard against becoming malnourished.
"But six of them agreed to lower their protein intake," Fontana explains, "and after three weeks their circulating IGF-1 declined dramatically."
Cutting back on your protein consumption is easier than cutting back on your calories.
Sticking to a full Mediterranean diet provides substantial protection against major chronic diseases including heart disease, cancer and Parkinson's and Alzheimer's disease, according to a study published on bmj.com today.
A 'score' based on adherence to the Mediterranean diet could be used as an effective preventive tool for reducing the risk of premature death in the general population, say the authors.
The Mediterranean diet from populations bordering the Mediterranean Sea has a reputation for being a model of healthy eating and contributing to better health and quality of life. It is rich in olive oil, grains, fruits, nuts, vegetables, and fish, but low in meat, dairy products and alcohol.
Make the grains whole grains and go light on them. Better to get your carbos from beans and other lower glycemic index foods.
People who stuck closest to the diet were healthier.
A team of researchers from the University of Florence assessed 12 international studies, which collectively included more than 1.5 million participants whose dietary habits and health were tracked for follow-up periods ranging from three to 18 years.
All the studies examined the concept of using a numerical score to estimate how much people stuck to the diet, called an 'adherence score'.
The researchers found that people who stuck strictly to a Mediterranean diet had significant improvements in their health, including a 9% drop in overall mortality, a 9% drop in mortality from cardiovascular disease, a 13% reduction in incidence of Parkinson and Alzheimer's disease, and a 6% reduction in cancer.
What vices do you have that pull you away from an ideal diet? Or do you find an ideal diet inconvenient due to work schedule and travel?
Among the 7,000 men and women aged 45 from across England, Scotland and Wales that they studied, those who were smokers, non-drinkers, the overweight and the underweight all reported higher rates of chronic pain.
Among the women, vitamin D levels also appeared to be important.
This finding was not explained by gender differences in lifestyle or social factors, such as levels of physical activity and time spent outdoors, say the authors.
Women with vitamin D levels between 75 and 99 mmol/litre - a level deemed necessary for bone health - had the lowest rates of this type of pain, at just over 8%.
Women with levels of less than 25 mmol/litre had the highest rates, at 14.4%.
Hey, vitamin D is good for you and there's a decent chance you do not have enough of it. Your odds of not getting enough go way up in winter.
Time for another in my continuing saga of why you need to get a lot of vitamin D. While previous studies have found evidence that higher vitamin D concentrations reduce the risk of death Johns Hopkins researchers think their new study is a big and sufficiently well controlled study to finally feel confident that vitamin D cuts death rates.
Researchers at Johns Hopkins are reporting what is believed to be the most conclusive evidence to date that inadequate levels of vitamin D, obtained from milk, fortified cereals and exposure to sunlight, lead to substantially increased risk of death.
In a study set to appear in the Archives of Internal Medicine online Aug. 11, the Johns Hopkins team analyzed a diverse sample of 13,000 initially healthy men and women participating in an ongoing national health survey and compared the risk of death between those with the lowest blood levels of vitamin D to those with higher amounts. An unhealthy deficiency, experts say, is considered blood levels of 17.8 nanograms per milliliter or lower.
Of the 1,800 study participants known to have died by Dec. 31, 2000, nearly 700 died from some form of heart disease, with 400 of these being deficient in vitamin D. This translates overall to an estimated 26 percent increased risk of any death, though the number of deaths from heart disease alone was not large enough to meet scientific criteria to resolve that it was due to low vitamin D levels.
Yet, researchers say it does highlight a trend, with other studies linking shortages of vitamin D to increased rates of breast cancer and depression in the elderly. And earlier published findings by the team, from the same national study, have established a possible tie-in, showing an 80 percent increased risk of peripheral artery disease from vitamin D deficits.
Breast cancer, depression, and peripheral artery disease should be on everyone's list of things to avoid.
Hey, they did a big study and have clearer results than other studies. So they are bragging. But they deserve to brag. So why not?
Researchers note that other studies in the last year or so in animals and humans have identified a connection between low levels of vitamin D and heart disease. But these studies, they say, were weakened by small sample numbers, lack of diversity in the population studied and other factors that limited scientists' ability to generalize the findings to the public at large.
"Our results make it much more clear that all men and women concerned about their overall health should more closely monitor their blood levels of vitamin D, and make sure they have enough," says study co-lead investigator Erin Michos, M.D., M.H.S.
Small amounts of sunlight can make the difference. Though in winter better think about taking a vitamin D pill. Your benefit probably tops out at 2000 IU per day. Though only a blood test would tell you whether you are at the 50 nanograms per milliliter concentration at which benefit is maximized.
Aware of the cancer risks linked to too much time spent in the sun, she says as little as 10 to 15 minutes of daily exposure to the sun can produce sufficient amounts of vitamin D to sustain health. The hormone-like nutrient controls blood levels of calcium and phosphorus, essential chemicals in the body.
If vitamin supplements are used, Michos says there is no evidence that more than 2,000 international units per day do any good. Study results show that heart disease death rates flattened out in participants with the highest vitamin D levels (above 50 nanograms per milliliter of blood), signaling a possible loss of the vitamin's protective effects at too-high doses.
The U.S. Institute of Medicine suggests that an adequate daily intake of vitamin D is between 200 and 400 international units (or blood levels nearing 30 nanograms per milliliter). Previous results from the same nationwide survey showed that 41 percent of men and 53 percent of women are technically deficient in the nutrient, with vitamin D levels below 28 nanograms per milliliter.
Are you still not taking vitamin D? If not, what's your problem? Secret death wish? A feeling of futility? Or maybe you are one of those rare people who like having doctors fuss all over you? In that case it is safer to use fake symptoms. So take the vitamin D anyhow.
Why would alcohol consumption cut the risk of an auto-immune disease? Does alcohol act like an anti-inflammatory and dampen the immune response to inflammation of joints?
Alcohol cuts the risk of developing rheumatoid arthritis by up to 50%, reveals research published ahead of print in the Annals of the Rheumatic Diseases.
The Scandinavian researchers base their findings on more than 2750 people taking part in two separate studies, which assessed environmental and genetic risk factors for rheumatoid arthritis.
Over half the participants (1650) had the disease and had been matched for age, sex, and residential locality with randomly selected members of the general public.
All participants were quizzed about their lifestyle, including how much they smoked and drank. And blood samples were taken to check for genetic risk factors.
The results showed that drinking alcohol was associated with a significantly lower risk of developing rheumatoid arthritis. And the more alcohol was consumed, the lower the risk of rheumatoid arthritis.
Among those who drank regularly, the quarter with the highest consumption were up to 50% less likely to develop the disease compared with the half who drank the least.
Rheumatoid arthritis (RA) is definitely a disease you want to avoid. Not only does it cause lots of pain. But this auto-immune disease appears to do wider damage. RA sufferers have a much greater risk of heart disease.
The researchers found that while 85 percent of the RA patients between the ages of 50 and 59 had an intermediate or high risk for developing heart disease within 10 years of diagnosis, just 27 percent of comparable non-RA patients did. Among patients between the ages of 60 and 69 at the start of the study, 100 percent of the RA patients had an intermediate or high risk for heart disease, compared with 79 percent of non-RA patients.
When looking at just "high risk" among the 60 to 69 age group, the difference was even more dramatic: 85 percent for RA patients, compared to just 40 percent for non-RA patients.
The researchers concluded that more than half of RA patients 50 to 59, and all RA patients over the age of 60, had a 10 percent or greater risk of developing heart disease within 10 years of an RA diagnosis.
An earlier report found a doubling to tripling of heart disease risk from rheumatoid arthritis.
Aside from drinking alcohol what else can you do to cut your RA risks? Turns out that vitamin D consumption is strongly inversely correlated with rheumatoid arthritis risk.
Life extension can't be found in most vitamin pills. But note they do not mention vitamin D.
Many people take antioxidants in the belief that they will prolong their life expectancy. However, data from 67 randomised trials that involved just under a quarter of a million people failed to support this idea, a Cochrane Systematic Review has discovered.
“We could find no evidence to support taking antioxidant supplements to reduce the risk of dying earlier in healthy people or patients with various diseases,” says Goran Bjelakovic, visiting researcher, who performed the systematic review at the Copenhagen Trial Unit at the Copenhagen University Hospital in Denmark.
The idea that antioxidants can extend life comes from human and animal laboratory research and has been boosted by some observational clinical studies. But other studies have indicated neutral or even harmful effects.
Cochrane reviews are based on peer reviewed published protocols that aim to identify randomised, published and unpublished, trials. Following Cochrane methodology, relevant data are extracted and pooled together from the identified trials, which are also assessed and subdivided into unbiased and biased in terms of methodology of their conductance, so that unbiased assessments of intervention effects can be conducted.
“The findings of our review show that if anything, people in trial groups given the antioxidants beta-carotene, vitamin A, and vitamin E showed increased rates of mortality. There was no indication that vitamin C and selenium may have positive or negative effects. So regarding these antioxidants we need more data from randomised trials,” says Bjelakovic. “The bottom line is that current evidence does not support the use of antioxidant supplements in the general healthy population or in patients with certain diseases.”
Nutrition still matters. Lots of types of food can cause harm. Charbroiled beef and foods with high glycemic index can cut your life expectancy while vegetables, fruits, and beans can keep you healthy longer. Try to eat good food while we wait for the biotechnological revolution to deliver real rejuvenating therapies. Within a couple of decades I expect life extension will come from stem cell therapies and gene therapies. We should try harder to make that real effective rejuvenation therapies come sooner.
I'm glad to see some medical experts have taken the time to write up a review of the lack of evidence for the claims that many glasses of water per day help you stay healthy. The idea that high water consumption delivers a health benefit is just a legend.
Washington, DC (Friday, March 28, 2008) — A recent look at what is known about the health effects of drinking water reveals that most supposed benefits are not backed by solid evidence. The findings indicate that most people do not need to worry about drinking their recommended 8 glasses of 8 ounces (“8x8”) of water per day. The editorial is published in the June 2008 issue of the Journal of the American Society of Nephrology (JASN).
While it is clear that humans cannot survive for longer than several days without water, very little research has assessed how average individuals’ health is affected by drinking extra fluids. Experts have claimed that ingesting water is helpful for everything from clearing toxins and keeping organs healthy to warding off weight gain and improving skin tone.
To investigate the true benefits of drinking water, Dan Negoianu, MD, and Stanley Goldfarb, MD, of the Renal, Electrolyte, and Hypertension Division at the University of Pennsylvania, in Philadelphia, PA, reviewed the published clinical studies on the topic. They found solid evidence that individuals in hot, dry climates, as well as athletes, have an increased need for water. In addition, people with certain diseases benefit from increased fluid intake. But no such data exist for average, healthy individuals. In addition, no single study indicates that people need to drink the recommended “8x8” amount of water each day. Indeed, it is unclear where this recommendation came from.
This scan of the literature included a look at studies related to the notion that increased water intake improves kidney function and helps to clear toxins. A variety of studies reveal that drinking water does have an impact on clearance of various substances by the kidney, including sodium and urea. However, these studies do not indicate any sort of clinical benefit that might result.
I've tried telling co-workers that their water habits were just the stuff of urban legends. But they were thoroughly wedded to their legends and kept on drinking. So just where did this urban legend originate? Maybe in some diet (wash that fat away) for losing weight? Or as part of some 1960s or 1970s fad about body detoxing?
How many weeks has it been since I last nagged you about how most of you don't get enough vitamin D? Vitamin D, which helps the immune system function better, seems to cut the incidence of the autoimmune disorder type 1 diabetes.
Vitamin D supplements in early childhood may ward off the development of type 1 diabetes in later life, reveals a research review published ahead of print in the Archives of Disease in Childhood.
Type 1 diabetes is an autoimmune disorder, in which insulin producing beta cells in the pancreas are destroyed by the body’s own immune system, starting in early infancy. The disease is most common among people of European descent, with around 2 million Europeans and North Americans affected.
Its incidence is rising at roughly 3% a year, and it is estimated that new cases will have risen 40% between 2000 and 2010.
A trawl of published evidence on vitamin D supplementation in children produced five suitable studies, the pooled data from which were re-analysed.
The results showed that children given additional vitamin D were around 30% less likely to develop type 1 diabetes compared with those not given the supplement.
Vitamin D also might cut your risk of the autoimmune disease rheumatoid arthritis (and see here too). Risk of Multiple Sclerosis also appears inversely associated with blood vitamin D levels. Avoid autoimmune disorders. Get enough vitamin D.
Eat your broccoli! That's the advice from UCLA researchers who have found that a chemical in broccoli and other cruciferous vegetables may hold a key to restoring the body's immunity, which declines as we age.
Published in this week's online edition of the Journal of Allergy and Clinical Immunology, the study findings show that sulforaphane, a chemical in broccoli, switches on a set of antioxidant genes and enzymes in specific immune cells, which then combat the injurious effects of molecules known as free radicals that can damage cells and lead to disease.
Immune system aging sets you up for getting killed by pneumonia or flu or a bacterial infection picked up while at a hospital. In fact immune system aging probably makes us more vulnerable to cancer and people with especially capable immune systems are probably at much lower risk of getting cancer. So keeping your immune system younger yields a big benefit.
The UCLA team not only found that the direct administration of sulforaphane in broccoli reversed the decline in cellular immune function in old mice, but they witnessed similar results when they took individual immune cells from old mice, treated those cells with the chemical outside the body and then placed the treated cells back into a recipient animal.
In particular, the scientists discovered that dendritic cells, which introduce infectious agents and foreign substances to the immune system, were particularly effective in restoring immune function in aged animals when treated with sulforaphane.
"We found that treating older mice with sulforaphane increased the immune response to the level of younger mice," said Hyon-Jeen Kim, first author and research scientist at the Geffen School.
To investigate how the chemical in broccoli increased the immune system's response, the UCLA group confirmed that sulforaphane interacts with a protein called Nrf2, which serves as a master regulator of the body's overall antioxidant response and is capable of switching on hundreds of antioxidant and rejuvenating genes and enzymes.
Nel said that the chemistry leading to activation of this gene-regulation pathway could be a platform for drug discovery and vaccine development to boost the decline of immune function in elderly people.
Sulforaphane concentration in broccoli sprout (1153 mg/100 g dry weight) was about 10 times higher than that of mature broccoli (44-171 mg/100 g dry weight).
Extracts of 3-day-old broccoli sprouts (containing either glucoraphanin or sulforaphane as the principal enzyme inducer) were highly effective in reducing the incidence, multiplicity, and rate of development of mammary tumors in dimethylbenz(a)anthracene-treated rats. Notably, sprouts of many broccoli cultivars contain negligible quantities of indole glucosinolates, which predominate in the mature vegetable and may give rise to degradation products (e.g., indole-3-carbinol) that can enhance tumorigenesis. Hence, small quantities of crucifer sprouts may protect against the risk of cancer as effectively as much larger quantities of mature vegetables of the same variety.
Some Johns Hopkins researchers have even founded a company that sells teas fortified with sulforaphane.
CORVALLIS, Ore. – A new study done with mice has discovered that supplements of lipoic acid can inhibit formation of arterial lesions, lower triglycerides, and reduce blood vessel inflammation and weight gain – all key issues for addressing cardiovascular disease.
Lipoic acid is involved in energy metabolism. Possibly it delivers a benefit by keeping energy generation up in cells in the circulatory system. Imagine we had a better way to keep up energy generation, for example a gene therapy that could replace damaged mitochondrial genes as we age. Well, our blood vessels might remain unclogged for decades longer.
Although the results cannot be directly extrapolated beyond the laboratory, researchers report that “they strongly suggest that lipoic acid supplementation may be useful as an inexpensive but effective intervention strategy . . . reducing known risk factors for the development of atherosclerosis and other inflammatory vascular diseases in humans.”
The findings were made by scientists from the Linus Pauling Institute and College of Veterinary Medicine at Oregon State University, and the Department of Medicine at the University of Washington. They were just published in Circulation, a journal of the American Heart Association.
Heart disease is the leading cause of death in the United States.
The study found that lipoic acid supplements reduced atherosclerotic lesion formation in two types of mice that are widely used to study cardiovascular disease, by 55 percent and 40 percent, respectively. The supplements were also associated with almost 40 percent less body weight gain, and lower levels of triglycerides in very low-density lipoproteins.
The reduced body weight gain: Do we gain weight as we age because our metabolisms slow down?
The dose used is the equivalent of 2 grams per day for humans. Mind you, your own arteries might be clean and you ought to eat a better diet of the sort that reduces cardiovascular (and cancer) risk before taking lipoic acid.
Alpha lipoic acid is a naturally occurring nutrient found at low levels in green leafy vegetables, potatoes and meats, especially organ meats such as kidney, heart or liver. The amounts used in this research would not be obtainable by any normal diet, researchers said, and for human consumption might equate to supplements of about 2,000 milligrams per day. Even at low, normal, dietary levels, the compound can play a key role in energy metabolism.
I would rather have gene therapies and cell therapies that turn back the biological clock than take vitamins and other nutrients in pills.
Time for another study on the benefits of vitamin D. The D2 form of vitamin D appears to reduce the frequency of falls among older women.
Vitamin D2 supplements appear to reduce the risk of falls among women with a history of falling and low blood vitamin D levels living in sunny climates, especially during the winter, according to a report in the January 14 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
“Approximately one-third of women older than 65 years fall each year, and 6 percent sustain a fracture as a result of the fall,” the authors write as background information in the article. “In addition, fear of falling is a major problem in older people.”
Richard L. Prince, M.D., of the Sir Charles Gairdner Hospital, Nedlands, Australia, and colleagues conducted a year-long clinical trial of 302 women age 70 to 90 years living in Perth, Australia. Because vitamin D is produced in response to sun exposure and the study was completed in a sunny climate, the researchers selected women with blood vitamin D levels below the median for the area (24 nanograms per milliliter). All participants had a history of falling in the previous year and received 1,000 milligrams of calcium citrate per day. Half were then randomly assigned to take either 1,000 international units of vitamin D2 (ergocalciferol) and half took an identical placebo. Data on falls were collected from participants every six weeks.
Eighty women (53 percent) in the vitamin D2 group and 95 women (62.9 percent) in the control group fell at least once during the study period. After adjusting for height, which affected the risk of falling and was significantly different between the two groups, vitamin D2 therapy reduced the risk of having at least one fall by 19 percent. “When those who fell were grouped by the season of first fall or the number of falls they had, ergocalciferol treatment reduced the risk of having the first fall in winter and spring but not in summer and autumn, and reduced the risk of having one fall but not multiple falls,” the authors write.
There is the falling. But there are also the injuries sustained by the falling. There is the substantial possibility that the vitamin D supplementation will reduce the risks of bone breakage per fall as well as reducing the risk of falling in the first place.
These results imply that older folks are at greater risk of falling down in the fall and winter. Interesting.
“It is interesting that the ergocalciferol therapy effect was confined to those who were to sustain one fall but not those destined to have more than one fall,” the authors write. “Older people who fall frequently tend to have more risk factors for falling, including greater degrees of disability and poorer levels of physical function.” It is possible that chemically correcting vitamin D levels in the blood is insufficient to prevent falls in these individuals, they note. “Ergocalciferol, 1,000 international units per day, added to a high calcium intake is associated with 23 percent reduction of the risk of falling in winter/spring to the same level as in summer/autumn,” the authors conclude.
In the comments section of my post on the value of vitamin D as D2 or D3 a researcher from UCSD pointed out that the study in that post doesn't prove the stated conclusion of the study. Well, be aware that when reading these sorts of posts that we aren't necessarily seeing the critical reactions to the studies (though in that case we did). Still, enough of the benefits of vitamin D are well established that even if some of the theorized benefits don't hold up getting more of the nutrient looks like a big benefit for most people in industrialized societies.
If you've been persuaded (certainly I've tried) that you need more vitamin D maybe (but probably not) you've wondered what form of vitamin D you should take. Well renowned vitamin D researcher Michael Holick, PhD, MD, basically has found that you can take vitamin D as D2 or D3 without worrying which is more potent.
Boston, MA— Researchers from Boston University School of Medicine (BUSM) have found that vitamin D2 is equally as effective as vitamin D3 in maintaining 25-hydroxyvitamin D status. The study appears online in the December 2007 issue of the Journal of Clinical Endocrinology & Metabolism.
Researchers studied healthy adults aged 18-84 who received either placebo, 1,000 International Units (IU) of vitamin D3, 1,000 IU of vitamin D2, or 500 IU of vitamin D2 plus 500 IU of vitamin D3 daily for three months at the end of winter to establish what effect it had on circulating levels of total 25 (OH)D as well as 25(OH)D2 and 25(OH)D3. Sixty percent of the adults were vitamin D deficient at the start of the study.
Adults who received the placebo capsule daily for three months demonstrated no significant change in their total 25(OH)D levels during the winter and early spring. Adults who ingested 1,000 vitamin D2/d gradually increased their total 25(OH)D levels during the first six weeks. Adults who ingested 1,000 IU of vitamin D3 had a baseline 25(OH)D that was statistically no different from the baselines of either the placebo group or the groups that took 1,000 IU of vitamin D2/d or 500 IU vitamin D2 plus 500 IU vitamin D3/d. The vitamin D3 group increased their serum 25(OH)D levels similar to that of the group that ingested vitamin D2.
The circulating levels of 25-hydroxyvitamin D increased to the same extent in the groups that received 1,000 IU daily as vitamin D2, vitamin D3, or a combination of 500 IU vitamin D2 and 500 IU vitamin D3. The 25-hydroxyvitamin D3 levels did not change in the group that received 1,000 IU vitamin D2 daily. One thousand IU of vitamin D2 or vitamin D3 did not raise 25-hydroxyvitamin D levels in vitamin D deficient subjects above 30 ng/ml.
Even if you haven't wondered about this particular burning vitamin D research question at least this serves as a reminder that vitamin D probably will reduce your odds of cancer, auto-immune disorders, infections, osteoporosis, and assorted other maladies.
Mormons have less heart disease — something doctors have long chalked up to their religion's ban on smoking. New research suggests that another of their "clean living" habits also may be helping their hearts: fasting for one day each month.
A study in Utah, where the Church of Jesus Christ of Latter-Day Saints is based, found that people who skipped meals once a month were about 40 percent less likely to be diagnosed with clogged arteries than those who did not regularly fast.
Thanks to James Bowery for the tip.
Though more than 90% of the people studied were Mormons, the findings held true even in those who had a different religious preference, says Benjamin D. Horne, PhD, director of cardiovascular and genetic epidemiology at Intermountain Medical Center in Salt Lake City.
Yes friends, even you can benefit. Step right up and choose your day to go hungry. I'm thinking the fasting day needs to be a day where there's a whole lot of constant distraction so you don't have to spend the day thinking how hungry you are. Maybe we need fasting amusement parks where you spend all day riding roller coasters.
The research was conducted at LDS Hospital using the Intermountain Heart Collaborative Study registry, made up of patients who had heart angiography between 1994 and 2002. The researchers focused on patients who are LDS to see if other church-dictated practices besides not smoking had an impact, said Benjamin Horne, director of cardiovascular and genetic epidemiology, now at the new Intermountain Medical Center. He's also an adjunct professor at the University of Utah.
Researchers looked at data from more than 4,600 people, average age 64, who had come through the cardiac cath lab, to see the degree of risk for someone who was LDS compared to others. They focused on those with obvious coronary artery disease (CAD), defined as 70 percent narrowing or blockage in at least one artery, and those who had little or no CAD (less than 10 percent narrowing). They found that while 66 percent of others had CAD, only 61 percent of LDS members did.
I am going to found a church which preaches a high vegetable, high fruit, and low glycemic index diet. Maybe call it the SENS Church for Strategies for Engineered Negligible Senescence Church. I need to find a barrel to look into to receive divine messages. What are my prospects for success?
SENS believers, you've got to suffer hunger pangs once a month to survive until the redemption of rejuvenation therapies. Once we receive the rejuvenation therapies we will enter the promised land of no harm daily Roman style feasts.
Instead of avoiding fats it probably makes a lot more sense to eat less carbo.
Eating foods high on the glycemic index, which measures the effect of carbohydrates on blood glucose levels, may be associated with the risk for developing type 2 diabetes in Chinese women and in African-American women, according to two studies in the November 26 issue of Archives of Internal Medicine, one of the JAMA/Archives journals. However, eating more cereal fiber may be associated with a reduced risk for type 2 diabetes in African-American women.
Researchers remain uncertain regarding exactly how diet, including carbohydrate intake, affects the development of type 2 diabetes, according to background information in the articles. Studies have revealed that the body absorbs carbohydrates from different foods at different rates. This leads to varying effects on levels of blood glucose and the hormone insulin, which converts glucose into energy. Foods high on the glycemic index, such as rice and other simple carbohydrates, cause a rapid spike and then a drop in blood glucose, whereas high-fiber foods tend to be lower on the glycemic index and have a more gradual effect. Some evidence has linked high–glycemic index foods with the risk of developing type 2 diabetes.In one study, Supriya Krishnan, D.Sc., of Boston University School of Public Health, and colleagues examined data from 40,078 U.S. black women who filled out a food questionnaire in 1995. The glycemic index and glycemic load—a measure of the amount of carbohydrates from glucose—were calculated. Every two years through 2003, the women answered follow-up questionnaires about their weight, health and other factors.
A high carbohydrate diet with high glycemic index foods almost doubled the risk of type 2 insulin resistant diabetes.
During the study, 1,608 of the women developed diabetes. Women who consumed more carbohydrates overall were more likely to develop diabetes—when they were split into five groups based on carbohydrate intake, those in the group consuming the most (about 337.6 grams per day) had a 28 percent higher risk than those in the group consuming the least (about 263.5 grams per day). Women who ate diets with a higher glycemic index and who ate more staples such as bread, noodles and rice specifically also had an increased risk. Women who ate 300 grams or more of rice per day were 78 percent more likely to develop diabetes than those who ate less than 200 grams per day.
Chinese women who eat more rice are at higher risk of type 2 diabetes mellitus. Cut way back on grains consumption. If you eat grains then at least eat whole grains. Also, pasta is lower in glycemic index than bread. Check out this long list of foods and their glycemic index values. Shift toward beans and away from grains. Eat more fruits and vegetables and nuts. Also see this cool sortable database of glycemic index and glycemic load of foods.
WASHINGTON, D.C. (November 8, 2007)- There is a new reason for the 76 million baby boomers to grab a glass of milk. Vitamin D, a key nutrient in milk, could have aging benefits linked to reduced inflammation, according to a new study published in the American Journal of Clinical Nutrition.
In a genetic study of more than 2,100 female twin pairs ages 19-79, British and American researchers found that higher vitamin D levels were linked to improved genetic measures of lifelong aging and chronic stress. Using a genetic marker called leukocyte telomere length (LTL), they found those with the highest vitamin D levels had longer LTL, indicating lower levels of inflammation and body stress. The telomere difference between those with the highest and lowest vitamin D levels was equivalent to 5 years of aging.
Previous research has found that shortened LTL is linked to risk for heart disease and could be an indication of chronic inflammation – a key determinant in the biology of aging. While there are several lifestyle factors that affect telomere length (obesity, smoking and lack of physical activity), the researchers noted that boosting vitamin D levels is a simple change to affect this important marker.
Why use telomere length as a proxy for aging and stress? See my post Telomere Length Indicates Mortality Risk.
Also see my posts Chronic Stress Accelerates Aging As Measured By Telomere Length and Telomeres Wear Down Quicker In Men Than Women. Don't stress out guys. It is slowly killing you.
Approximately one in four patients who suffer from chronic pain also have inadequate blood levels of vitamin D, possibly contributing to their ongoing pain, according to a new study. Patients lacking sufficient vitamin D also required higher doses of morphine for a longer period of time.
Researchers recorded the serum vitamin D levels of 267 adults undergoing outpatient treatment for chronic pain, as well as their pain medication (morphine) dose and duration of use, and physical and general health functioning.
Of the patients tested, 26 percent had vitamin D inadequacy. Among these patients, the morphine dose was nearly twice that of the group with adequate vitamin D levels. In addition, the vitamin D inadequacy group used morphine for an average of 71.1 months versus 43.8 months. The vitamin D deficient group also reported lower levels of physical functioning and had a poorer view of their overall health.
It has long been known that inadequate levels of vitamin D can cause pain and muscle weakness, according to the study author, W. Michael Hooten, M.D., medical director, and anesthesiologist at Mayo Comprehensive Pain Rehabilitation Center, Rochester, Minnesota. Previous studies also have suggested that pain-related symptoms of vitamin D inadequacy respond poorly to pain medications.
I think its been a few weeks since I last gave you all a reason to get more vitamin D in your body. Is this nagging doing any good?
HONOLULU, Sept. 20 – Women with low levels of vitamin D have an increased risk of hip fracture, according to a study led by the University of Pittsburgh Graduate School of Public Health presented this week at the 29th annual meeting of the American Society for Bone and Mineral Research at the Hawaii Convention Center.
Jane A. Cauley, Dr.P.H., professor of epidemiology, and colleagues evaluated patient data on 400 women enrolled in the Women’s Health Initiative Observational Study Cohort who had experienced hip fracture, confirmed by their medical record, over a median of 7.1 years. Levels of 25 hydroxyvitamin D, an indicator of vitamin D status, in the bloodstream were measured for these patients and compared with those of a control group matched for age, race, ethnicity and the date of relevant blood work. As vitamin D concentrations decreased, the risk of hip fractures climbed.
“The risk of hip fractures was 77 percent higher among women whose 25 hydroxyvitamin D levels were at the lowest concentrations,” said Dr. Cauley, who has spent much of the past 15 years investigating the physical changes that take place in postmenopausal women. “This effect persisted even when we adjusted for other risk factors such as body mass index, family history of hip fracture, smoking, alcohol use and calcium and vitamin D intake.”
Vitamin D deficiency might well cause more damage than any other nutrient deficiency in industrialized countries.
Juvenile onset type 1 diabetes is an auto-immune disease where the body's immune cells attack pancreatic cells that make insulin. Omega-3 fatty acids, which are known to have anti-inflammatory properties, appear to substantially reduce risk of type 1 diabetes.
Preliminary research suggests that in children at increased risk for type 1 diabetes, dietary intake of omega-3 fatty acids was associated with a reduced risk of pancreatic islet autoimmunity, which is linked to the development of diabetes, according to an article in the Sept. 26 issue of JAMA.
“Type 1 diabetes mellitus is an autoimmune disease that is characterized by the destruction of insulin-producing beta cells in the pancreatic islets. Although it is not yet known what initiates the autoimmune process, it is likely that both genetic background and environmental factors contribute to the disease process,” the authors write. Certain dietary factors have been associated with the onset of type 1 diabetes as well as the autoimmune process that leads to the disease.
Jill M. Norris, M.P.H., Ph.D., of the University of Colorado at Denver and Health Sciences Center, Denver, and colleagues examined whether consumption of omega-3 and omega-6 fatty acids are associated with the development of pancreatic islet autoimmunity (IA; development of antibodies against the cells in pancreas that produce insulin) in children. The study, conducted between 1994 and 2006, included 1,770 children at increased risk for type 1 diabetes, defined as either possession of a high diabetes risk HLA (human leukocyte antigen) genotype or having a sibling or parent with type 1 diabetes. The average age at follow-up was 6.2 years. Islet autoimmunity was assessed in association with reported dietary intake of polyunsaturated fatty acids starting at age 1 year. Fish is the primary source of marine polyunsaturated fatty acids. Childhood diet was measured using a food frequency questionnaire (FFQ).
A case-cohort study (n = 244) was also conducted in which risk of IA by polyunsaturated fatty acid content of erythrocyte membranes (outer portion of the red blood cell) was examined.
Fifty-eight children became positive for IA during follow-up. Adjusting for HLA genotype, family history of type 1 diabetes, caloric intake, and total omega-6 fatty acid intake, total omega-3 fatty acid intake was inversely associated with IA risk (a 55 percent reduced risk). The association was strengthened when the definition of the outcome was limited to those positive for two or more autoantibodies. In the case-cohort study, omega-3 fatty acid content of erythrocyte membranes was associated with a 37 percent decreased risk of IA.
Children who eat fish are also getting more vitamin D and hence might have less auto-immune disease for that reason. It has long been noticed that in the United States the incidence of multiple sclerosis (such is very likely an auto-immune disorder) is higher at northern latitudes. Further north people spend more time in-doors and get less vitamin D made in their skin as a result of sunlight hitting their skin. So the effect here might not entirely come from the omega-3 fatty acids. Either way, this result is an argument for eating fish. The research on omega 3 fatty acids and chronic inflammatory diseases also supports the idea that fish oil delivers real benefit.
Parents were surveyed annually about what their children ate and children were tested for specific antibodies in the blood that marked the destruction of the cells that make insulin (i.e. diabetes autoimmunity). In a subset of this population, the researchers also examined whether risk of diabetes autoimmunity was associated with omega-3 fatty acid content of red blood cell membranes, which is a marker of omega-3 fatty acid status.
Of the children followed, those who reported eating more omega-3 fatty acids were less likely to develop diabetes autoimmunity. The investigators also showed that omega-3 fatty acid content of red blood cell membranes was inversely associated with risk of diabetes autoimmunity.
I go out of my way to make sure I get enough omega 3 fatty acids and eat salmon several times a week. Suggest you do the same.
Time for yet another FuturePundit post on why vitamin D is probably the best nutrient to take as a supplement. A meta-analysis of 18 randomized controlled trials using vitamin D supplements found a 7% lower risk of death among vitamin D supplement users.
Individuals who take vitamin D supplements appear to have a lower risk of death from any cause over an average follow-up time of six-years, according to a meta-analysis of 18 previously published studies in the September 10 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Past studies have suggested that deficiencies in vitamin D might be associated with a higher risk of death from cancer, heart disease and diabetes—illnesses that account for 60 percent to 70 percent of deaths in high-income nations, according to background information in the article. “If the associations made between vitamin D and these conditions were consistent, then interventions effectively strengthening vitamin D status should result in reduced total mortality,” the authors write.
Philippe Autier, M.D., of the International Agency for Research on Cancer, Lyon, France, and Sara Gandini, Ph.D., of the European Institute of Oncology, Milano, Italy, searched for randomized controlled trials of vitamin D supplements published before November 2006. They analyzed 18 separate trials that included 57,311 participants and evaluated doses of vitamin D ranging from 300 to 2,000 international units, with an average dose of 528 international units. Most commercially available supplements contain between 400 and 600 international units.
Over an average follow-up period of 5.7 years, 4,777 of the participants died. Individuals who took vitamin D had a 7 percent lower risk of death than those who did not. In the nine trials that collected blood samples, those who took supplements had an average 1.4- to 5.2-fold higher blood level of vitamin D than those who did not.
The reduction in all cause mortality suggests that vitamin D doesn't just reduce one risk while boosting another. Too many things that might help in some ways end up hurting in other ways. Vitamin D looks like a big net benefit.
Aside from vitamin D I'm hard pressed to think of a single vitamin that holds the promise of such a large benefit if taken as a supplement by most people in developed countries. Most likely you could do much better for your health by eating more vegetables and fruits than by taking any other vitamin.
Vitamin D deficiency early in pregnancy is associated with a five-fold increased risk of preeclampsia, according to a study from the University of Pittsburgh Schools of the Health Sciences reported this week in the Journal of Clinical Endocrinology and Metabolism.
The Hannaford Brothers Company grocery store chain in Maine tried putting stars on foods (the more stars the better the food) to steer customers toward healthier food choices. Given better information about the health benefits of foods while in grocery stores customers will select healthier meats but won't buy more vegetables.
After analyzing a year’s worth of sales data, Hannaford found that customers tended to buy leaner cuts of meat. Sales of ground beef with stars on their labels increased 7 percent, and sales of chicken that had a star rating rose 5 percent. Sales of ground beef labeled with no stars dropped by 5 percent, while sales of chicken that had a zero-star rating declined 3 percent. Similarly, sales of whole milk, which received no stars, declined by 4 percent, while sales of fat-free milk (three stars) increased 1 percent. Sales of fruits and vegetables, however, remained about the same as they did before the ratings were introduced. All fresh produce received stars.
People ask me to write a post describing the ideal diet. Well, the best thing you can do to improve your health is to eat lots more vegetables and fruits and less of just about everything else. But people want fats and red meat and starchy foods. They don't want vegetables. This latest result demonstrates this basic problem with the human diet. We have food instincts that are aimed at ensuring survival in environments where food is in short supply. So our instincts lead us to eat foods which are far from optimal for us today.
Antioxidant vitamins C, E, and beta carotene failed to cut risk of heart attacks in women. (but remember that you probably need more vitamin D)
Vitamins C and E and beta carotene, either individually or in combination, do not appear to reduce the risk of cardiovascular events or death among women at high risk for heart disease, according to a report in the August 13/27 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
The search for why vegetables and fruits improve your health isn't finding that antioxidant vitamins are the cause.
Oxidative damage—harm to cells caused by exposure to oxygen—may contribute to the development of cardiovascular disease, according to background information in the article. In addition, compounds known as free radicals may damage artery linings, encourage blood clots and alter the function of blood vessels. “Antioxidants scavenge free radicals and limit the damage they can cause,” the authors write. “Diets high in fruit and vegetable intake, and thus rich in such antioxidants, have been associated with reduced rates of coronary heart disease and stroke. Vitamins C and E and beta carotene are potential mediators of the apparent protective effect of a plant-based diet on cardiovascular disease.”
Nancy R. Cook, Sc.D., of Brigham & Women’s Hospital and Harvard Medical School, Boston, and colleagues tested the effects of these compounds in the Women’s Antioxidant Cardiovascular Study, which followed 8,171 women 40 years or older (average age 60.6) beginning in 1995 to 1996. The women, who either had a history of cardiovascular disease or three or more risk factors, were randomly assigned to take 500 milligrams of ascorbic acid (vitamin C) or placebo every day; 600 international units of vitamin E or placebo every other day; and 50 milligrams of beta carotene or placebo every other day. Participants were followed up for the occurrence of heart events (including stroke, heart attack and bypass surgery) or death through 2005.
Vitamin C and E in combination might cut risk of stroke.
During the average study period of 9.4 years, 1,450 women had one or more cardiovascular events, including 274 heart attacks, 298 strokes, 889 coronary revascularization procedures (bypass surgery or angioplasty) and 395 cardiovascular deaths (out of a total 995 deaths). “There was no overall effect of ascorbic acid, vitamin E or beta carotene on the primary combined end point or on the individual secondary outcomes of myocardial infarction, stroke, coronary revascularization or cardiovascular disease death,” the authors write. “There were no significant interactions between agents for the primary end point, but those randomized to both active ascorbic acid and vitamin E experienced fewer strokes.”
While scientists try to figure out what exactly in fruits and vegetables extend the lives of many people your best bet is to eat more fruits and vegetables. Vegetables are boring. But vegetables are good for you. They are probably good for you for the same reason they are boring: They have low glycemic index and so do not taste as sweet as other higher glycemic index foods. Also, their fibers have tastes that aren't as appealing as starchy grains. If you want to live longer then find ways to make vegetables more palatable.
If you can't find it in you to eat lots of vegetables (and few people can) then you should find the time to promote accelerated research into the development of therapies that reverse the damage caused by eating lots of meat and grains. Donate to research. Ask your government to fund more research into stem cells and gene therapy. Invest in biotech start-ups.
Scientists have provided new evidence that using more fish oil than vegetable oil in the diet decreases the formation of chemicals called prostanoids, which, when produced in excess, increase inflammation in various tissues and organs. The results, by William L. Smith, Professor and Chair of Biological Chemistry at the University of Michigan, Ann Arbor, and colleagues, may help in designing new anti-inflammatory drugs with fewer side effects than the ones currently available.
“Prostanoids help control blood pressure, fight allergies, and modulate inflammation, but too much of them – especially those made from vegetable oils – can also lead to increased pain, swelling, and redness in various tissues,” Smith says. “Our study shows that prostanoids made from fish oil are less effective at causing pain and swelling than those made from vegetable oil and that adding fish oil to the diet decreases the amount of prostanoids made from vegetable oil.”
Increased expression of genes involved in inflammation is one of the characteristics of aging tissues. Reducing the extent of this age-related inflammation will probably yield health dividends.
The experiments were done with cell cultures.
Smith and colleagues looked at the mutual effects of both oils by changing their respective amounts in cultured cells. As expected, a relative increase in fish oil lowered the amount of prostanoids from vegetable oil, although not always in the expected proportions.
Both fish and vegetable oils are converted into prostanoids through chemical reactions that are aided by enzymes called cyclo-oxygenases (COX), two types of which – COX-1 and COX-2 – are involved in the reactions. The scientists showed that, in reactions involving COX-1, when more fish oil is present, it preferentially binds to COX-1, thus limiting vegetable oil’s access to this enzyme. But in reactions involving COX-2, increasing the amount of fish oil did not change the way it binds to COX-2, so a significant portion of vegetable oil was still converted to prostanoids.
Eat more fish oils to get more omega 3 fatty acids. Also, eat less corn oil and other oils which have more omega 6 fatty acids.
Free radicals and other types of reactive oxygen species (ROS) will accelerate aging if present in higher than optimal concentrations. Flavonoids in orange juice quench reactive oxygen species (ROS)
BUFFALO, N.Y. -- Orange juice, despite its high caloric load of sugars, appears to be a healthy food for diabetics due to its mother lode of flavonoids, a study by endocrinologists at the University at Buffalo has shown.
But some reactive oxygen species (ROS) are needed to carry out basic metabolic functions. So would consumption of too much flavonoids make one lethargic?
Consumption of glucose sugar boosts blood ROS. That spike in ROS is probably harmful and best avoided. So one should probably prefer foods that one can eat without getting the ROS spike.
"Many major diseases are associated with oxidative stress and inflammation in the arterial wall, so the search for foods that are least likely to cause these conditions must be pursued," said Paresh Dandona, M.D., Ph.D., head of the Diabetes-Endocrinology Center of Western New York and senior author on the study.
"Our previous work has shown that 300 calories of glucose induces ROS and other proinflammatory responses," said Dandona, who is Distinguished Professor of Medicine in the UB School of Medicine and Biomedical Sciences.
Orange juice did not boost blood ROS. But plain fructose without any flavonoids didn't boost blood ROS either.
The resulting study involved 32 healthy participants between the ages of 20 and 40, who were of normal weight, with a body mass index of 20-25 kg/m2. Participants were assigned randomly and evenly into four groups, who would drink the equivalent of 300 calories-worth of glucose, fructose, orange juice or saccharin-sweetened water.
Fasting blood samples were taken before the test and at 1, 2 and 3 hours after a 10-minute period to consume the drinks.
Results showed a significant increase in ROS within 2 hours in samples from the glucose group but not in those from the fructose, orange juice or water group.
However, two flavonoids found in orange juice inhibit ROS generation.
An additional round of test on the samples showed that neither fructose nor vitamin C suppressed the oxygen free radicals. However the two types of flavonoids in orange juice -- hesperetin and naringenin -- inhibited ROS generation by 52 percent and 77 percent, respectively.
We need orange juice that contains less fructose and more flavonoids.
More generally: We need better availability of fruits that haven't been bred to be very sweet. I always look for apple varieties that taste less sweet but which have tangier taste. Red Delicious is too sweet for my taste. I try to avoid calories while getting more beneficial compounds which have no calorie content.
Vitamins and minerals supplements aren't automatic sure wins on the health front. Too much selenium might boost the risk for the form of diabetes that makes cells resistant to the effects of insulin.
PHILADELPHIA -- A new analysis of data from a large national study found that people who took a 200 microgram selenium supplement each day for almost eight years had an increased risk of developing type 2 diabetes than those who took a placebo or dummy pill.
The data came from the Nutritional Prevention of Cancer Trial (NPC), a large randomized, multi-center, clinical trial from the eastern United States, designed to evaluate whether selenium supplements prevent skin cancer. In the study being published, researchers selected 1,202 participants who did not have diabetes when they were enrolled in the NPC Trial. Half received a 200 microgram selenium supplement and half received a placebo pill for an average of 7.7 years.
Saverio Stranges, MD, PhD, lead author of the study, says that the findings from this study suggest that selenium supplements do not prevent diabetes and that they might be harmful. “At this time, the evidence that people should take selenium supplements is extremely limited. We have observed an increased risk for diabetes over the long term in the group of participants who took selenium supplements.”
Overweight people did not experience a boost in type 2 diabetes risk from taking selenium.
In the current study, 58 out of 600 participants in the selenium group and 39 out of 602 participants in the placebo group developed type 2 diabetes. After 7.7 years of follow-up, the relative risk rate was approximately 50 percent higher among those randomly selected for the selenium group than among those randomly placed in the placebo group.
The results consistently showed higher risks of disease among participants receiving selenium across subgroups of baseline age, gender, and smoking status. However, the selenium supplements had no impact on the most overweight participants. The risk of developing diabetes tended to be higher in people who had higher blood selenium levels at the start of the study.
Whether a selenium supplement would help or hurt you probably depends on how much selenium you have in your body from your diet. People who eat Brazil nuts already are getting lots of selenium and shouldn't take a supplement.
The lack of increased risk from selenium for those who are overweight suggests that selenium works to boost type 2 diabetes by the same mechanism which fat cells boost that risk. Maybe the fat cells already flip some molecular switches to the same position selenium causes the switches to get set to and therefore when selenium comes along it can't flip the switches.
We need implanted sensors that'll tell us when we are getting too much or two little of each nutrient. We also need nutritional genomics: genetic tests that will tell us what levels of nutrients are ideal for our individual bodies.
According to the new findings, levels of the flavonoids quercetin and kaempferol were found to be on average 79 and 97 per cent higher, respectively, in organic tomatoes. Flavonoids such as these are known antioxidants and have been linked to reduced rates of cardiovascular disease, some forms of cancer and dementia, says Alyson Mitchell, a food chemist who led the research at the University of California, Davis.
The quality of tomatoes varies enormously from pale unmoist tomatoes sold in supermarkets in the winter to the best stuff from sandy acidic soil picked fully ripe in summer. Of course this stuff varies greatly in how much flavonoids it contains.
That meant growers didn't need to use as much compost to keep nitrogen levels high. And without that extra boost of growth-promoting nitrogen, plants seemed to devote more energy to producing flavonoids.
The findings don't necessarily mean that all organic tomatoes would contain more flavonoids, Mitchell stressed, because soils and growing methods on different farms could vary tremendously.
My own experience with garden-grown versus farmed tomatoes is that home grown tomatoes taste much better and look more colorful than most tomatoes sold in stores.. Either soil conditions or types of tomatoes used or the ability to let the tomatoes fully ripen on the vine in gardens might account for the difference. My guess is that the tangier and more colorful tomatoes have more beneficial chemicals.
Every time I write a post about the health benefits of chocolate I eat some chocolate while writing the post. This time was no exception. How often does science tell you to do exactly what you want to do? (usually science tells you to eat vegetables you aren't excited to eat)
Eating about 30 calories a day of dark chocolate was associated with a lowering of blood pressure, without weight gain or other adverse effects, according to a study in the July 4 issue of JAMA.
Previous research has indicated that consumption of high amounts of cocoa-containing foods can lower blood pressure (BP), believed to be due to the action of the cocoa polyphenols (a group of chemical substances found in plants, some of which, such as the flavanols, are believed to be beneficial to health). “A particular concern is that the potential BP reduction contributed by the flavanols could be offset by the high sugar, fat and calorie intake with the cocoa products,” the authors write. The effect of low cocoa intake on BP is unclear.
Dirk Taubert, M.D., Ph.D., of University Hospital of Cologne, Germany, and colleagues assessed the effects of low regular amounts of cocoa on BP. The trial, conducted between January 2005 and December 2006, included 44 adults (age 56 through 73 years; 24 women, 20 men) with untreated upper-range prehypertension (BP 130/85 – 139/89) or stage 1 hypertension (BP 140/90 – 160/100). Participants were randomly assigned to receive for 18 weeks either 6.3 g (30 calories) per day of dark chocolate containing 30 mg polyphenols or matching polyphenol-free white chocolate.
That 6.3 grams of dark chocolate is about one and a third teaspoon or almost half a tablespoon of chocolate.
The researchers found that from baseline to 18 weeks, dark chocolate intake reduced average systolic BP by −2.9 (1.6) mm Hg and diastolic BP by −1.9 (1.0) mm Hg without changes in body weight, plasma levels of lipids or glucose. Hypertension prevalence declined from 86 percent to 68 percent.
The white chocolate didn't help any. You have to eat the dark stuff, the darker and less sweet the better.
A population of adults in Hawaii who averaged about 29 hours a week of sun exposure still mostly did not have an optimal amount of vitamin D in their blood.
Participants: The study population consisted of 93 adults (30 women and 63 men) with a mean (SEM) age and body mass index of 24.0 yr (0.7) and 23.6 kg/m2 (0.4), respectively. Their self-reported sun exposure was 28.9 (1.5) h/wk, yielding a calculated sun exposure index of 11.1 (0.7).
Main Outcome Measures: Serum 25(OH)D concentration was measured using a precise HPLC assay. Low vitamin D status was defined as a circulating 25(OH)D concentration less than 30 ng/ml.
Results: Mean serum 25(OH)D concentration was 31.6 ng/ml. Using a cutpoint of 30 ng/ml, 51% of this population had low vitamin D status. The highest 25(OH)D concentration was 62 ng/ml.
I wonder what their racial and age breakdown was. First off, darker skinned people will make less vitamin D from a given amount of sun exposure. Second, as skin ages it very likely becomes less efficient at harnessing sun to make vitamin D.
Another report on this study says only about 22 of those hours were without sunscreen on average. But 22 hours a week is a lot more than people get in colder climates except maybe during the summer times.
Another recent study by Paul Lips and colleagues using subjects from the Longitudinal Aging Study Amsterdam found that blood vitamin D below 20 ng/ml was associated with a more rapid decline in physical performance among the elderly.
Conclusions: Serum 25-OHD concentrations below 20 ng/ml are associated with poorer physical performance and a greater decline in physical performance in older men and women. Because almost 50% of the population had serum 25-OHD below 20 ng/ml, public health strategies should be aimed at this group.
This doesn't prove a cause and effect. It could be that sicker people get out into the sun less. Or people who get out more exercise more and therefore do a better job of maintaining muscle mass as they age.
Another study from 2005 found that even women receiving anti-osteoporosis therapy do not have enough vitamin D.
Conclusions: More than half of North American women receiving therapy to treat or prevent osteoporosis have vitamin D inadequacy, underscoring the need for improved physician and public education regarding optimization of vitamin D status in this population.
Think about what this says about doctors. These women have crumbling bones. Did the doctors prescribe vitamin D to boost their deficient blood vitamin D levels? Probably not. Yet vitamin D is essential for good bone health.
DETROIT, June 11, 2007 -- Adding to a growing body of evidence, new research shows that a daily dose of pistachios may offer protective benefits against cardiovascular disease, according to a study published in the Volume 26, Number 2 issue of the Journal of the American College of Nutrition.
The study, conducted by James N. Cooper M.D., of George Mason University and Michael J. Sheridan, Sc.D., of Inova Fairfax Hospital, found that in people with moderately high cholesterol levels, a daily diet consisting of 15% of calories from pistachios (about two to three ounces or one to two handfuls of kernels) over a four-week period favorably improved some blood lipid levels.
"These results are exciting because the research indicates that adding pistachios to the daily diet can help protect the heart without a dramatic dietary lifestyle change," said Dr. James Cooper. "This research challenges the previously-held belief that a low-fat diet is best for heart health. Studies now show that a diet with a moderate amount of healthful monounsaturated fat, like the kind found in pistachios, is a more effective way to prevent heart disease than reducing overall fat intake. What's more, we noted very good compliance and a positive response from participants during the four-week period."
Nuts are good.
Different studies produce conflicting results on the question of which diet is best for weight loss. A recent study that looked insulin response to sugar consumption found that for people whose bodies produce more insulin in response to an oral glucose tolerance test the best diet is one that lowers glycemic index.
Overweight individuals who secrete insulin at a higher level may experience greater weight loss by selecting a low-glycemic load diet, compared to a low-fat diet, according to a study in the May 16 issue of JAMA. The researchers also found a low-glycemic load diet to have beneficial effects on HDL cholesterol and triglyceride concentrations.
"With prevalence approaching one-third of the population, obesity is among the most important medical problems in the United States and identification of effective dietary treatment has become a major public health priority. Three popular diets—low fat, low carbohydrate, and low glycemic load—have recently received much attention. However, clinical trials have produced inconsistent findings, with some suggesting that one diet is superior for weight loss and others indicating no difference between diets," the authors write. They add that one explanation for the inconsistent findings could relate to the inherent physiological differences among study participants. "One physiological mechanism that might relate weight loss to dietary composition is individual differences in insulin secretion."
A low glycemic index diet is one which contains carbohydrates in forms that break down slowly in the intestine.
A low glycemic index diet works best for people whose bodies secrete more insulin in response to consuming glucose.
The researchers found that change in body weight and body fat percentage did not differ between the diet groups overall. However, for those with insulin concentration at 30 minutes above the median (midpoint), the low–glycemic load diet produced a greater decrease in weight (12.8 lbs. vs. 2.6 lbs.) and body fat percentage (–2.6 percent vs. –0.9 percent) than the low-fat diet at 18 months. There were no significant differences in these end points between diet groups for those with insulin concentration at 30 minutes below the median level. Among all the participants in the study, high-density lipoprotein cholesterol (the "good" cholesterol) and triglyceride concentrations improved more on the low–glycemic load diet, whereas low-density lipoprotein cholesterol (the "bad" cholesterol) concentration improved more on the low-fat diet.
"The main finding of our study is that a simple measure of insulin secretion predicted weight and body fat loss on low–glycemic load and low-fat diets," the authors write. "For obese individuals with high insulin concentration at 30 minutes during an oral glucose tolerance test, a low–glycemic load diet may promote more weight and body fat loss than a low-fat diet. Regardless of insulin secretion, a low–glycemic load diet has beneficial effects on concentrations of HDL cholesterol and triglycerides but not on LDL cholesterol. Additional research is needed to examine these effects in other populations and to explore the mechanistic basis for the observed diet-phenotype interaction."
The big insulin response could cause more weight gain by a couple of mechanisms. First off, the greater amount of insulin causes the sugar to get cleared from the blood more rapidly. Therefore blood sugar drops and the more rapid return to a state of lower blood pressure probably brings with it hunger pangs. Second, some of the sugar that gets moved out of the blood gets converted into fat for storage. If the sugar came into the blood and exited the blood more slowly the body could probably burn more of it before it gets converted to fat.
A diet that does not much stimulate the islets of Langerhans. on your pancreas to pump out a lot of insulin in response to what you eat is probably a better diet regardless of whether you are trying to lose weight. Big blood sugar spikes cause sugar to bind in places harmful to your health and that accelerates aging. That is why diabetics have much shorter life expectancies.
If you want to lower the glycemic index of your diet then choose among foods that have low glycemic index. Here is the glycemic index for hundreds of foods. Also see David Mendosa's satiety index for foods.
Here is the research paper: Effects of a Low–Glycemic Load vs Low-Fat Diet in Obese Young Adults.
A research team at Wake Forest University Baptist Medical Center found obese old women who diet and lose weight maintain or increase their mobility.
Her study evaluated 23 obese, postmenopausal, sedentary women with a mean age of 58 who participated in the DEMO study. For five months, their meals and snacks were provided by the study and contained 400 fewer calories than they needed to maintain their weight.
Participants’ body composition and physical function were measured before and after the five-month period. Tests of physical function measured knee strength, hand-grip strength, walking speed, aerobic fitness and ability to quickly rise from a chair without using their arms. The women lost an average of 25 pounds, with muscle representing about 35 percent of the total loss.
“Despite the large amount of muscle loss, their aerobic fitness and their ability to rise from a chair showed a trend toward improvement,” said Demons. “Their strength and walking speed did not change. This suggests that their weight loss through dieting wouldn’t be expected to lead to increased disability.”
So far, so good. But the overwhelming majority of people who lose weight regain it. Well, they regained proportionately less muscle than they lost.
Lyles’ project evaluated 30 women from the DEMO study to determine body composition when weight was regained. Body composition was measured before and after the five-month period of calorie restriction. A third measurement was taken 12 months later.
The women lost an average of 25 pounds – about 32 percent of the lost weight was muscle and 68 percent was fat. The women regained an average of 11 pounds. About 27 percent of the regained weight was muscle and 73 percent was fat.
35% of their loss was muscle. But only 27% of their gain was muscle. That's not good. Some of that could be due to aging. But it seems too large a change to attribute only to aging.
I'm skeptical of the benefit of dieting for these women. Almost all of them are going to regain most or all the lost weight. Dieting might be worse than not dieting. Exercise to build up muscle mass might provide a clearer benefit. I'm skeptical that people can defeat the appetite regulation mechanism in the brain which starts telling them to eat more when they get their weight down. We need drugs that reduce appetite or for most people weight loss diets are going to do more harm than good.
The diets included a Step I Diet – a standard heart healthy diet with 25 percent fat and 8 percent saturated fat, a diet containing 1.5 ounces of pistachios that was a Step I Diet with 30 percent total fat and 8 percent saturated fat and a diet containing 3 ounces of pistachios that was a Step I Diet containing 34 percent fat and 8 percent saturated fat. At the end of each four-week diet regime, the researchers measured blood pressure and total peripheral vascular resistance at rest and during two stress tests.
The two tests consisted of a physical test and a psychological test. The physical test consists of putting one foot in a bucket of ice water for 2.5 minutes. The psychological test asks participants to listen to two numbers, add them in their head and say the answer. Then they hear another number and they must add it to the second number they heard, not the sum they spoke.
Note these results go against the simple rule that more fats are bad. Nuts are a more complicated story in part because their fats are less saturated.
Pistachios reduced the effects of stress on blood pressure. Stressful conditions did not increase blood pressure as much in people who were on diets that included pistachios. Pistachios caused artery relaxation.
The researchers found that both pistachio containing diets reduced the stress effects on blood pressure, but that the 1.5 ounce pistachio diet reduced systolic blood pressure by 4.8 millimeters of mercury while the 3-ounce pistachio diet only reduced systolic blood pressure by 2.4 millimeters of mercury. The diets had no effect on normal, resting blood pressure.
"When we only look at blood pressure, these results are confusing," says West. "If it is the pistachios, why is it not dose related?"
When the researchers looked at total peripheral vascular resistance, it was clear that the 3-ounce diet caused greater relaxation of arteries. Because the body tightly regulates blood pressure, rather than allowing blood pressure to drop further, the heart compensated by pumping more forcefully.
The artery benefits might come from the high concentrations of arginine found in pistachios and some other nuts. Pistachios have two and a half grams of arginine in a cup. The arginine helps boost nitric acid which relaxes arteries.
The multi-week study, which received funding from the California Pistachio Commission , concluded that three ounces of pistachios a day reduced LDL levels by 11.6 percent, total cholesterol levels by 8.4 percent, and non-high density lipoproteins (non-HDL) by 11.2 percent.
Lower cholesterol, less reaction to stress, lower blood pressure. Does the arginine story get any better? A different study by the University of Toronto’s Dr. Cyril Kendall and Dr. David Jenkins (he who developed his "ape diet" to lower cholesterol in humans) finds that pistachios reduce blood sugar rise after high carbohydrate meals.
Drs. Jenkins and Kendall and their research colleagues studied 10 healthy individuals who participated in a number of acute dietary studies over the course of two months. After an overnight fast, participants were given a one-, two- or three-ounce serving of pistachios alone or served with a slice of white bread and blood sugar levels were measured over a two-hour period. The findings suggest that consumption of pistachios with a carbohydrate-rich meal significantly lowered the d blood glucose response. As consumption of pistachios increased, the blood sugar lowering response was enhanced. In addition, when pistachios were consumed alone, the rise in blood glucose was minimal.
The researchers also monitored the effect of pistachios consumed with different common carbohydrate foods on postprandial glycemia, or blood sugar levels after eating. The addition of pistachios to a number of other commonly consumed carbohydrate-rich foods – such as mashed potatoes, pasta and rice – also resulted in significant reductions in the blood sugar response, compared to when these foods were eaten alone.
These results are consistent with a larger body of research showing health benefits from consumption of nuts. Curiously, pistachios have more carbohydrates than a lot of other nuts. Yet they provided blood sugar benefits.
Things that boost the level of inflammation in human bodies generally accelerate aging and are to be avoided. With that in mind, the popular use of conjugated linoleic acid (CLA) to take off fat might be a bad idea. In a controlled trial CLA lowered the good HDL cholesterol but boosted some markers for inflammation such as C-Reactive Protein (CRP).
Lean body mass increased by 0.64 kg in the 6.4 g/d CLA group (P < 0.05) after 12 wk of intervention. Significant decreases in serum HDL-cholesterol and sodium, hemoglobin, and hematocrit, and significant increases in serum alkaline phosphatase, C-reactive protein, and IL-6, and white blood cells occurred in the 6.4 g/d CLA group, although all values remained within normal limits. The intervention was well tolerated and no severe adverse events were reported, although mild gastrointestinal adverse events were reported in all treatment groups. In conclusion, whereas CLA may increase lean body mass in obese humans, it may also increase markers of inflammation in the short term.
Anyone taking CLA or thinking of doing so ought to think twice.
Susan Steck (University of North Carolina, Chapel Hill, USA) and colleagues performed a randomized, double-blind, placebo-controlled trial among 48 adults who were obese but otherwise healthy.
I'd love to see the equivalent of this trial performed for a very large assortment of foods and supplements. Which foods raise HDL, lower inflammation, and maybe even reduce body fat? So an foods exist which provide benefits on all these measures at once?
For the current study, researchers analyzed data from the InCHIANTI study, which evaluated factors contributing to the decline of mobility in late life. The study involved 976 people who were 65 years and older from two towns in the Chianti area of Italy. The mean age of participants was 74.8 years. Data were collected from Sept. 1998 through March 2000.
Participants completed a short physical performance test of their walking speed, ability to stand from a chair and ability to maintain their balance in progressively more challenging positions. In addition, handgrip strength, a predictor of future disability, was measured using a hand-held dynamometer.
The researchers found that physical performance and grip strength were about five to 10 percent lower in those who had low levels of vitamin D. After looking at other variables that could influence the results, such as body mass index, physical activity, the season of the year, mental abilities, health conditions and anemia, the results held true.
The study wasn’t designed to evaluate whether low vitamin D levels actually cause poor physical performance, but the results suggest the need for additional research in this area, said Houston. She said vitamin D plays an important role in muscle function, so it is plausible that low levels of the vitamin could result in lower muscle strength and physical performance.
“But it’s also possible that those with poor physical performance had less exposure to sunlight resulting in low vitamin D levels,” she said.
Current recommended daily intake for vitamin D might be too low.
Current recommendations call for people from age 50 to 69 to get 400 international units (IUs) of vitamin D per day and for those over age 70 to get 600 IUs. Many researchers, however, suggest that higher amounts may be needed.
“Higher amounts of vitamin D may be needed for the preservation of muscle strength and physical function as well as other conditions such as cancer prevention,” said Houston. “The current recommendations are based primarily on vitamin D’s effects on bone health.”
We spend less time outside than our ancestors did. It seems likely we do not make enough vitamin D from sun exposure. At the same time, many of us do not get much vitamin D from foods. So vitamin D deficiency might be common.
A team at Harvard Medical School have the proof for what you already thought you knew: Yes, eating too much salt really is bad for your heart and cardiovascular system.
Boston, MA- Researchers at Brigham and Women's Hospital (BWH), in an extended follow-up of a randomized trial, found that reducing sodium intake among men and women lowered subsequent risk of cardiovascular disease by 25 percent more than 10 years after the trial ended.
BWH researcher, Nancy Cook, ScD, in a study to be published in the British Medical Journal, expanded upon the most recent findings from the analysis of the Trials of Hypertension Prevention (TOHP)- in which participants, ages 30 to 54 years with high normal blood pressure took part in a sodium intervention during which participants were taught to identify, select and prepare low-salt foods. The study demonstrated that by reducing dietary salt intake, an individual could lower the risk of developing cardiovascular disease 10 to 15 years post-trial. Specifically, participants who were randomized to a sodium lifestyle intervention during the study period experienced a 25 percent decreased risk of cardiovascular disease up to 15 years later. Total mortality was also reduced by 20%, a finding that was consistent, although not statistically significant. This study marks the only randomized sodium intervention that has been followed for later long-term cardiovascular disease risk.
It is not like you didn't already know this. But think of it as a reminder.
Heart disease and cancer are the two biggest killers. Heart disease is far easier to avoid than cancer. Don't smoke. Avoid saturated fats and trans fats. Eat lots of vegetables. Do not use table salt and avoid highly salted prepared foods. Try using vinegar and spices in place of salt. Works for me. Get exercise. How much? More than you are getting now in all likelihood (you long distance runners excepted).
Cancer is the tougher one. Just about all the things you should do for your heart will also reduce your cancer risk (and stop eating carcinogen-laden charbroiled foods - which are bad for your heart anyway). But with a great diet and lifestyle the cancer risk won't go down near as much as the heart disease risk. We really need cures for cancer. Given my diet and weight and blood lipids I do not worry about dying from heart disease. But cancer is something that strikes me as a big dice roll where the odds get higher every year. I'm always a few mutations away from a fatal case of cancer. The sooner it becomes curable the better.
Frequent consumption of cured meats results in lower lung function test scores and increases the odds of developing chronic obstructive pulmonary disease (COPD), according to a large cross-sectional survey of adults in the U.S.
The study results appear in the second issue for April 2007 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.
Rui Jiang, M.D., Dr.P.H., of Columbia University Medical Center in New York, and three associates showed that the "odds ratio" for developing COPD among individuals who consumed cured meat products 14 times or more per month was 1.93, as compared with those who did not consume cured meats. An odds ratio greater than 1 implies that the event is more likely to occur within that group.
"Cured meats, such as bacon, sausage, luncheon meats and cured hams, are high in nitrites, which are added to meat products as a preservative, an anti-microbial agent, and a color fixative," said Dr. Jiang. "Nitrates generate reactive nitrogen species that may cause damage to the lungs, producing structural changes resembling emphysema."
What I'd like to see: studies on blood oxidative stress indicators with people who eat cured meat versus fresh meat. Do hot dog eaters have more signs of free radicals in their blood?
Will you lose weight and keep it off if you diet? No, probably not, UCLA researchers report in the April issue of American Psychologist, the journal of the American Psychological Association.
"You can initially lose 5 to 10 percent of your weight on any number of diets, but then the weight comes back," said Traci Mann, UCLA associate professor of psychology and lead author of the study. "We found that the majority of people regained all the weight, plus more. Sustained weight loss was found only in a small minority of participants, while complete weight regain was found in the majority. Diets do not lead to sustained weight loss or health benefits for the majority of people."
Mann and her co-authors conducted the most comprehensive and rigorous analysis of diet studies, analyzing 31 long-term studies.
The researchers analyzed all studies that followed dieters from 2 to 5 years. None of them worked. Worse, these studies contain biases that overstate the benefits of the diets.
Mann said that certain factors biased the diet studies to make them appear more effective than they really were. For one, many participants self-reported their weight by phone or mail rather than having their weight measured on a scale by an impartial source. Also, the studies have very low follow-up rates — eight of the studies had follow-up rates lower than 50 percent, and those who responded may not have been representative of the entire group, since people who gain back large amounts of weight are generally unlikely to show up for follow-up tests, Mann said.
Dieting is even worse than not dieting.
"Several studies indicate that dieting is actually a consistent predictor of future weight gain," said Janet Tomiyama, a UCLA graduate student of psychology and co-author of the study. One study found that both men and women who participated in formal weight-loss programs gained significantly more weight over a two-year period than those who had not participated in a weight-loss program, she said. Another study, which examined a variety of lifestyle factors and their relationship to changes in weight in more than 19,000 healthy older men over a four-year period, found that "one of the best predictors of weight gain over the four years was having lost weight on a diet at some point during the years before the study started," Tomiyama said. In several studies, people in control groups who did not diet were not that much worse off — and in many cases were better off — than those who did diet, she said.
In a way this is great news for anyone who doesn't want to diet. You don't need to feel guilty about it. If you diet you'll just gain more weight in the long run. My guess is the body treats the scarcity of food while on a diet as a sign that it needs to build up fat stores in case another lean period happens.
So how to lose weight? The Mann and Tomiyama suspect that exercise will best keep people skinny. But their latest analysis was restricted to the effects of dieting.
People faced with morbid obesity can do the stomach surgey that restricts stomach size. That appears to work pretty reliably. Also, get enough sleep. Lack of sleep has been found a contributor to weight gain in other studies. Also, at least eat healthy foods regardless of how much food you eat.
I'd like to see more studies on the effect of eating various ratios of different types of fats and sugars. Does fructose consumption contribute to obesity? Do some fats sate hunger for longer than other fats? Do low glycemic index foods sate hunger for longer? In addition to how much we eat, what we eat might matter for weight control.
ORLANDO, Fla., March 2 -- Eating whole-grain breakfast cereals seven or more times per week was associated with a lower risk of heart failure, according to an analysis of the observational Physicians’ Health Study. Researchers presented findings of the study today at the American Heart Association’s 47th Annual Conference on Cardiovascular Disease Epidemiology and Prevention. For the present study, breakfast cereals that contain at least 25 percent oat or bran content were classified as whole grain cereals.
The analysis shows that those who ate a whole-grain breakfast cereal seven or more times per week were less likely (by 28 percent) to develop heart failure over the course of the study than those who never ate such cereal. The risk of heart failure decreased by 22 percent in those who ate a whole-grain breakfast cereal from two to six times per week and by 14 percent in those who ate a whole-grain breakfast cereal up to once per week.
The oats and bran might have provided a benefit by displacing less healthy breakfast foods.
Some people take vitamins in search of longer life expectancy. My advice: Make small improvements in regular food choices before going for pills. More vegetables, fruits, and whole grains stand a better chance of extending your life than anything you take in a pill (with the possible exception of vitamin D).
Remember, the goal isn't just to live longer. The goal is to still be alive when full aging reversal becomes possible using rejuvenation therapies such as stem cells, gene therapies, grown replacement organs, artificial organs, and nanobots.
The health benefits of epicatechin, a compound found in cocoa, are so striking that it may rival penicillin and anaesthesia in terms of importance to public health, reports Marina Murphy in Chemistry & Industry, the magazine of the SCI. Norman Hollenberg, professor of medicine at Harvard Medical School, told C&I that epicatechin is so important that it should be considered a vitamin.
Hollenberg has spent years studying the benefits of cocoa drinking on the Kuna people in Panama. He found that the risk of 4 of the 5 most common killer diseases: stroke, heart failure, cancer and diabetes, is reduced to less then 10% in the Kuna. They can drink up to 40 cups of cocoa a week. Natural cocoa has high levels of epicatechin.
'If these observations predict the future, then we can say without blushing that they are among the most important observations in the history of medicine,' Hollenberg says. ‘We all agree that penicillin and anaesthesia are enormously important. But epicatechin could potentially get rid of 4 of the 5 most common diseases in the western world, how important does that make epicatechin?... I would say very important’
The best way to get rid of the most common degenerative diseases is to develop rejuvenation therapies using stem cells, gene therapy, nanobots, and other methods to totally repair all the damage caused by aging. But if we can slow aging down with cocoa I'll take it while waiting for the methods that'll reverse aging.
Among the Kuna people of Panama, who can drink up to 40 cups of cocoa per week, rates of stroke, heart disease, cancer and diabetes are less than 10%.
The Kuna also appear to live longer than other Panama inhabitants and do not get dementia, a US scientist reports in Chemistry and Industry.
This is an observational study. But I'm going to try to put cocoa into apple sauce more often.
Anyone know the best food source for epicatechin?
CORVALLIS, Ore. – Flavonoids, a group of compounds found in fruits and vegetables that had been thought to be nutritionally important for their antioxidant activity, actually have little or no value in that role, according to an analysis by scientists in the Linus Pauling Institute at Oregon State University.
However, these same compounds may indeed benefit human health, but for reasons that are quite different – the body sees them as foreign compounds, researchers say, and through different mechanisms, they could play a role in preventing cancer or heart disease.
Bioflavonoids join an existing known list of plant compounds that deliver health benefits because they alter metabolism in ways that reduce damage caused by toxins. For example, cabbage and other cruciferous vegetables contain compounds called isothiocyanates such as sulforaphane and indole-3-carbinol. The liver reacts to these isothiocyanates as if they are toxins and the liver therefore makes more enzymes that break down toxins. As a result any real toxins get broken down more quickly and therefore do less harm to the body.
The body metabolises flavonoids into forms that have little antioxidant activity.
“What we now know is that flavonoids are highly metabolized, which alters their chemical structure and diminishes their ability to function as an antioxidant,” said Balz Frei, professor and director of the Linus Pauling Institute. “The body sees them as foreign compounds and modifies them for rapid excretion in the urine and bile.”
Attempts to turn up big health benefits of antioxidant vitamins have been somewhat of a disappointment. The foods that appear to be associated with longer and healthier lives probably deliver most of their benefit due to compounds in them that alter human metabolism in a large assortment of ways.
Flavonoids alter metabolism in several health-promoting ways.
The large increase in total antioxidant capacity of blood observed after the consumption of flavonoid-rich foods is not caused by the flavonoids themselves, Frei said, but most likely is the result of increased uric acid levels.
But just because flavonoids have been found to be ineffectual as antioxidants in the human body does not mean they are without value, Frei said. They appear to strongly influence cell signaling pathways and gene expression, with relevance to both cancer and heart disease.
“We can now follow the activity of flavonoids in the body, and one thing that is clear is that the body sees them as foreign compounds and is trying to get rid of them,” Frei said. “But this process of gearing up to get rid of unwanted compounds is inducing so-called Phase II enzymes that also help eliminate mutagens and carcinogens, and therefore may be of value in cancer prevention.
“Flavonoids could also induce mechanisms that help kill cancer cells and inhibit tumor invasion,” Frei added.
It also appears that flavonoids increase the activation of existing nitric oxide synthase, which has the effect of keeping blood vessels healthy and relaxed, preventing inflammation, and lowering blood pressure – all key goals in prevention of heart disease.
If we could optimally turn up every enzyme pathway that breaks down toxins we could reduce our rate of aging and delay the onset of cancer and other disorders of old age.
Biogerontologist Aubrey de Grey makes what to my mind is a persuasive argument against the expectation that antioxidants will deliver large health benefits: The metabolic cost of making and retaining antioxidants in the body is pretty low. If antioxidants could deliver benefits as large as some of their advocates claim then natural selection would long ago have selected for mutations that boost body antioxidant levels. So why expect consumed antioxidants to deliver a big benefit?
So (I hear you asking) why wouldn't the body make more detoxifying enzymes even in the absence of foods consumed that up-regulate detoxifying enzymes? My guess is that those enzymes are more metabolically expensive to keep around.
Taking only the 47 low-bias trials, involving 180,938 people, they found that supplements as a whole increased the death rate by 5 per cent. When the supplements were taken separately, beta carotene increased death rates by 7 per cent, vitamin A by 16 per cent, and vitamin E by 4 per cent. Vitamin C gave contradictory results, but when given singly or in combination with other vitamins in good-quality trials, increased the death rate by 6 per cent.
Selenium was the only supplement to emerge with any credit. It appears to cut death rates by 10 per cent when given on its own or with other supplements in high-quality trials, but the result is not statistically significant.
The researchers wrote: "Our findings contradict the findings of observational studies claiming that antioxidants improve health.
"Considering that 10% to 20% of the adult population in Europe and North America may consume the supplements, the public health consequences may be substantial."
They said there were several different explanations for this increase in risk - and suggested that knocking out 'free radicals' might actually interfere with a natural defence mechanism within the body.
One of the uses of free radicals in the body is in the immune system to kill invading pathogens. Taking big doses of antioxidant vitamins might render aged immune systems less able to take on invader pathogens. So the higher mortality rate of vitamin takers might be due to dampened immune systems.
Another use is for intracellular and intercellular signalling. Denman Harman MD, who first proposed the free radical theory of aging back in the 1950s, once described in an interview (sorry, no link, this is from faded memory) how he felt sluggish if he took very high doses of antioxidant vitamins. His explanation for this effect was that the vitamins were quenching free radicals that were needed for signalling and by doing so they were suppressing his metabolism.
What is in your diet still matters. But the mystery remains as to just which compounds in which foods provide the most benefit. But what about vitamin supplements? My guess: the most beneficial nutrients from a supplementation standpoint are the non-antioxidant vitamins. Most people probably do not get enough vitamin D, for example. Others do not get enough calcium for their bones or iron for red blood cells. But for antioxidants we probably should look more toward non-vitamin compounds found in some foods.
But what we most need are biotechnologies that will let us repair the damage caused by free radicals. Gene therapies, cell therapies, replacement organs, and nanobots will all eventually let us repair the aging damage caused by free radicals. We should treat the development of these technologies as an urgent priority. We are getting older every year. Aging is a defeatable malady. We should defeat it.
The dietary trial involved 30 healthy men and 30 healthy women (including 30 smokers) eating an 85g bag (a cereal bowl full) of fresh watercress every day for eight weeks. The beneficial changes were greatest among the smokers. This may reflect the greater toxic burden or oxidative stress amongst the smokers, as smokers were also found to have significantly lower antioxidant levels at the start of the study compared to the non-smokers.
Here are the major results from eating a daily bowl of watercress:
The reduction in DNA damage argues for a reduced risk of cancer. DNA mutations probably are the biggest cause of cancer.
Results: Watercress supplementation (active compared with control phase) was associated with reductions in basal DNA damage (by 17%; P = 0.03), in basal plus oxidative purine DNA damage (by 23.9%; P = 0.002), and in basal DNA damage in response to ex vivo hydrogen peroxide challenge (by 9.4%; P = 0.07). Beneficial changes seen after watercress intervention were greater and more significant in smokers than in nonsmokers. Plasma lutein and ß-carotene increased significantly by 100% and 33% (P < 0.001), respectively, after watercress supplementation.
What I'd like to know: If this experiment was repeated for a wide range of vegetables how would they rank in potency? How do cabbage, celery, tomatoes, broccoli, radishes, kale, and other vegetables compare?
Writing in the current issue of the American Journal of Clinical Nutrition, Greenberg and his co-workers from the State University of New York and the City University of New York report the results of their epidemiological study of 6594 men and women aged between 32 and 86 using data from the 1971–1973 National Health and Nutrition Examination Survey (NHANES I) and follow-up until 1992.Intake of caffeinated beverages, including coffee, tea, and caffeinated cola and chocolate, was calculated from food frequency questionnaires, and classified according to average daily intake: less than half a serving, between half and two servings, two to four servings, four or more servings.
Was the protective effect from caffeine or from other compounds in the caffeinated foods? I wonder if the researchers tried excluding caffeinated colas or tried weighting the foods based on amounts of bioflavonoids to see if the effect tracked better with the amount of caffeine or the amount of other compounds..
Note that this effect was found only for those over age 65. Does this beneficial effect require a lifetime of caffeine consumption? Or could one wait till one reaches one's 60s before becoming a regular consumer of tea, coffee, and chocolate? (I err on the safe side and eat the chocolate many years before reaching the elderly stage)
For this age group, the researchers report that increasing intake of caffeinate beverages was associated with decreasing risk of mortality from these conditions. Indeed, drinking four or more servings per day reduced the risk of heart disease mortality by 53 per cent.
Over the next 15 years, men who consumed cocoa regularly had significantly lower blood pressure than those who did not.
Over the course of the study, 314 men died, 152 due to cardiovascular diseases.
Men in the group with the highest cocoa consumption were half as likely as the others to die from cardiovascular disease.
Their risk remained lower even when other factors, such as weight, smoking habits, physical activity levels, calorie intake and alcohol consumption were taken into account.
The men who consumed more cocoa were also less likely to die of any cause.
The Dutch researchers suspect that polyphenol compounds in cocoa are responsible for the protective effects. But the effective dose needed is quite high. You are best off eating dark rather than milk chocolate and better yet cocoa powder. I put cocoa powder on apple sauce for this reason.
Thanks to Lou Pagnucco for the heads up.
Two biologists at Penn State have discovered a master regulator that controls metabolic responses to a deficiency of essential amino acids in the diet. They also discovered that this regulatory substance, an enzyme named GCN2 eIF2alpha kinase, has an unexpectedly profound impact on fat metabolism. "Some results of our experiments suggest interventions that might help treat obesity, prevent Type II diabetes and heart attacks, or ameliorate protein malnutrition," said Douglas Cavener, professor and head of the Department of Biology, who led the research along with Feifan Guo, a research assistant professor. Their research will appear in the 7 February 2007 issue of the scientific journal Cell Metabolism.
Can one get some of the weight loss benefit on a low leucine diet that has enough leucine for basic needs?
A leucine-free diet is the fast path to big time weight loss?
Organisms adapt metabolically to episodes of malnutrition and starvation by shutting down the synthesis of new proteins and fats and by using stores of these nutrients from muscle, fat, and the liver in order to continue vital functions. Cavener and Guo found that the removal of a single amino acid, leucine, from the diet is sufficient to provoke a starvation response that affects fat metabolism. "These findings are important for treating two major problems in the world," Cavener says. "The starvation response we discovered can repress fat synthesis and induce the body to consume virtually all of its stored fat within a few weeks of leucine deprivation. Because this response causes a striking loss of fatty tissue, we may be able to formulate a powerful new treatment for obesity."
Do any readily available protein sources have no leucine in them? Would one need to stop eating all protein in order to avoid leucine? If you wanted to avoid the amino acid tryptophan then gelatin will serve as a cheap easily available tryptophan-free food. But gelatin is 3.5% leucine. So that's not a solution.
Note that leucine is an essential amino acid. Someone who wants to go on a leucine-free diet could not continue on it indefinitely. Also, ingestion of extra leucine with protein stimulates muscle protein synthesis. So leucine has advantages to bodybuilders. Avoidance of leucine involves trade-offs.
Thanks to Lou Pagnucco for the heads-up.
Research published on-line (Tuesday 9 January) in European Heart Journal has found that the protective effect that tea has on the cardiovascular system is totally wiped out by adding milk.
Tests on volunteers showed that black tea significantly improves the ability of the arteries to relax and expand, but adding milk completely blunts the effect. Supporting tests on rat aortas (aortic rings) and endothelial (lining) cells showed that tea relaxed the aortic rings by producing nitric oxide, which promotes dilation of blood vessels. But, again, adding milk blocked the effect.
The findings, by cardiologists and scientists from the Charité Hospital, Universitätsmedizin-Berlin, Campus Mitte, Germany, are bad news for tea-drinking nations like the British, who normally add milk to their beverage. The results have led the researchers to suggest that tea drinkers who customarily add milk should consider omitting it some of the time.
Proteins in milk probably bind to the catechins and render them unavailable.
Their study showed that the culprit in milk is a group of proteins called caseins, which they found interacted with the tea to decrease the concentration of catechins in the beverage. Catechins are the flavonoids in tea that mainly contribute to its protection against cardiovascular disease.
Senior researcher Dr Verena Stangl, Professor of Cardiology (Molecular Atherosclerosis) at the hospital, said: "There is a broad body of evidence from experimental and clinical studies indicating that tea exerts antioxidative, anti-inflammatory and vasodilating effects, thereby protecting against cardiovascular diseases. As worldwide tea consumption is second only to that of water, its beneficial effects represent an important public health issue. But, up to now, it's not been known whether adding milk to tea, as widely practised in the UK and some other countries, influences these protective properties. So, we decided to investigate the effects of tea, with and without milk, on endothelial function, because that is a sensitive indicator of what is happening to blood vessels."
In East Asian countries where green tea is popular the use of milk in tea is relatively rare. So they are deriving a greater benefit from tea drinking.
High resolution ultrasound allowed measure of the effects of tea and milk on an artery.
Sixteen healthy postmenopausal women drank either half a litre of freshly brewed black tea, black tea with 10% skimmed milk, or boiled water (as a control) on three separate occasions under the same conditions. The endothelial function of the brachial artery in the forearm was measured by high resolution ultrasound before and two hours after drinking, with measurements being taken every 15 seconds for up to two minutes a time.
Said first author Dr Mario Lorenz, a molecular biologist: "We found that, whereas drinking tea significantly increased the ability of the artery to relax and expand to accommodate increased blood flow compared with drinking water, the addition of milk completely prevents the biological effect. To extend our findings to a functional model, we determined vasodilation in rat aortic rings by exposing them to tea on its own and tea with individual milk proteins added, and got the same result."
Milk contains a number of different proteins: by testing each one separately, the researchers found that it was the three caseins that accounted for the inhibiting effect, probably by forming complexes with tea catechins.
Casein proteins make up a substantial portion of cheese. This suggests that red wine (which has a healthy amount of catechins) and cheese is a bad combination. Chocolate milk similarly blunts the effects of the catechins in the chocolate. Drink your wine with nuts. The nuts have their own beneficial compounds such as another type of flavonoids called anthocyanins (tea has some too). As for chocolate milk: Why dilute something as great as chocolate with mere milk?
Casein proteins show up as food additives in a variety of foods and you can watch for the terms caseinate, casein, milk solids, milk protein, and curds as indicators of their presence.
A link between obesity and the microbial communities living in our guts is suggested by new research at Washington University School of Medicine in St. Louis. The findings indicate that our gut microbes are biomarkers, mediators and potential therapeutic targets in the war against the worldwide obesity epidemic.
In two studies published this week in the journal Nature, the scientists report that the relative abundance of two of the most common groups of gut bacteria is altered in both obese humans and mice. By sequencing the genes present in gut microbial communities of obese and lean mice, and by observing the effects of transplanting these communities into germ-free mice, the researchers showed that the obese microbial community has an increased capacity to harvest calories from the diet.
"The amount of calories you consume by eating, and the amount of calories you expend by exercising are key determinants of your tendency to be obese or lean," says lead investigator Jeffrey Gordon, M.D., director of the Center for Genome Sciences and the Dr. Robert J. Glaser Distinguished University Professor. "Our studies imply that differences in our gut microbial ecology may determine how many calories we are able to extract and absorb from our diet and deposit in our fat cells."
That is, not every bowl of cereal may yield the same number calories for each person. People could extract slightly more or slightly less energy from a serving depending upon their collection of gut microbes. "The differences don't have to be great, but over the course of a year the effects can add up," Gordon says.
Small differences add up.
Up with the great Bacteroidetes and down with those heinous Firmicutes.
The researchers focused on two major groups of bacteria - the Bacteroidetes and the Firmicutes - that together make up more than 90 percent of microbes found in the intestines of mice and humans. In an earlier study, they compared genetically obese mice and their lean littermates. The obese mice had 50 percent fewer Bacteroidetes and proportionately more Firmicutes. Moreover, the differences were not due to a bloom of one species in the Firmicutes or a diminution of a single or a few species of Bacteroidetes: virtually all members of each group were altered.
In one of this week's Nature articles, Ruth Ley, Ph.D., a microbial ecologist in Gordon's group, reports on her investigation into whether these findings also held true among obese humans. She followed 12 obese patients at a Washington University weight loss clinic over a one-year period. Half the patients were on a low-calorie, low-fat diet and half were on a low-calorie, low carbohydrate diet.
At the outset of the study, the obese patients had the same type of depletion of Bacteroidetes and relative enhancement of Firmicutes as the obese mice. As the patients lost weight, the abundance of the Bacteroidetes increased and the abundance of Firmicutes decreased, irrespective of the diet they were on. Moreover, not one particular species of Bacteroidetes but the entire group increased as patients lost weight.
So then does the obesity cause the bacterial difference? Or does the bacterial difference cause the obesity? Or do these two factors act in a reinforcing cycle?
Part of the research was made possible by DNA sequencing technology. Answers to questions about human biology will come much more rapidly in the future because scientific instrumentation advances continue to accelerate the rate at which scientists can collect data and to allow measurement of things that were previously unmeasurable.
In a companion paper in the same journal, Peter Turnbaugh, a Ph.D. student in Gordon's lab, compared the genes present in the gut microbial communities of the obese and lean mice using the newest generation of massively parallel DNA sequencers.
Transfer of bacteria from fat rats to sterile rats made those rats gain weight more rapidly.
The results of these so-called comparative metagenomic studies revealed that the obese animals' microbial community genome (microbiome) had a greater capacity to digest polysaccharides, or complex carbohydrates. By transferring the gut microbial communities of obese and lean mice to mice that had been raised in a sterile environment (germ-free animals), he confirmed that the obese microbial community prompted a significantly greater gain in fat in the recipients.
There's an obvious opening here for yogurt makers? Can bacterial blends for yogurt get formulated to encourage the flourishing of bacteria that keep the weight off?
Boston, MA – The possibility that vitamin D could help protect people from developing multiple sclerosis (MS) has been posited by researchers in recent decades, but evidence to support that link has been scant. In the first large-scale, prospective study to investigate the relationship between vitamin D levels and MS, researchers at the Harvard School of Public Health (HSPH) have found an association between higher levels of vitamin D in the body and a lower risk of MS. The study appears in the December 20, 2006, issue of the Journal of the American Medical Association.
What I wonder: Does Vitamin D reduce the risk by helping the immune system knock out pathogens at a very early stage before the can replicate enough to invoke a more specific immune response? MS might be caused by an immune reaction to a pathogen that has a protein on it that is similar to a surface protein on human nerves. If the immune system can knock out a pathogen at a very early stage (and vitamin D might help do this) then the larger immune response could be avoided and production of T cells carrying antibodies which have affinity for nerves could be avoided.
A big reduction in the incidence of MS could avoid hundreds of thousands of future cases.
MS is a chronic degenerative disease of the central nervous system. It affects some 350,000 people in the U.S. and 2 million worldwide, and occurs most commonly in young adults. Women, who are affected more than men, have a lifetime risk of about 1 in 200 in the U.S. Vitamin D is a hormone manufactured naturally in the body, and its levels can be increased with exposure to sunlight, consumption of foods rich in vitamin D, such as fatty fish, and by taking supplements.
The research was done on a population of 7 million military personnel and former personnel.
The researchers, led by Ascherio, worked in collaboration with colleagues in the U.S. Army and Navy to determine whether vitamin D levels measured in healthy young adults predict their future risk of developing MS. The investigation relied on a study population of more than 7 million individuals, whose serum samples are stored in the Department of Defense Serum Repository. Between 1992 and 2004, 257 U.S. Army and Navy personnel with at least two serum samples stored in the repository were diagnosed with MS. A control group, consisting of participants who did not develop MS, was randomly selected from the study population. Serum samples were analyzed for levels of 25-hydroxyvitamin D, a good indicator of vitamin D availability to tissues, and individuals were divided into five groups of equal size according to their average levels. Because vitamin D levels are strongly influenced by skin color, separate analyses were conducted among whites, blacks, and Hispanics.
The results showed that, among whites, MS risk declined with increasing vitamin D levels--the risk was 62% lower among individuals in the top fifth of vitamin D concentration (corresponding approximately to levels above 100 nmol/L or 40 ng/mL) than among those in the bottom fifth (approximately below 63 nmol/L or 25 ng/mL). The association was strongest among individuals who were younger than 20 when they first entered the study. No significant association was found among blacks and Hispanics, possibly because of a smaller sample size and the lower levels of vitamin D found in those groups. The average age of onset of MS cases was 28.5 years old; there was no significant difference in the results between men and women.
Doug of the Exoteric brought to my attention an abstract of a research paper which suggests influenza might be more common in the winter in part because of vitamin D deficiency. That abstract argues vitamin D prevents respiratory infections by strengthening the initial immune response to pathogens.
vitamin D deficiency is common in the winter, and activated vitamin D, 1,25(OH)2D, a steroid hormone, has profound effects on human immunity. 1,25(OH)2D acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the ‘oxidative burst’ potential of macrophages. Perhaps most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in neutrophils, monocytes, natural killer cells, and in epithelial cells lining the respiratory tract where they play a major role in protecting the lung from infection. Volunteers inoculated with live attenuated influenza virus are more likely to develop fever and serological evidence of an immune response in the winter.
Could avoidance of full blown infections reduce the risk of auto-immune disorder? Can we protect ourselves from infections, MS, and even cancer by taking vitamin D?
Resveratrol occurs in such low concentrations in wines as compared to the doses used in experiments to tweak sirtuin genes that some scientists suspect that other compounds in wines are delivering the heart healthy benefits claimed for wine consumption. British researchers think the've identified which compounds in wines deliver the biggest benefit and which wines have the most of such compounds.
"The endothelial cells which line our arteries are an important site of action for the vascular protective effects of polyphenols," Roger Corder, of Queen Mary's School of Medicine and Dentistry in London, said in a prepared statement. "We purified the most biologically active polyphenols and identified them as procyanidins."
The researchers then tested wines from two regions in southwest France and Sardinia and compared them with wines from other countries. The wines from France and Sardinia had surprisingly high levels of procyanidins, often five to 10 times more than wines produced elsewhere, the researchers found.
Wines high in tannins are the ticket.
Procyanidins, however, suppressed the synthesis of a peptide called endothelin-1 that constricts blood vessels.
"The traditional production methods used in Sardinia and southwestern France ensure that the beneficial compounds, procyanidins [tannins], are efficiently extracted," says researcher Roger Corder of Queen Mary's William Harvey Research Institute of the University of London, in a news release.
"This may explain the strong association between consumption of traditional tannic wines with overall well-being, reflected in greater longevity," he says.
The winemakers of that region tend to use more traditional techniques in which Tannat grapes are soaked with their seeds longer, boosting the procyanidins.
You could also take pills that contain grape seed extract. Maybe swallowing grape seeds while eating seeded grapes is a good idea?
I'm eating dark chocolate and cranberries to get the same compounds. Walnuts, raspberries, blueberries, apples, and dark grape juice are all good source. I would expect that vintners in other regions could adjust their wine preparation techniques to greatly increase the concentrations of the procyanidins as well.
You have options. Choose a way to get more procyanidins.
I got half way through reading this report about health benefits of dark chocolate and had to go get a couple of pieces of dark chocolate to eat. This happens every time yet another study comes out that documents the health benefits of the flavonoid compounds found in chocolate. Now, that I'm on a chocolate high I'm thrilled to pass along this information. Might chocolate work to lower blood clot and heart attack risk?
"What these chocolate 'offenders' taught us is that the chemical in cocoa beans has a biochemical effect similar to aspirin in reducing platelet clumping, which can be fatal if a clot forms and blocks a blood vessel, causing a heart attack," says Diane Becker, M.P.H., Sc.D., a professor at The Johns Hopkins University School of Medicine and Bloomberg School of Public Health.
Becker cautions that her work is not intended as a prescription to gobble up large amounts of chocolate candy, which often contains diet-busting amounts of sugar, butter and cream. But as little as 2 tablespoons a day of dark chocolate - the purest form of the candy, made from the dried extract of roasted cocoa beans - may be just what the doctor ordered.
Parenthetically, Mars claims they've changed their chocolate processing process to retain more flavonoids than typical chocolate processing techniques retain. So Dove Dark is probably a great way to get the flavonoids.
Regular chocolate eaters have blood that clots more slowly.
In the study, 139 people Becker - whom Becker somewhat tongue in cheek calls "chocolate offenders" - were disqualified from a much larger study looking at the effects of aspirin on blood platelets. The Genetic Study of Aspirin Responsiveness (GeneSTAR) was conducted at Hopkins from June 2004 to November 2005 and enrolled more than 500 men and 700 women participants nationwide.
Shortly before aspirin dosing began for the subjects, they were told to stay on a strict regimen of exercise and to refrain from smoking or using foods and drinks known to affect platelet activity. These included caffeinated drinks, wine, grapefruit juice - and chocolate.
The non-compliers - who admitted to eating chocolate - were a diverse group who got their flavonoid "fix" from a variety of sources, including chocolate bars, cups of hot cocoa, grapes, black or green tea, and strawberries. And while they were excluded from the aspirin study, Becker and her team scoured their blood results for chocolate's effect on blood platelets, which the body recycles on a daily basis.
When platelet samples from both groups were run through a mechanical blood vessel system designed to time how long it takes for the platelets to clump together in a hair-thin plastic tube, the chocolate lovers were found to be less reactive, on average taking 130 seconds to occlude the system. Platelets from those who stayed away from chocolate as instructed clotted faster, at 123 seconds.
In another key test of urine for waste products of platelet activity, primarily urinary thromboxane (11-dehydro-thromboxane B2), scientists found that chocolate eaters showed less activity and waste products on average, at 177 nanograms per millimol of creatinine, versus an average of 287 nanograms per millimol of creatinine in the group that abstained.
Proanthocyanin compounds might be particularly beneficial. Lou Pagnucco has recently pointed me to a USDA document that places cocoa beans as highest in proanthocyanins followed by sorghum bran (PDF format). Have you ever seen sorghum bran for sale? Cinnamon added to apple sauce ups its proanthocyanin content even higher. Berries are good sources. Check out the charts in the document.
The darker and less sweetened the chocolate the more potent it is in health effects. Also, eat more berries and cherries. They are probably the most beneficial fruits.
The presence of higher levels of docosahexaenoic acid (DHA) in the blood has been found to be associated with reduced Alzheimer's Disease and dementia risks in participants in the Framingham Heart Study.
Individuals who have higher levels of a fatty acid known as docosahexaenoic acid (DHA) in their blood may have a significantly lower risk of developing dementia and Alzheimer’s disease, according to a report in the November issue of Archives of Neurology, one of the JAMA/Archives journals.
Age, family history and genetic factors have all been found to increase the risk of dementia and Alzheimer’s disease, a neurodegenerative disorder that causes 70 percent of cases of dementia in the elderly, according to background information in the article. Recent studies have found that high levels of homocysteine, an amino acid that is derived from proteins in the diet and that can accumulate in the blood and contribute to heart disease, increase the risk for Alzheimer’s disease and dementia. In addition, DHA, an omega-3 polyunsaturated fatty acid found in fish, appears to affect dementia risk and to be important for the proper functioning of the central nervous system.
Anything that so improves the metabolism of the brain that it reduces risk of Alzheimers and dementia probably yields shorter term benefits in terms of enhanced cognitive function. So even if a demented old age seems a distant prospect you might want to get more DHA in your diet or as a supplement just to make your mind work better.
Ernst J. Schaefer, M.D., Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, and colleagues studied the association between DHA levels and dementia in the blood of 899 men and women who were part of the population-based Framingham Heart Study. The participants of an average age of 76 years provided blood samples and underwent neuropsychological testing, and were followed for an average of nine years. A subgroup of 488 also filled out a questionnaire assessing their diet, including information about fish consumption. None of the participants had dementia at the beginning of the study; and they were given a mental examination every two years to screen for its development.
Through the nine-year study period, 99 out of 899 participants developed dementia, including 71 with Alzheimer’s disease. After controlling for other known risk factors for dementia, including age and homocysteine levels, and dividing the study population into fourths (quartiles) based on levels of DHA, the researchers found that men and women in the quartile with the highest DHA levels had a 47 percent lower risk of developing dementia and 39 percent lower risk of developing Alzheimer’s disease than the other three quartiles with lower DHA levels. Among the participants who completed the dietary questionnaire, those in the top quartile of blood DHA levels reported that they ate an average of .18 grams of DHA a day and an average of three fish servings a week. Participants in the other quartiles ate substantially less fish.
DHA levels in the blood vary by the degree to which the liver converts alpha-linolenic acid, an essential fatty acid, to DHA and also by the amount of DHA in the diet. “In our study, the correlation between [blood] DHA content and fish intake was significant, indicating that fish intake is an important source of dietary DHA,” the authors write.
The .18 grams per day is only 180 milligrams per day. I've decided to take a daily DHA/EPA supplement so I don't have to count how many days its been since the last salmon meal.
You can get a lot of alpha linolenic (ALA) acid from walnuts. Though I've found one source that claims the conversion rate of ALA to DHA and EPA is very low. Still, nut consumption is also associated with heart benefits and other health benefits. So occasional walnuts are a good idea anyway.
TUCSON, Ariz. – An ancient spice, long used in traditional Asian medicine, may hold promise for the prevention of both rheumatoid arthritis and osteoporosis, according to a recently completed study at The University of Arizona College of Medicine.
Turmeric, the spice that flavors and gives its yellow color to many curries and other foods, has been used for centuries by practitioners of Ayurvedic medicine to treat inflammatory disorders. Turmeric extract containing the ingredient curcumin is marketed widely in the Western world as a dietary supplement for the treatment and prevention of a variety of disorders, including arthritis.
At the UA College of Medicine, Janet L. Funk, MD, working with Barbara N. Timmermann, PhD, then-director of the National Institutes of Health (NIH)-funded Arizona Center for Phytomedicine Research at the UA, set out to determine whether (and how) turmeric works as an anti-arthritic. They began by preparing their own extracts from the rhizome, or root, of the plant, providing themselves with well-characterized materials to test and to compare with commercially available products. (Dr. Timmermann since has joined the faculty of the University of Kansas, Lawrence, Kan.)
Sounds like extracts sold as curcumin have the active ingredients.
Dr. Funk and her colleagues then tested in animal models a whole extract of turmeric root, only the essential oils, and an oil-depleted extract containing the three major curcuminoids found in the rhizome. Of the three extracts, the one containing the major curcuminoids was most similar in chemical composition to commercially available turmeric dietary supplements. It also was the most effective, completely inhibiting the onset of rheumatoid arthritis.
Dr. Funk, an endocrinologist in the UA Department of Medicine, says this study provides several noteworthy "firsts." Completed with the researchers' own prepared, well-defined extracts, the study represents the first documentation of the chemical composition of a curcumin-containing extract tested in a living organism, in vivo, for anti-arthritic efficacy. It also provides the first evidence of anti-arthritic efficacy of a complex turmeric extract that is analogous in composition to turmeric dietary supplements.
Turmeric extract might also help prevent osteoporosis.
In addition to preventing joint inflammation, Dr. Funk's study shows that the curcuminoid extract blocked the pathway that affects bone resorption. Noting that bone loss associated with osteoporosis in women typically begins before the onset of menopause, she has begun work on another NIH-funded study to determine whether turmeric taken as a dietary supplement during perimenopause can prevent bone loss and osteoporosis. Both of the studies are supported by the National Center for Complementary and Alternative Medicine (NCCAM) and the Office of Dietary Supplements (ODS), both of the NIH.
Note that any compound that suppresses an inflammation response runs the risk of causing harmful side effects.
The current research, which was funded by the Office of Dietary Supplements and National Center for Complementary and Alternative Medicine of the National Institutes of Healthis the first study to document the composition of a turmeric-containing compound that is similar to commercially available products and to document the mechanisms by which it reduces the effects of arthritis. The authors were able to find an effective dose in rats that would be equivalent in humans to 1.5 milligrams per day of a portion of the turmeric root that makes up 3% of dried turmeric powder. The inhibition of NF-KB and of key inflammatory genes directly or indirectly activated by NF-KB suggests that inhibition of this protein may be an important mechanism in turmeric's anti-arthritic effects. In fact, the authors state that "it would appear that turmeric dietary supplements share the same mechanism of action as antiarthritic pharmaceuticals currently under development that target NF-KB." It is also possible that turmeric blocks other inflammatory pathways, given its chemical complexity. Turmeric seems to block early inflammatory responses, as evidenced by the fact that it was effective when started 3 days but not 8 days after arthritis was induced, the authors note.
"In summary," the authors state, "just as the willow bark provided relief for arthritis patients before the advent of aspirin, it would appear that the underground stem (rhizome) of a tropical plant [turmeric] may also hold promise for the treatment of joint inflammation and destruction." They note that the anti-inflammatory effects of botanicals can only be utilized if their chemical content is analyzed. The authors conclude: "Finally, before turmeric supplements can be recommended for medicinal use, clinical trials are clearly needed to verify/determine whether treatment with adequate doses of well-characterized turmeric extracts can indeed prevent/suppress disease flares in RA [rheumatoid arthritis] patients, as well as to explore any potential benefits of turmeric dietary supplements in the prevention or treatment of more common forms of arthritis in the general population."
If only 3% of dried turmeric powder has the useful component and you need 1.5 mg of that component that suggests you need 33 times 1.5 mg of turmeric extract powder to get a useful dose. That's about 50 mg.
The turmeric extract curcumin might also help prevent Alzheimer's Disease. See my post: Curcumin Stimulates Immune Cells To Clear Alzheimers Plaque.
Boston, MA – Many studies have shown the nutritional benefits of eating fish (finfish or shellfish). Fish is high in protein and omega-3 fatty acids. But concerns have been raised in recent years about chemicals found in fish from environmental pollution, including mercury, PCBs and dioxins. That has led to confusion among the public--do the risks of eating fish outweigh the benefits?
Researchers from the Harvard School of Public Health (HSPH) tackled that question by undertaking the single most comprehensive analysis to date of fish and health. In the first review to combine the evidence for major health effects of omega-3 fatty acids, major health risks of mercury, and major health risks of PCBs and dioxins in both adults and infants/young children, the results show that the benefits of eating a modest amount of fish per week--about 3 ounces of farmed salmon or 6 ounces of mackerel--reduced the risk of death from coronary heart disease (CHD) by 36%. Notably, by combining results of randomized clinical trials, the investigators also demonstrated that intake of fish or fish oil reduces total mortality--deaths from any causes--by 17%.
Included with the paper, which appears in the October 18, 2006, issue of The Journal of the American Medical Association (http://jama.ama-assn.org/), is the first comprehensive summary of levels of omega-3 fatty acids, mercury, PCBs and dioxins in various species of fish and other foods, including chicken, beef, pork, butter and eggs.
"Overall, for major health outcomes among adults, the benefits of eating fish greatly outweigh the risks," said Dariush Mozaffarian, lead author of the study and an instructor in epidemiology at HSPH and in medicine at Brigham and Women's Hospital. "Somehow this evidence has been lost on the public."
Don't worry. Be happy. Eat fish.
Since the study did not examine the effects of all potential benefits of fish the results may understate the benefit of fish consumption.
The researchers, Mozaffarian and Eric Rimm, associate professor of epidemiology and nutrition at HSPH, did a comprehensive search of publications through April 2006 to evaluate the evidence from studies that looked at the relationship between fish intake and major health benefits as well as at the health risks of mercury, dioxins and PCBs. For benefits, the researchers focused on cardiovascular health in adults and brain development in infants, areas in which the scientific evidence is strongest (other potential benefits of fish consumption--for example, for cognitive decline or depression--might make the overall benefits even greater). The researchers focused on evidence from large prospective studies and randomized clinical trials.
Eat oily fish.
The evidence across different studies showed that fish consumption lowers the risk of death from heart disease by 36%. The benefit was related to the level of intake of omega-3 fatty acids, and thus benefits are greater for oily fish (e.g. salmon, bluefish), which are higher in beneficial omega-3 fatty acids, than lean fish (haddock, cod).
Avoid high mercury fish types.
The evidence was suggestive that mercury may have subtle effects on brain development for a child exposed in the womb, or in early childhood. To obtain the benefits of omega-3 fatty acids for brain development and minimize the potential risk of mercury, the investigators' findings agreed with the recommendations of the Environmental Protection Agency and Food and Drug Administration that women of childbearing age, nursing mothers and young children should eat up to two servings per week of a variety of fish (for example, salmon, light tuna, shrimp, mackerel, and up to 6 oz. per week of albacore tuna) and avoid only four species of fish--golden bass (also known as tilefish), king mackerel, shark and swordfish--larger, predatory fish that have higher levels of mercury. The researchers emphasized that this advisory is only for women of childbearing age, nursing mothers and young children, not the general population. Importantly, the evidence suggests that, for those women, it is as important for their health and for the brain development of their infants that they eat a variety of other types of fish as it is to avoid the four fish species higher in mercury.
Do not worry about dioxins in fish unless you get fish from fresh water sources which are contaminated.
Some studies have shown that PCBs and dioxins may be carcinogenic. The authors found that the benefits of eating fish far outweighed the potential cancer risks from these chemicals. "The levels of PCBs and dioxins in fish species are low, similar to other commonly consumed foods such as beef, chicken, pork, eggs, and butter. Importantly, the possible health risks of these low levels of PCBs and dioxins in fish are only a small fraction of the much better established health benefits of the omega-3 fatty acids," said Mozaffarian. "For example, for farmed salmon, the cardiovascular benefits are greater than the cancer risks by a factor of at least 300:1. With the exception of some locally caught sport fish from contaminated inland waters, the levels of PCBs and dioxins in fish should not influence decisions about fish intake."
The study also points out that only 9% of the PCBs and dioxins in the U.S. food supply come from fish and other seafood; more than 90% comes from other foods such as meats, vegetables, and dairy products.
I continue to be partial to salmon. It has the most omega 3 fatty acids of many types of fish that I've compared. It also has very little mercury.
Depressed people also ought to eat fish. The omega 3 fatty acids might lessen your feelings of pain and depression.
For the study, Dr. Ros and his colleagues recruited 24 nonsmoking adults with normal body weights and blood pressures. Half of the participants had normal cholesterol levels and half had moderately high levels. Each was asked to follow a cholesterol-lowering Mediterranean diet for two weeks prior to the study and throughout its duration. A Mediterranean diet includes foods low in saturated fat but high in fiber or monounsaturated fat, such as fruits and vegetables, whole grains and olive oil.
Study participants were randomly assigned to one of two groups. Each was provided with two high-fat meals, eaten one week apart. The meals were identical, consisting of a salami-and-cheese sandwich on white bread and a small serving of full-fat yogurt. For one meal, the researchers added about 5 teaspoons (25 ml) of olive oil. For the other, they added 40 grams of walnuts, or about eight shelled nuts.
According to their findings, both the olive oil and the walnuts helped to decrease the sudden onset of inflammation and oxidation in the arteries. These harmful processes, which typically follow consumption of high-fat meals, can lead to hardening of the arteries, or atherosclerosis, a precursor to heart disease.
But unlike olive oil, adding walnuts also helped to preserve the elasticity and flexibility of the arteries, regardless of people's cholesterol levels. This elasticity allows the arteries to expand when needed to increase blood flow to the body.
The walnuts contain arginine. Arginine is a precursor to nitric oxide. Nitric oxide is a signalling agent used by the body to (among other things) cause blood vessels to dilate and let more blood through. Saturated fats are known from previous research to cause the body to produce inflammation molecules which block nitric oxide production. But perhaps higher arginine availability counteracts that effect and keeps nitric oxide production higher.
"The inner lining of the arteries produces a substance called nitric oxide that is needed to keep the arteries flexible," Dr. Ros said. "When we eat high-fat meals, the fat molecules temporarily disrupt the production of nitric oxide, preventing the arteries from increasing blood flow in response to physical activity."
One of the nutrients found in walnuts, he said, is arginine, an amino acid used by the body to produce nitric oxide. Walnuts also contain antioxidants and alpha-linolenic acid (ALA), a plant-based omega-3 fatty acid. Olive oil does not contain ALA, a specific type of healthy, polyunsaturated fat.
The ability of walnuts to enhance nitric oxide production has other implications. Some drugs work by releasing nitric oxide (NO). Among the NO releasing compounds are Minoxidil for treating male pattern baldnessa and Viagra and Cialis for treating erectile dysfunction. There's a chance that consumption of walnuts might therefore provide other benefits as well.
According to the National Osteoporosis Foundation, approximately 55 percent of Americans, mostly women, are at risk of developing osteoporosis, a disease of porous and brittle bones that causes higher susceptibility to bone fractures. Now, Katherine Tucker, PhD, director of the Epidemiology and Dietary Assessment Program at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, and colleagues have reported findings in the American Journal of Clinical Nutrition that cola, a popular beverage for many Americans, may contribute to lower bone mineral density in older women, a condition which increases risk for osteoporosis.
Tucker, also a professor at the Friedman School of Nutrition Science and Policy at Tufts, and colleagues analyzed dietary questionnaires and bone mineral density measurements at the spine and three different hip sites of more than 2,500 people in the Framingham Osteoporosis Study whose average age was just below 60. In women, cola consumption was associated with lower bone mineral density at all three hip sites, regardless of factors such as age, menopausal status, total calcium and vitamin D intake, or use of cigarettes or alcohol.
However, cola consumption was not associated with lower bone mineral density for men at the hip sites, or the spine for either men or women. The results were similar for diet cola and, although weaker, for decaffeinated cola as well.
Men reported drinking an average of six carbonated drinks a week, with five being cola, and women reported consuming an average of five carbonated drinks a week, four of which were cola. Serving size was defined as one bottle, can or glass of cola. “The more cola that women drank, the lower their bone mineral density was,” says Tucker, who is corresponding author of the study. “However, we did not see an association with bone mineral density loss for women who drank carbonated beverages that were not cola.”
“Carbonated soft-drink consumption increased more than three-fold” between 1960 and 1990, cite the authors. They also note that more than 70 percent of the carbonated beverages consumed by people in the study were colas, all of which contain phosphoric acid, an ingredient that is not likely to be found in non-cola carbonated beverages.
Why the cola drinks might cause osteoporosis is unclear. Consumption of less calcium due to colas displacing milk or other foods might be to blame. Or the phosphorus in the form of phosphoric acid might create acidic conditions in the blood that mobilize calcium from the bones. Or perhaps women who drink colas eat less of some foods which are beneficial in other ways.
While previous studies have suggested that cola contributes to bone mineral density loss because it replaces milk in the diet, Tucker determined that women in the study who consumed higher amounts of cola did not have a lower intake of milk than women who consumed fewer colas. However, the authors did conclude that calcium intake from all sources, including non-dairy sources such as dark leafy greens or beans, was lower for women who drank the most cola. On average, women consumed 1,000 milligrams of calcium per day, and men consumed 800 milligrams per day, both lower than the daily recommended 1,200 daily milligrams for adults over age 50.
“Physiologically, a diet low in calcium and high in phosphorus may promote bone loss, tipping the balance of bone remodeling toward calcium loss from the bone. Although some studies have countered that the amount of phosphoric acid in cola is negligible compared to other dietary sources such as chicken or cheese,” Tucker says, “further controlled studies should be conducted to determine whether habitual cola drinkers may be adversely affecting their bone health by regularly consuming doses of phosphoric acid that do not contain calcium or another neutralizing ingredient.”
Sugary drinks are a bad idea because they displace healthier foods. You are better off drinking pure fruit juices that come with anthocyanins and other beneficial flavonoid compounds. Given a choice between empty calories and nutritionally richer foods you should opt for the latter.
If you want caffeine then your best bet is probably green tea or perhaps black tea. A recent study found that black tea reduces blood levels of the stress hormone cortisol after humans are exposed to stressful situations. Tea might also reduce the risk of colorectal cancer. Though the evidence for reduced cancer risk from tea is mixed. Tea cancer reduction success in animal models may be due to use of doses far higher than humans will get from drinking tea.
A new study by Jane Lukacs of the University of Michigan School of Nursing suggests that the impairment of vitamin K function could compromise bone health and contribute to the development of osteoporosis. The study found that one of the early effects of declining estrogen is the impairment of vitamin K function in bone even before any bone loss that could be attributed to menopause can be measured.
"Our study suggests that the generally accepted level of vitamin K in healthy women is inadequate to maintain bone health just at the onset of menopause," Lukacs said.
Vitamin K is essential for making a bone protein called osteocalcin fully functional. This protein is part of the bone structure when it is "carboxylated" (a chemical modification of the protein that changes its shape making it easy to bind to calcium) in the presence of sufficient vitamin K. With adequate vitamin K, this protein can bind to calcium in the bone environment—sort of like glue, Lukacs said.
Vitamin K is good for the bones of guys too.
Check out what the Harvard School of Public Health says about vitamin K. The Nurse's Health Study showed a diet high in vitamin K slashes the risk of bone breaks.
Lately, researchers have demonstrated that vitamin K is also involved in building bone. Low levels of circulating vitamin K have been linked with low bone density, and supplementation with vitamin K shows improvements in biochemical measures of bone health.(31) A report from the Nurses' Health Study suggests that women who get at least 110 micrograms of vitamin K a day are 30% less likely to break a hip as women who get less than that.(32) Among the nurses, eating a serving of lettuce or other green leafy vegetable a day cut the risk of hip fracture in half when compared with eating one serving a week. Data from the Framingham Heart Study also shows an association between high vitamin K intake and reduced risk of hip fracture.(33)
Optimal Intake: The recommended daily intake for vitamin K is 80 micrograms for men and 65 for women. Because this vitamin is found in so many foods, especially green leafy vegetables and commonly used cooking oils, most adults get enough of it. According to a 1996 survey, though, a substantial number of Americans, particularly children and young adults, aren't getting the vitamin K they need.(34)
Note that the 65 mcg recommended daily intake is probably too low for post-menopausal women. So what to do about it? 3 and a half ounces of kale or swiss chard will give you over 800 mcg of vitamin K. Spinach will give you half that amount. Collard greens and turnip greens are also very high sources of vitamin K. Parsley, broccoli, and brussel sprouts are all good vitamin K sources as well.
Adults in Japan who consumed higher amounts of green tea had a lower risk of death due to all causes and due to cardiovascular disease, according to a study in the September 13 issue of JAMA. But there was no link between green tea consumption and a reduced risk of death due to cancer.
Tea is the most consumed beverage in the world aside from water. Three billion kilograms of tea are produced each year worldwide, according to background information in the article. Because of the high rates of tea consumption in the global population, even small effects in humans could have large implications for public health. Among teas, green tea polyphenols have been extensively studied as cardiovascular disease (CVD) and cancer chemopreventive agents. Although substantial evidence from in vitro and animal studies indicates that green tea preparations may impede CVD and carcinogenic processes, the possible protective role of green tea consumption against these diseases in humans remains unclear.
Shinichi Kuriyama, M.D., Ph.D., of the Tohoku University School of Public Policy, Sendai, Japan, and colleagues examined the association between green tea consumption and mortality (death rate) due to all causes, CVD, and cancer within a large population. The study, initiated in 1994, included 40,530 adults (age 40 to 79 years) in northeastern Japan, where green tea is widely consumed. Within this region, 80 percent of the population drinks green tea and more than half of them consume 3 or more cups and day. The participants, who had no history of stroke, coronary heart disease, or cancer at baseline, were followed for up to 11 years (1995-2005) for all-cause death and for up to 7 years (1995-2001) for cause-specific death.
Over 11 years of follow-up, 4,209 participants died, and over 7 years of follow-up, 892 participants died of cardiovascular disease and 1,134 participants died of cancer. The researchers found that green tea consumption was inversely associated with death due to all causes and due to cardiovascular disease. Compared with participants who consumed less than 1 cup/d of green tea, those who consumed 5 or more cups/d had a risk of all-cause mortality and CVD mortality that was 16 percent lower (during 11 years of follow-up) and 26 percent lower (during 7 years of follow-up), respectively.
These inverse associations of all-cause and CVD mortality were stronger among women, although the inverse association for green tea consumption was observed in both sexes. In women, compared with those who consumed less than 1 cup/d of green tea, those who consumed 5 or more cups/d had a 31 percent lower risk of CVD death.
Actuarial Escape Velocity (AEV) is the point where the rate of advance in the development of rejuvenating medical therapies becomes faster than the rate of aging. Bodies will become rejuvenated faster than they age. Your odds of living to the day when AEV is reached depends on a couple of factors that are under your control. First off, you can help speed up the rate of biomedical advance by supporting efforts like the Methuselah Mouse Prize to provide scientists with more incentives to work on rejuvenation therapies. You can also let your elected officials know that you want to see governments aggressively fund the development of Strategies for Engineered Negligible Senescence (SENS) to develop the technologies that will make it possible to repair the accumulation of damage which is aging.
Of course, even if you do all you can to support biotechnological advances needed to conquer aging you still are at risk of dying before the SENS treatments become available. So what to do about that? Eat better. Drink better too. Get exercise too.
For a larger discussion of polyphenols, flavonoids, and other chemicals in foods that lower disease risk see my post Fruit And Vegetable Juices Make Big Cut In Alzheimers Risk.
A cup of coffee may cause a heart attack in some people within an hour of drinking it, according to a study reported in the journal Epidemiology (“Transient Exposure to Coffee as a Trigger of a First Nonfatal Myocardial Infarction,” (Volume 17, Issue 5, September 2006.) The risk was highest among people with light or occasional coffee intake, and those with a sedentary lifestyle or other risk factors for coronary heart disease.
Studying 503 cases of non-fatal myocardial infarction in Costa Rica, Ana Baylin of Brown University and her colleagues of Harvard School of Public Health surveyed participants about their coffee consumption in the hours and days before their heart attack. They also studied the participants’ socio-demographic characteristics, lifestyle, and medical history. They theorized that caffeine causes short-term increases in blood pressure and sympathetic nervous activity that could affect a vulnerable atherosclerotic plaque, and trigger a heart attack.
The researchers found that the moderate coffee drinkers, by having a cup of coffee, increased their risk of having a heart attack by 60%. There was little effect among heavy coffee drinkers, but light coffee drinkers increased their risk of heart attack by more than four times. This may be because lighter drinkers are less acclimated to the effects of caffeine. Baylin and her team also found that patients with three or more risk factors for coronary heart disease more than doubled their risk.
“People at high risk for a heart attack who are occasional or regular coffee drinkers might consider quitting coffee altogether,” comments Baylin, adding that for these individuals, a cup of coffee could be “the straw that broke the camel’s back.”
Also see my quite useful post Scientists Demonstrate Best Way To Use Caffeine.
Update: A New York Times survey of the health effects of coffee finds it has anti-inflammatory effects and studies have found that coffee reduces the risk of diabetes, liver cirrhosis, heart disease, and other disorders. The heart health benefit of coffee comes only in a sub-range of coffee consumption.
Some studies show that cardiovascular risk also decreases with coffee consumption. Using data on more than 27,000 women ages 55 to 69 in the Iowa Women’s Health Study who were followed for 15 years, Norwegian researchers found that women who drank one to three cups a day reduced their risk of cardiovascular disease by 24 percent compared with those drinking no coffee at all.
But as the quantity increased, the benefit decreased. At more than six cups a day, the risk was not significantly reduced.
The identification of the beneficial and harmful compounds in coffee and other foods will eventually lead to the development of foods which contain optimal concentrations of beneficial compounds and much less of the harmful compounds. Genetic engineering, breeding, and food processing methods will all be used to optimize the health benefits of foods based on increasing amounts of scientific knowledge..
Hackettstown, NJ – July 31, 2006 -- Flavanol-rich cocoa could offer powerful cardiovascular benefits for the nearly 78 million baby boomers in the United States today, suggests a new study published in the August issue of the Journal of Hypertension.
Researchers at Harvard Medical School and the Brigham and Women's Hospital in Boston found that drinking a standardized flavanol-rich cocoa beverage improved several measures of blood vessel function, especially among older study participants. Flavanols are the natural compounds in cocoa that are increasingly being linked to promising circulatory benefits – including improved blood flow and a reduced tendency to form damaging clots.
In the current study, 15 healthy young adults under age 50, and 19 healthy adults over age 50 drank the specially-made flavanol rich cocoa beverage daily for four to six days. The researchers tracked changes in the function of their peripheral arteries using several measures, including peripheral arterial tonometry a standard method for evaluating the health of an individual's blood vessels. At the study's completion, significant improvements in vessel function following the consumption of flavanol rich cocoa were seen in both young and older adults. While aging has previously been shown to lead to a deterioration of blood vessel function, this study is the first to demonstrate that the consumption of flavanol-rich cocoa can improve this age-related loss of vessel function in older adults. In agreement with previous studies using this same cocoa, these improvements in both young and older adults appear to be linked to the ability of cocoa flavanols to influence the body's production of nitric oxide, a key regulator of blood vessel tone.
Compared to the younger subjects, the vessel responses of the older men and women were significantly more pronounced after drinking the flavanol-rich cocoa beverage -- suggesting that the consumption of this flavanol rich cocoa offers a dietary approach for maintaining endothelial vessel function, and indicates the possibility that this cocoa could be useful for improving endothelial function in our aging population.
We have to eat foods to get various nutrients. But then there are the foods with a variety of non-nutrient compounds that have medicinal value: decreased cancer risk, decreased heart risk, and other benefits. It is hard to figure out how to make optimal choices.
A lot of chocolates have low levels of flavonols. Mars has seen to it that Dark Dove chocolate is higher in flavonols than other chocolates. But it still contains plenty of sugar and cocoa fat of course. So its net benefit is far from clear - at least to me. Lower calorie foods that have healthy compounds seem better choices. But if you are going to eat chocolate make it as dark and low sugar as possible.
You can't just take a pill to avoid health problems. At least not yet. Some day biotechnological advances will free us from the need to select our diets carefully. But for now drugs can not do the job alone.
Boston, MA -- A prospective study of 42,847 middle-aged and older U.S. men participating in the Health Professionals Follow-up Study has found that a healthy lifestyle is associated with a lower risk of coronary heart disease (CHD), even among men taking antihypertensive or lipid-lowering medications. The research, which is the first to look at the role of a healthy lifestyle and CHD in men in this age group, is published in the July 3, 2006, online edition of Circulation.
The research team, led by Eric Rimm, associate professor of epidemiology and nutrition at Harvard School of Public Health (HSPH) and Stephanie Chiuve, research fellow in nutrition at HSPH, did a 16-year follow-up of men aged 40-75 in the Health Professionals Follow-up Study, a men's health study that began in 1986. The researchers defined healthy lifestyle factors as not smoking, daily exercise, moderate alcohol consumption, a healthy body weight and a healthy diet (based upon the Alternate Healthy Eating Index developed by HSPH, which targets food and nutrients associated with lower risk of chronic disease). The study, which documented 2,183 coronary events, found that men with all five healthy lifestyle factors had a lower risk of CHD compared to men with none of those factors. It also found that 62 percent of coronary events may have been prevented if all men in the study population adhered to all five healthy lifestyle factors; for those men taking medications, 57 percent could have been prevented. Men who adopted two or more low-risk factors during the study period (1986-2002) had a 27 percent lower risk of CHD. Overall, for each healthy lifestyle factor, the authors found an inverse association with CHD risk.
Well, statins used to lower cholesterol will not provide an optimal outcome. Diet still matters, not surprisingly.
If you want to follow their dietary recommendations then check out the food pyramid for the Alternate Healthy Eating Index. My guess is you can do even better than that food pyramid by enhancing it with the "Ape Diet" recommendations of David Jenkins at U Toronto.
New research suggests one reason vegetables may be so good for us – a study in mice found that a mixture of five common vegetables reduced hardening of the arteries by 38 percent compared to animals eating a non-vegetable diet. Conducted by Wake Forest University School of Medicine, the research is reported in the current issue of the Journal of Nutrition.
“While everyone knows that eating more vegetables is supposed to be good for you, no one had shown before that it can actually inhibit the development of atherosclerosis,” said Michael Adams, D.V.M., lead researcher. “This suggests how a diet high in vegetables may help prevent heart attacks and strokes.”
The study used specially bred mice that rapidly develop atherosclerosis, the formation on blood vessel walls of fatty plaques that eventually protrude into the vessel’s opening and can reduce blood flow. The mice have elevated low-density lipoprotein ( LDL), or “bad” cholesterol, which is also a risk factor for atherosclerosis in humans.
Half of the mice in the study were fed a vegetable-free diet and half got 30 percent of their calories from a mixture of freeze-dried broccoli, green beans, corn, peas and carrots. These five vegetables are among the top-10 vegetables in the United States based on frequency of consumption.
After 16 weeks, the researchers measured two forms of cholesterol to estimate the extent of atherosclerosis. In mice that were fed the vegetable diet, researchers found that plaques in the vessel were 38 percent smaller than those in the mice fed vegetable-free diets. There were also modest improvements in body weight and cholesterol levels in the blood.
The estimates of atherosclerosis extent involved measuring free and ester cholesterol, two forms that accumulate in plaques as they develop. The rate of this accumulation has been found to be highly predictive of the actual amount of plaque present in the vessels.
Most people do not eat an optimal amount of vegetables. Another report providing yet more evidence on the benefits of vegetables won't cause many to alter their diets. Maybe what we need is some sort of Pop-Tart that is mostly vegetables but with flavoring designed to hide the vegetable taste.
Veggies reduce inflammation.
He said that a 37 percent reduction in a certain marker of inflammation in mice suggests that vegetable consumption may inhibit inflammatory activity.
“It is well known that atherosclerosis progression is intimately linked with inflammation in the arteries,” Adams said. “Our results, combined with other studies, support the idea that increased vegetable consumption inhibits atherosclerosis progression through antioxidant and anti-inflammatory pathways.”
Since mouse studies can be done more rapidly and cheaply than human studies I'd love to see this study repeated with different vegetables diluted with conventional mouse chow to see which veggies are most potent. Potent veggies could be used in smaller doses in veggie Pop-Tarts. High potency veggie Pop-Tarts are our only hope.
We need high potency veggie Pop-Tarts to buy us some extra time while we wait for the development of SENS technologies.
GAINESVILLE, Fla., - A lifelong habit of trimming just a few calories from the daily diet can do more than slim the waistline - a new study shows it may help lessen the effects of aging.
Scientists from the University of Florida's Institute on Aging have found that eating a little less food and exercising a little more over a lifespan can reduce or even reverse aging-related cell and organ damage in rats.
The discovery, described this month in the journal Antioxidants and Redox Signaling, builds on recent research in animals and humans that has shown a more drastic 20 percent to 40 percent cut in calories slows aging damage. The UF findings indicate even small reductions in calories could have big effects on health and shed light on the molecular process responsible for the phenomenon, which until now has been poorly understood.
"This finding suggests that even slight moderation in intake of calories and a moderate exercise program is beneficial to a key organ such as the liver, which shows significant signs of dysfunction in the aging process," said Christiaan Leeuwenburgh, Ph.D., an associate professor of aging and geriatric research at the UF College of Medicine and the paper's senior author.
UF scientists found that feeding rats just 8 percent fewer calories a day and moderately increasing the animals' activity extended their average lifespan and significantly overturned the negative effects of cellular aging on liver function and overall health.
An 8 percent reduction is the equivalent of a few hundred calories in an average human diet and moderate exercise is equivalent to taking a short walk.
But most people can't reduce their calorie consumption at all for a sustained length of time. So this is an interesting result and a reason to eat slightly less. But few will manage to pull that off.
The researchers also found that RNA is an earlier biomarker for aging than DNA.
To reveal the workings of the body's chemical climate when aging-related damage happens, UF researchers tracked levels of biomarkers - chemicals and molecules present in the liver - in groups of rats. The liver, a crucial organ for maintaining good health during aging, cleans the blood and helps regulate the body's immune system. The researchers also plan to assess the same biomarkers in a study of rats' hearts, muscle and brains.
The research team was surprised to find one of the biomarkers, RNA, which is important for coding DNA and for protein synthesis, is more quickly damaged by aging than the more frequently studied DNA. RNA damage, therefore, could be an excellent early signal to indicate the onset of aging, researchers say.
"Because it is more sensitive to oxidative stress, RNA can be useful as an early marker of oxidative damage and even aging," said Arnold Y. Seo, a doctoral student in UF's Institute on Aging.
Better aging biomarkers that detect changes at earlier stages allow more rapid testing of potential life extending therapies.
Another study on rats found important clues for how calorie restriction lengthens life expectancy. Mice lacking a growth hormone receptor and with lower resulting insulin live longer than normal mice.
"The implication ... for pharmaceutical development would be that the signaling pathways of growth hormone and insulin may be logical targets for development of anti-aging medicine," Dr. Andrezej Bartke from Southern Illinois University in Springfield told Reuters Health.
However, in sharp contrast to its effects in normal mice, calorie restriction failed to increase lifespan in mutant mice lacking growth hormone receptor. "The present findings show that growth hormone resistant mice fail to respond normally to calorie restriction, a very effective life-extending intervention," Bartke said.
I think the idea here is that the reduction in growth hormone receptor delivers the life extension benefit that calorie reduction would normally deliver. So when calories are reduced in these mice there is not an additional benefit from the calorie reduction.
Update: You can read the paper in the Proceedings of the National Academy Of Science by Bartke's group in abstract and the full paper in open access.
Robert Beelman at Penn State and some Finnish scientists have discovered that UV light shined on mushrooms is an easy way to boost dietary vitamin D.
The ongoing work, so far, has found that a single serving of white button mushrooms the most commonly sold mushroom will contain 869 percent the daily value of vitamin D once exposed to just five minutes of UV light after being harvested. If confirmed, that would be more than what's in 2 tablespoons of cod liver oil, one of the richest and most detested natural sources of the vitamin, according to the National Institutes of Health.
Details were being presented this week at the FDA's annual science forum. The FDA proposed the research, which was funded by the Mushroom Council, as the agency looks for ways to increase the amounts of vitamin D consumed by Americans.
Overall, each additional unit of the Mediterranean diet adherence score (a zero to nine-point scale) was associated with a 9% to 10% decreased risk for Alzheimer's, reported Nikolaos Scarmeas, M.D., of Columbia University here, and colleagues, in the April issue of the Annals of Neurology and published online.
Compared with participants who had the lowest adherence to the diet, the risk for those with the highest adherence was 39% to 40% lower, while those in the middle tertile had a decreased Alzheimer's risk of 15% to 21%. This, the investigators said, showing a significant dose response, and sensitivity analysis did not change these findings.
Scarmeas followed more than 2,000 cognitively normal elderly people from Manhattan, with an average age of 77 years, for about four years. Every 18 months the participants filled out a dietary questionnaire asking them about what they consumed and how often. In total, 262 of the participants developed Alzheimer's during the course of the study.
The changes that lead to Alzheimer's start happening decades before the full blown disease. Therefore following a better diet makes sense even if you are fairly young.
Good news! Cocoa really does help you live longer.
A study of elderly Dutch men indicates that eating or drinking cocoa is associated with lower blood pressure and a reduced risk of death, according to an article in the February 27 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
Cocoa has been linked to cardiovascular health benefits since at least the 18th century, but researchers are just beginning to collect scientific evidence for these claims, according to background information in the article. Cocoa is now known to contain chemicals called flavan-3-ols, which have been linked to lower blood pressure and improved function of the cells lining the blood vessels.
Brian Buijsse, M.Sc., National Institute for Public Health and the Environment, Bilthoven, the Netherlands, and colleagues examined cocoa's relationship to cardiovascular health in 470 Dutch men aged 65 to 84 years. The men underwent physical examinations and were interviewed about their dietary intake when they enrolled in the study in 1985 and at follow-up visits in 1990 and 1995. The researchers then placed them into three groups based on their level of cocoa consumption. Information about their subsequent illnesses and deaths were obtained from hospital or government data.
Over the next 15 years, men who consumed cocoa regularly had significantly lower blood pressure than those who did not. Over the course of the study, 314 men died, 152 due to cardiovascular diseases. Men in the group with the highest cocoa consumption were half as likely as the others to die from cardiovascular disease. Their risk remained lower even when considering other factors, such as weight, smoking habits, physical activity levels, calorie intake and alcohol consumption. The men who consumed more cocoa were also less likely to die of any cause.
Although blood pressure is usually linked with risk of cardiovascular death, that was not the case in this study. "The lower cardiovascular mortality risk associated with cocoa intake could not be attributed to the lower blood pressure observed with cocoa use," the authors write. "Our findings, therefore, suggest that the lower cardiovascular mortality risk related with cocoa intake is mediated by mechanisms other than lowering blood pressure." The benefits associated with flavan-3-ols may play a role.
Of course some people are determined to believe that nothing that you love could possibly be good for you. Cathy Ross, medical spokesperson for the British Heart Foundation, still discourages chocolate consumption.
"Cocoa is rarely tolerable in large amounts in its raw state and therefore to consume the suggested therapeutic amount you would have to have 100g of dark chocolate per day.
"This would mean an average intake of 500 calories per 100g and an average 30% of fat. Eating less did not produce the same effect.
"We are certainly not suggesting people never eat chocolate - everyone can enjoy a treat from time to time.
"But there are much better ways of improving your heart health."
If you are going to eat chocolate then the darker and the lower in sugar the better. I personally get semi-sweet cooking chocolate. I'd like to find some lower in sugar and cocoa butter. To keep the calories down as an alterrnative I've started eating cocoa powder straight on occasion. Might try it in apple sauce and eat it more regularly instead of dark chocolate.
Not all dark chocolates are the same. Processing removes some of the antioxidants. Mars dark chocolate has more of the antioxidants than the average chocolate. But I'm not clear on how big a difference there is between the various dark chocolates. I'd really like to find a cocoa powder that has the least amount of flavanoids and flavanols removed. Such a cocoa powder might be more bitter tasting though.
What I want to know: Does cocoa keep down blood pressure by increasing nitric acid synthesis? If so, it might just be a mild aphrodisiac as well.
Adopting a low-fat diet in later life and following such a regimen for nearly a decade does not appear to have a significant impact on reducing the overall risk of breast cancer, colorectal cancer or heart disease, according to a Women's Health Initiative study that involved nearly 50,000 postmenopausal women across the United States. The results of the federally funded dietary modification study will be published in a series of three papers – two with lead authors at Fred Hutchinson Cancer Research Center and all three involving co-authors from the Hutchinson Center – in the Feb. 8 issue of the Journal of the American Medical Association, or JAMA.
The study – the first attempt to test the health impact of a low-fat diet in a randomized, controlled trial, considered the gold standard of clinical and public-health study design – did, however, uncover some encouraging trends, according to Hutchinson Center biostatistician Ross L. Prentice, Ph.D., lead author of the JAMA paper that describes the impact of a low-fat diet on breast-cancer risk, one of the primary goals of the study.
"Women in the low-fat-diet group reduced their overall rate of breast cancer by about 9 percent as compared to the women who didn't change their eating patterns, but that difference was not statistically significant; it could have been due to chance. So at this point we're not able to say with certainty that a low-fat diet reduces the risk of breast cancer," said Prentice, member and former director of the Hutchinson Center's Public Health Sciences Division. A 9 percent reduction in breast-cancer incidence means that, out of 10,000 women, 42 in the low-fat-diet group and 45 in the comparison group developed breast cancer each year.
Prentice and colleagues did find, however, that a low-fat diet was associated with a statistically significant 15 percent reduction in estradiol, a form of blood estrogen that increases the risk of breast cancer.
My guess is that if people could manage to stay on diets for decades then we'd see larger differences in results.
The 30% reduction in a single subtype of breast cancer suggests they really did find an effect from lower fat diets but that only some mechanisms by which cancer is generated are affected much by fat level in the diet.
Women in the low-fat group also experienced a 30 percent risk reduction for a certain subtype of breast cancer: tumors that were progesterone-receptor negative. "This finding provides an interesting hypothesis for further development and reinforces that breast cancer is multifaceted; it is not a single disease," Prentice said. PR-negative tumors, while relatively rare, are difficult to treat and associated with a higher mortality rate because they are unresponsive to hormone-blocking drugs such as tamoxifen.
The larger the decrease in fat in the diet (due to starting with a higher percentage of fat to begin with) the bigger the measured benefit:
Significant results were seen also among women in the low-fat-diet group who began the study with the highest baseline fat consumption and among women who most strictly adhered to the study's dietary-fat goals. Women in these categories experienced a 15 percent to 20 percent overall reduction in breast-cancer incidence.
"The bottom line is that changing to a low-fat diet may reduce breast-cancer risk, especially among women who have a relatively high-fat diet to begin with, but we don't view our data as strong enough at this time to make a broad recommendation that all women initiate a low-fat diet for that purpose," Prentice said. "Additional follow up with these women may yield a stronger, statistically significant conclusion."
With regard to colorectal cancer, the study did not reveal a reduction of cancer incidence overall, but it did show a modest 9 percent decrease in self-reported colon polyps – a precursor to colon cancer – among the women in the low-fat intervention group, according to Shirley A.A. Beresford, Ph.D., lead author of the paper describing the colorectal-cancer findings.
"It is important to remember that cancers often take decades to develop, and we may only be seeing the early stages of the impact of a low-fat diet intervention on the risk of colorectal cancer and other diseases," said Beresford, a member of the Hutchinson Center's Public Health Sciences Division and a professor of epidemiology at the University of Washington School of Public Health and Community Medicine. "The reduction in polyps suggests a possible reduction in colorectal-cancer risk could emerge over a longer time period." No significant reduction in heart disease emerged among the women in the low-fat intervention group, who achieved only a 2.4 percent reduction in low-density lipoprotein, or LDL, the so-called "bad" cholesterol, and a 3 percent lower rate of heart disease.
The study did, however, find trends toward reduction in heart-disease risk among the subset of women in the low-fat-diet group who made the greatest reduction in consumption of saturated fat and trans fat, both of which can raise the risk of heart disease because they increase production of LDL cholesterol.
"For heart-disease prevention, the data suggests that a greater emphasis on reduction of saturated and trans fats will be needed to have a major difference," Prentice said. Barbara V. Howard, Ph.D., president of MedStar Research Institute/Howard University in Washington, D.C., was the lead author of the heart-disease paper.
A reduction of dietary fat to only 20% of calories still falls well short of a Pritikin style diet where one might get only 10% of calories from fat. If they'd tried for a larger fat reduction they might have picked up a stronger signal in the data.
In my mind I hear Joe Jackson singing.
Everything gives you cancer
Everything gives you cancer
There’s no cure, there’s no answer
Everything gives you cancer
Forty percent of the participants were assigned to the low-fat diet, in which they were asked to reduce their fat intake to 20 percent of their total calories while eating five or more daily servings of vegetables and fruits and six servings of grains. The remaining 60 percent served as a comparison group and did not change their diet.
Although the primary hypotheses of protective effects of a low-fat diet on breast and colorectal cancer failed the test, the WHI researchers pointed out that the majority of women assigned to the low-fat diet didn't meet the 20 percent fat goal: On average, the women reduced their fat intake to 24 percent in the first year, but slowly increased their fat intake to 29 percent by the eighth year.
Furthermore, the study showed that women who had the highest fat intake at the study's outset showed greater evidence for reducing their breast cancer risk on the diet program. There was also a suggestive trend of breast cancer risk reduction for women who initially had the lowest consumption of vegetables and fruits and then increased their intake by one serving per day as part of the diet.
So the study was only for 8 years and yet our risk of cancer is the result of decades of accumulation of damage to our bodies. Also, the ladies didn't stay on their diets just like people do not stick to all the other diets they go on. Expecting people to stick with a diet for years isn't realistic.
A final point: I predict that in 10 years time we'll have plenty of genetic tests that tell us not only our genetic predisposition to various cancers (we already have some such tests) but also the genetic tests will tell us how much our individual risk will be modified by various dietary changes. Some people will be told that lowering their dietary fat won't matter much. Others will be told that lowering their dietary fat (or perhaps just specific kinds of fat) will have a big impact on their cancer risks. I hope the conductors of the study above took and stored DNA samples from the participants in this study. 10 or so years from now when DNA testing will be orders of magnitude cheaper testing of the DNA sequences of study participants could yield very useful information on how DNA variations and diet interact to influence cancer and heart disease risks.
Vitamin D may play a role in keeping our lungs healthy, with greater concentrations of vitamin D resulting in greater lung health benefits. A study in the December issue of CHEST, the peer-reviewed journal of the American College of Chest Physicians (ACCP), shows that patients with higher concentrations of vitamin D had significantly better lung function, compared with patients with lower concentrations of vitamin D.
"Low levels of vitamin D have been associated with osteoporosis, hypertension, diabetes, and cancer," said lead author Peter Black, MB, ChB, Department of Medicine, University of Auckland, Auckland, New Zealand. "Our research shows that vitamin D may also have a strong influence on lung health, with greater levels of vitamin D associated with greater and more positive effects on lung function."
Researchers from the University of Auckland examined the relationship between vitamin D and lung function using participants from the United States National Health and Nutrition Examination Survey (NHANES III) carried out during 1988 to 1994. The study included 14,091 people aged >= 20 years, who were interviewed at mobile examination centers, had spirometry performed, and had serum 25-hydroxyvitamin D measured. Vitamin D measurements were divided into five groups (quintiles), ranging from more than 85.7 mL to less than 40.4 mL. After adjusting for gender, age, ethnicity, body mass index, and smoking status, the differences between the lowest quintile of vitamin D and the next quintile were 79 mL for FEV1 and 71 mL for FVC. In comparison, the differences between the highest and lowest quintiles of vitamin D were 126 mL for FEV1 and 172 mL for FVC. With further adjustment for physical activity, intake of vitamin D supplements and milk, and antioxidant level, the difference between the highest and lowest quintiles of vitamin D also was significant at 106 mL for FEV1 and 142 mL for FVC. In addition, an association between vitamin D and FEV1 was seen in non-Hispanic whites and blacks and was greater for those over 60 years and current or former smokers.
Here is the most amazing part.
"The difference in lung function between the highest and lowest quintiles of vitamin D is substantial and greater than the difference between former and nonsmokers," said Dr. Black. "Although there is a definite relationship between lung function and vitamin D, it is unclear if increases in vitamin D through supplements or dietary intake will actually improve lung function in patients with chronic respiratory diseases."
Overall, male gender, younger age, white ethnicity, nonsmoking status, and regular, vigorous physical activity were associated with the highest lung function. Vitamin D was higher in men than women, was inversely related to BMI, and declined with age. Vitamin D also was lower in non-Hispanic blacks and Mexican-Americans, compared with non-Hispanic whites, and it was lower in participants smoking more than 20 cigarettes a day compared with nonsmokers.
"Vitamin D would be a relatively simple, low-cost intervention that would likely have high compliance to prevent or slow loss of lung function in susceptible subgroups. However, further studies examining the relationship between vitamin D and lung function are warranted to identify who may benefit from such an intervention," said author of the study's corresponding editorial Rosalind Wright, MD, MPH, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
"Chronic lung conditions compromise quality of life for millions of people in the United States and around the world," said W. Michael Alberts, MD, FCCP, President of the American College of Chest Physicians. "By understanding the effect that vitamins have on lung function, we may be able to identify new and more effective treatments for these debilitating diseases."
People working indoors do not get the sun exposure that their ancestors got as farmers and manual laborers. Vitamin D deficiency is a common problem.
Also see my previous posts Vitamin D Could Decrease Overall Cancer Risk 30% and Higher Vitamin D Reduces Aging Bone Fracture Risks.
Don't want to become less muscular as you age? Here is news you can probably use.
Muscle in adults is constantly being built and broken down. As young adults we keep the two processes in balance, but when we age breakdown starts to win. However, adding the amino acid leucine to the diet of old individuals can set things straight again. This is the finding of research performed by Lydie Combaret, Dominique Dardevet and colleagues at the Human Nutrition Research Centre of Auvergne, INRA, Clermont-Ferrand, France.
After the age of 40, humans start loosing muscle at around 0.5–2% per year. Immediately after a meal degradation of protein slows down and synthesis doubles. This process is triggered by the arrival of a plentiful supply of amino acids. In older animals this stimulus is less effective; synthesis slows down, and previous work also suggests that breakdown may be affected. While adding leucine to the diet restores protein building there was no knowledge about this supplement's effect on breakdown.
To address this, researchers compared protein breakdown in young (8-month) and old (22-month) rats. They discovered that the slow down in degradation that normally follows a meal does not occur in old animals, so there is excessive breakdown. But adding leucine to the diet restored a balanced metabolism.
The team of researchers believe that the age-related problem results from defective inhibition of ubiquitin-proteasome dependent proteoloysis, a complex degradative machinery that breaks down contractile muscle protein, and that leucine supplementation can fully restore correct function.
"Preventing muscle wasting is a major socio-economic and public health issue, that we may be able to combat with a leucine-rich diet," says senior co-author Didier Attaix.
Commenting on the work Michael Rennie from the University of Nottingham Medical School at Derby says: "This is exciting because it strengthens the idea of a co-ordinated linkage between the meal-related stimulation of protein synthesis and the inhibition of breakdown."
Here for the convenience of American readers is a Froogle Google search on Leucine.
No, I do not know what would be an appropriate human daily dose. Does any reader have an informed basis for estimating a reasonable daily leucine dose?
DURHAM, N.C. -- People who followed a low-carbohydrate diet for six months raised their good cholesterol and lowered their triglycerides, changes that can help lower the risk of heart disease, Duke University Medical Center researchers found.
The Duke study compared the effects of a low-carbohydrate diet, which included nutritional supplements, with a low-fat, low-cholesterol, low-calorie diet. The two diets improved cardiac risk in different ways, said lead researcher Eric Westman, M.D., associate professor of medicine at Duke University Medical Center.
The low-carb diet improved HDL, or good cholesterol levels, and lowered triglycerides, the researchers found. The reduced fat diet lowered total cholesterol levels and triglyceride levels. Both diets brought down blood levels of small LDL particles, the form of bad cholesterol most likely to lead to hardened arteries, they found.
The results appeared early online November 16, 2005 in the International Journal of Cardiology and will appear in print in 2006. The research was funded by an unrestricted grant from the Robert C. Atkins Foundation. The study authors have no financial interest in Atkins Nutritionals, Inc.
"I think the emerging science shows different diets improve cardiac risk in different ways. We are moving from a one-size-fits-all approach to considering many different diets to fit the many different types of cardiac risk," Westman said.
Triglycerides fell much more on the low carb diet.
Overall, both diets had positive effects on cholesterol, Westman said. The triglyceride levels improved significantly in both groups, falling 74.2 points for the low-carb group and 27.9 points for the low-fat group. People on the low-carb diet showed an increase in HDL cholesterol by 5.5 points, a positive change, while those following the low-fat diet did not have a significant change. LDL cholesterol levels did not change significantly in either group but small LDL particles decreased 17.4 points for the low-carb dieters and 19.2 points for the low-fat dieters, a similar improvement. The total cholesterol of the low-fat dieters saw a 13.7 point decline over 6 months but did not change significantly in the low-carb dieters.
My guess is there is enough genetic variability in how bodies respond to different diets that one would benefit from trying different diets and then getting one's cholesterol tested.
They say the participatns were "in generally good health". But some of the participants have body mass indexes as high as 60. Er, this doesn't strike me as compatible with the "generally good health" label. Also, these people all had high cholesterol levels.
The 120 study participants were randomly assigned to either the low-carbohydrate diet or the low-fat, low-cholesterol, low-calorie diet. All were between 18 and 65 years old and in generally good health, with a body mass index (BMI) between 30 and 60, indicating obesity, and a total cholesterol level of more than 200 mg/dL. None had tried dieting or weight loss pills in the previous six months.
There's also the possibility that people who have low cholesterol levels react to low fat and low carbohydrate diets differently than do people with high cholesterol. So if you have low cholesterol yet still want to optimize your diet be aware this study might not provide useful guidance.
The low carb dieters were allowed unlimited meat and eggs. But the details matter a great deal. My guess is you'd be a lot better off eating unlimited salmon than unlimited beef and then fowl would fall somewhere in between salmon and beef in terms of health effects. But what proportion of each meat type did the dieters choose?
The low-carbohydrate group was permitted daily unlimited amounts of animal foods (meat, fowl, fish and shellfish); unlimited eggs; 4 oz. of hard cheese; two cups of salad vegetables such as lettuce, spinach or celery; and one cup of non-starchy vegetables such as broccoli, cauliflower or asparagus. They also received daily nutritional supplements -- a multivitamin; essential oils including flax seed oil, borage oil and fish oil; and chromium picolinate. There were no restrictions on total calories, but carbohydrates were kept below 20 grams per day at the start of the diet.
The low-carbohydrate diet appears to have a favorable effect on cardiac risk, Westman said. "While the low-carbohydrate group received extra nutritional supplements, and experienced greater weight loss, these differences did not fully account for the changes in cardiac risk factors that we saw," he said.
The low-fat, low-cholesterol, low-calorie group followed a diet consisting of less than 30 percent of daily caloric intake from fat; less than 10 percent of calories from saturated fat; and less than 300 milligrams of cholesterol daily. They were also advised to cut back on calories. The recommended daily calorie level was 500 to 1,000 calories less than the participant's maintenance diet -- the calories needed to maintain current weight.
The size of the cutback in fat does not seem that radical to me and falls far short of a Pritikin-style diet.
Both diets leave out junk foods.
Westman noted that the diets have one often-ignored similarity. "It's possible that the common denominator of these diets is what they're not eating – both diets did not allow refined sugar or junk food," Westman said.
Study participants were encouraged to exercise 30 minutes at least three times per week, but no formal exercise program was provided. Both sets of dieters had group meetings at an outpatient research clinic regularly for six months.
I have a hard time coming to a conclusion on the debate about the ideal relative ratio of carbos to proteins to fats. Certainly the types of fats matter a great deal with differences as a function of omega 3 versus omega 6 fats and also fats of various levels of saturation. Plus, particular fatty acids might have especially harmful or healthful effects.
I'd like to see blood fat and cholesterol comparisons of diets with different types of carbs. How does a fruit diet differ from, say, a potato diet? Carb glycemic index differences cause differences in the size of blood spikes when consuming carbs and that might lead to differences in amounts of triglycerides and cholesterol. Imagine two groups ate equal amounts of rice but one group ate low glycemic index basmati rice and another ate the really sticky high glycemic index rice found at Chinese restaurants. My guess is the latter rice diet would have worse effects on blood fats and cholesterol than a basmati rice diet.
The benefit from eating a lot of fruits and vegetables seems more certain that the benefit of changing the relative proportion of fats, proteins, and carbs. Also, a number of foods have clear health risks. For example, charcoal cooked steak should be avoided. The flames and fossil fuels burning with the steak fat are a guaranteed way to produce a lot of carcinogens. Also, trans fatty acids found in many processed foods such as potato chips and many commercial cookies are definitely health unhealthy.
If you want to start improving your diet first remove the very bad foods from it while adding clear winners such as fruits and vegetables.
With an aging population, and with people living longer, experts say bone fractures will become a bigger and more costly problem unless more is done to prevent them. Osteoporosis (reduced bone mineral density) is most common in older adults, particularly women. It is a major risk factor for bone fractures, which can cause significant suffering while carrying high economic costs. While vitamin D has been shown to reduce the risk of fracture in the elderly, a study recently published in the Journal of the American Medical Association (JAMA) raises the question of how much vitamin D is enough.
The Recommended Dietary Allowance (RDA) of vitamin D for older adults is between 400 and 600 International Units (IU) per day. In their review of the existing literature, a team of scientists including senior author Bess Dawson-Hughes, MD, director of the Bone Metabolism Laboratory at the Jean Mayer USDA Human Nutrition and Research Center on Aging at Tufts University, found that this dose was not effective in reducing nonvertebral fracture rates among study participants. The researchers concluded, though, that higher daily doses, in the range of 700 to 800 IU, may reduce the risk of fracture by approximately 25 percent.
Dawson-Hughes and her colleagues analyzed the results of seven experimental trials that all compared fracture rates among subjects 60 years of age and older given vitamin D supplements (with or without calcium supplements) to those among similar subjects given only calcium or placebo. Each study lasted between one and five years, and looked specifically at hip fractures or other fractures that did not involve the spine. The researchers found that only subjects receiving higher doses of vitamin D supplementation had significantly fewer fractures than did subjects in the comparison groups.
"In the future, we may need to reconsider the current recommended daily values of vitamin D for older adults," says Dawson-Hughes. She adds, "We also need to look more closely at the possible role that calcium supplementation may have in mediating the effects of vitamin D. Fractures in the elderly can lead to severe health consequences, including death. One promising prevention strategy may be dietary supplementation with both calcium and vitamin D."
Another meta-analysis on vitamin D published in JAMA last year found that older adults can reduce their risk related to falls by more than 20 percent by ensuring they get enough vitamin D. Dawson-Hughes, an author on that paper, noted that "vitamin D may also improve muscle strength, thereby reducing fracture risk through fall prevention."
Reduction of broken bone risk and improved muscle strength are not the only reasons to up your vitamin D. See my post "Vitamin D Could Decrease Overall Cancer Risk 30%".
At best vitamin D can reduce the rate of decay of bones with age. Your bones are still going to age unless something more is done. In the future stem cell therapies to rejuvenate the cells that build up bones will also reduce the risk of bone fractures by putting in place cells that can make bones young again. Plus, the youthful and carefully selected and modified stem cells will have much lower risk of going cancerous. We need to accelerate the rate of progress in stem cell research.
BERKELEY, CA – Why does it seem like some people can eat all the ice cream they want without increasing their cholesterol or gaining much weight, while others with high cholesterol have to watch their diets like a hawk? Because no matter what their lifestyle, people's genes play an overriding role in their cholesterol response.
So says a new study by researchers at the Department of Energy's Lawrence Berkeley National Laboratory and the Children's Hospital Oakland Research Institute (CHORI), conducted by Paul Williams of Berkeley Lab's Life Sciences Division in collaboration with Robin Rawlings and Patricia Blanche of CHORI and Ronald M. Krauss of CHORI and Berkeley Lab's Genomics Division. They report their findings in the July 8, 2005, issue of the American Journal of Clinical Nutrition.
The investigators analyzed how "bad" cholesterol (low-density lipoprotein, or LDL, cholesterol) responded to diets that were either high or low in fat in 28 pairs of identical male twins — one twin a vigorous exerciser, the other a comparative couch potato.
"Although identical twins share exactly the same genes, we chose these twins because they had very different lifestyles," says Williams. "One member of each pair was a regular long-distance runner, someone we contacted through Runner's World magazine or at races around the country. His brother clocked 40 kilometers a week less, at least, if he exercised at all."
For six weeks the twins ate either a high-fat diet (40 percent of its calories from fat) or a low-fat diet (only 20 percent of its calories from fat); then the pairs switched diets for another six weeks. After each six-week period the twins' blood cholesterol levels were tested.
The researchers were interested in learning if blood cholesterol changes due to the different diets would be the same or different in each pair of genetically identical twins, even though their lifestyles were very different. A correlation of zero between the two would mean that their responses to the diets had no relation to each other, while a correlation of 1.0 would mean that their responses were identical.
The researchers found an astounding 0.7 correlation in responses to the change in diet, an incredibly strong similarity in the way each pair of twins responded — even though the responses themselves among different pairs of twins differed considerably.
"If one of the twins could eat a high-fat diet without increasing his bad cholesterol, then so could his brother," says Williams. "But if one of the twins' LDL cholesterol shot up when they went on the high-fat diet, his brother's did too."
The correlations showed that the twins had very similar changes in LDL cholesterol because they had the same genes. Some twins had one or more genes that made them very sensitive to the amount of fat in their diets. Other twins had genes that made them insensitive to dietary fat, no matter how much they exercised.
The genes which cause this difference in response to fats will be identified. A more immediate benefit of identifying those genes would come from genetic tests that would tell you whether your cholesterol level is sensitive to your diet. If your cholesterol level is not sensitive to the amount or types of fat you eat then you could stop fighting your desires to eat higher fat foods - at least for the sake of your cholesterol.
A longer term benefit will come from using this knowledge to guide the genetic reengineering of one's cholesterol metabolosm. My guess is that these genes exercise their influence in the liver. For people who have diet-sensitive cholesterol gene therapy could reprogram the liver cells to keep overall cholesterol low and HDL cholesterol high regardless of diet or exercise. Either the existing liver could be reprogrammed or stem cells from your body could be removed, genetically modified, and then grown to create a replacement liver that more optimally regulates cholesterol.
Not everyone who has cholesterol levels that are insensitive to diet have low cholesterol. Some have cholesterol that is stuck at dangerously high levels. Those people who have high cholesterol without much dietary sensitivity for cholesterol levels would derive the greatest benefit from geneticaly reengineered livers. For now the best they can do is take statin drugs.
If you were willing to make the effort and spend some money you could discover with the help of your doctor whether your cholesterol level is diet sensitive. Try different diets with different fat levels and fat types and get a test of your various types of cholesterol after eating each diet. for 6 weeks as these researchers did. If you want to try this then consider putting the ape diet on your list of diets to try. If even the ape diet doesn't lower cholesterol then you might as well enjoy ice cream for breakfast.
Dr. Arch G. Mainous, III and colleagues at the Medical University of South Carolina in Charleston have found that having a combination of either high VLDL cholesterol or low HDL cholesterol with high iron in the blood raises cancer risk by a factor of 2.68 and 2.82 respectively.
Iron and lipids combine to create oxidative stress, and oxidative stress has a role in the development of cancer. The objective was to determine the risk of cancer among persons who had both elevated iron and lipids. The authors conducted an analysis of the cohort available in the Framingham Offspring Study. Adults aged 30 or more years at baseline had serum iron and high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol, and very low density lipoprotein cholesterol (VLDL-C) assessed in 1979–1982 and were followed for development of cancer until 1996–1997 (n = 3,278). Cox regression models were computed while controlling for age, gender, smoking status, and body mass index. In adjusted models, both elevated iron (hazard ratio (HR) = 1.66, 95% confidence interval (CI): 1.11, 2.46; 29 cases) and VLDL-C (HR = 1.54, 95% CI: 1.04, 2.28; 93 cases) had significant independent risks for development of cancer. When elevated iron was combined with elevated VLDL-C, the adjusted relative risk of cancer increased (HR = 2.68, 95% CI: 1.49, 4.83; 18 cases). Elevated iron and low HDL-C also had a significant adjusted relative risk of cancer (HR = 2.82, 95% CI: 1.50, 5.28; 14 cases). The results suggest that elevated serum iron levels coupled with either high VLDL-C or low HDL-C appear to interact to increase cancer risk in this cohort.
Those are huge increases in risk, almost tripling the best case risk. The high iron is probably generating free radicals that are oxidizing the LDL and VLDL cholesterol. Perhaps the HDL cholesterol removes or neutralizes the reactive forms of LDL and VLDL and hence lower HDL raises the risks.
Exercise will raise HDL cholesterol. What will lower VLDL cholesterol? Same factors that lower LDL cholesterol? Then there is iron. Are the high iron people in this study that way due to genetic factors? In other words, what can be done to lower cancer risk due to cholesterol and iron interactions? Keep in mind as well, the oxidative stress that produces the higher cancer risk also probably accelerates general aging. So anything that reduces cancer risk from cholesterol and iron probably slows down aging in general.
Brace yourselves for a study which produced results which are, to say the least, counterintuitive. A group of Finnish researchers found in an epidemiological study on twins that those overweight people who intended to lose weight who lost weight were most at risk of dying over the study period. (the higher the hazard ratio the greater the risk of dying)
Weight loss in the obese improves risk factors for cardiovascular diseases and diabetes. However, several studies have shown inconsistent long-term effects of weight loss on mortality. We investigated the influence on mortality of intention to lose weight and subsequent weight changes among overweight individuals without known co-morbidities.
Methods and Findings
In 1975, a cohort of individuals reported height, weight, and current attempts (defined as “intention”) to lose weight, and in 1981, they reported current weight. Mortality of the 2,957 participants with body mass index ≥ 25 kg/m2 in 1975 and without pre-existing or current diseases was followed from 1982 through 1999, and 268 participants died. The association of intention to lose weight in 1975 and actual weight change until 1981 with mortality was analysed while controlling for behavioural and psychosocial risk factors and hypertension as possible confounders. Compared with the group not intending to lose and able to maintain stable weight, the hazard ratios (with 95% confidence intervals) in the group intending to lose weight were 0.84 (0.49–1.48) for those with stable weight, 1.86 (1.22–2.87) for those losing weight, and 0.93 (0.55–1.56) for those gaining weight. In the group not intending to lose weight, hazard ratios were 1.17 (0.82–1.66) for those who did lose weight, and 1.57 (1.08–2.30) for those gaining weight.
Deliberate weight loss in overweight individuals without known co-morbidities may be hazardous in the long term. The health effects of weight loss are complex, possibly composed of oppositely acting processes, and need more research.
That is the abstract of the study. Since it was published in PLoS Medcine you can click through and read the whole study. The body of the study has an extensive discussion of previous relevant research, more details of this study, and analyses of what it all means.
But don't rush to conclusions. Epidemiologist Meir Stampfer of the Harvard School for Public Health says epidemiology studies of the effect of weight on mortality need to correct for a number of problems.
Epidemiologic studies of the relation between overweight and mortality typically must address three principal concerns . First, in many populations, cigarette smokers tend to be leaner than nonsmokers. Because cigarette smoking is such a strong risk factor for mortality, failure to adjust for this adequately can lead to confounding, with the erroneous conclusion that leanness carries increased risk of death. Statistical adjustment for smoking is often insufficient to account for this difficulty. Smoking can lead to medical conditions, sometimes sub-clinical, that are associated with decreased body weight, such as chronic obstructive pulmonary disease. The presence of symptoms or diagnosed conditions may induce smokers to quit. Moreover, the intensity of smoking is related to both risk of death and body mass index. For these reasons, the best way to assess the impact of overweight on risk of mortality is simply to exclude current and past smokers. Kaprio and colleagues' study differentiated only current smoker or nonsmoker. Thus, never-smokers were included in the same category as past smokers, regardless of how much the past smokers had smoked or their reasons for quitting.A second difficulty in some epidemiologic studies is the inclusion of intermediary factors as co-variates. Weight loss improves hypertension and diabetes, so including these as co-variates would tend to attenuate the apparent benefit of weight loss. In the present study, the authors appropriately excluded people with diabetes, and adjustment for hypertension appeared to have little impact. The third and most difficult issue in studies of overweight and mortality is reverse causation, the impact of disease on body weight. This can occur either through the biological impact of a condition (diagnosed or preclinical) or as an inducement to attempt to lose weight as a means to improve health. The authors' keen recognition of this problem provides a significant strength to the present study. The authors appropriately excluded individuals with a wide range of conditions to identify an apparently healthy cohort. This critical step is often ignored. Sometimes, investigators also exclude deaths that occur in the first few years after follow-up, to reduce the impact of reverse causation. Such lagged analyses can be helpful, but some chronic conditions of long duration, such as depression, chronic lung disease, and heart failure (conditions that often may not reach the level of clinical diagnosis) can lead to lower body weight and higher mortality risk. Hence, that strategy (not employed by Kaprio and colleagues) may not fully avoid the problem.
Stampfer points out that the people who lost more weight may not have done so as a result of a desire to lose weight. They may have intended to lose weight. But when they finally did lose weight it might have been due to diseases that eventually killed them. Plus the study size was not big enough and the degree of obesity was fairly small.
As a further step toward reducing the potential bias of the impact of disease on body weight, the authors identified individuals with intent to lose weight. Unintended weight loss is well known as an ominous clinical sign, usually signifying a serious illness. Just over a third of the overweight subjects in the Kaprio cohort had expressed intent to lose weight at baseline in 1975. It is interesting to note that despite this intention, as a group, the median weight change in the ensuing six years was a gain of 0.33 kg/m2, almost identical to the weight change in the group that had not expressed intent to lose weight (gain of 0.31 kg/m2). Thus, this study cannot fairly be characterized as an assessment of intentional weight loss and its subsequent effect on mortality. Because the changes in weight are so similar in these two groups, it is implausible to attribute the weight loss in the intent-to-lose group to that intention. These findings render the results particularly difficult to interpret.Other important limitations include the very small number of endpoints—only 268 total deaths in the cohort. When further subdivided according to intention to lose weight, and categories of weight change, the numbers are far from sufficient for reliable estimates. For example, the main conclusions are based on the subgroup of those with intent to lose weight who actually lost weight; this group had only 42 deaths, of which ten were violent. Another related difficulty is that this cohort, though overweight, is not drastically obese. The median body mass index (BMI) was 26.7 kg/m2, and fewer than 10% of people had a BMI greater than 30. With such a narrow range of BMI, coupled with the very small changes in weight during the six years of initial follow-up, even a very large study would not have sufficient power to detect plausible relative risks associated with weight change.
At the extreme it seems very unlikely that people who are morbidly obese (e.g. the people who are so large they can no longer even stand up) would suffer a net harm from losing weight. Also, people who have various risk factors that show up more among the obese such as hypertension and type II diabetes would probably benefit more from weight loss than those who do not have those risk factors who are equally overweight.
If you are overweight, then losing weight is good for your health, surely? Unfortunately, the evidence on which an answer to this seemingly simple question might be based is at best equivocal, and at worst very controversial. Previous work has shown that weight loss in obese people improves risk factors associated with cardiovascular diseases and diabetes, but studies are conflicting on the long-term effects of weight loss on mortality. A study in this month's PLoS Medicine by Jaakko Kaprio and colleagues on a Finnish dataset adds more evidence to this debate, but experts are divided on what can be concluded from it.
The major difficulty in getting clear results on this question is that it is virtually impossible to do a controlled trial to answer it. Hence, the evidence accumulated has come mostly from epidemiological studies, but it is notoriously difficult to remove all confounding factors from these studies. Kaprio and colleagues' study is another epidemiological study, but we should not simply dismiss the data as unreliable just because of the problems inherent to such a study design. Instead, we should consider their study in the light of all the other evidence available.
Suppose the Finnish study's results hold up in a larger study. How could this be? One possibility is that loss of non-fat cell mass while on a diet may cause harm.
The study leaves us with the question of how intentional weight loss could lead to excess mortality. The authors suggest that this could be due to the unavoidable loss of lean body mass, which according to several other studies may increase mortality, and which may outweigh the beneficial effects of losing fat mass in healthy individuals. The authors therefore conclude that “the long-term effects of weight loss are complex, and they may be composed of oppositely operating effects with net results reflecting the balance between these effects.”
The research paper (which is the first link above) discusses this idea at greater length.
Suppose loss of lean body mass during dieting inflicts real harm. Large amounts of high calorie burning aerobic exercise might be the solution. If one could burn off calories with exercise then perhaps the lean muscle mass loss could be avoided. Though possibly internal organ mass might still be lost while dieting.
Another possible solution might be slower diets. But in the longer term the ideal solution would be drugs for regulating appetite that avoid obesity in the first place. For those already obese we probably need drugs that signal only fat cells to burn fat while leaving other tissue types unchanged.
Once effective weight loss drugs make it to market then fairly well prospective studies on the effect of weight loss will become possible. Without weight loss drugs few people currently succeed in keeping off the weight that they lose. I've seen references (sorry, no URL) to studies which purport to show that yo yo dieting where the weight goes on and off repeatedly is more harmful than no dieting at all. This makes intuitive sense when you consider the discussion above about the loss of lean body mass during diets. Someone who repeatedly diets puts their body through many episodes of lean body mass loss. Also, someone who is binging to gain weight will put their body through higher calorie consumption periods and probably therefore periods of even higher lipid levels from consuming mass quantites. My guess is that while people from Remulac can consume mass quantities safely humans can not.
My advice: Concentrate less on weight loss and more on improving the quality of the food you eat. Also, change how you go about your daily activities to inject more exercise into what you do. Try to walk rather than drive where that is practical. Take stairs rather than elevators. Get a totally manual mower rather than a gas engine mower. If your dog wants you to take him or her for a run then do so. Dogs are great personal fitness trainers if you will only obey them.
In April, the United States Centers for Disease Control and Prevention released a study challenging the conventional wisdom that eating less promotes longevity. The study found that the very thin run roughly the same risk of early death as the overweight. And now the tide seems to be turning against a common explanation for the long-standing observation that restricting food in lab organisms from yeast to mice prolongs life.
Many studies have indicated that it’s calorie reduction, rather than the specific source of calories, that increases longevity. That this effect occurs in such diverse organisms suggests a common mechanism may be at work, though none has been definitively characterized. And while calorie restriction enhances longevity in mice, it has not always done so in rats. In a new study, William Mair, Matthew Piper, and Linda Partridge show that flies can live longer without reducing calories but by eating proportionally less yeast, supporting the notion that calorie-restriction-induced longevity may not be as universal as once thought.
Dietary restriction in Drosophila involves diluting the nutrients in the fly’s standard lab diet of yeast and sugar to a level known to maximize life span. Since both yeast (which contributes protein and fat) and sugar (carbohydrates) provide the same calories per gram, the authors could adjust nutrient composition without affecting the calorie count, allowing them to separate the effects of calories and nutrients. The standard restricted diet had equivalent amounts of yeast and sugar (65 grams each) and an estimated caloric content of 521, while the yeast-restricted (65 g yeast/150 g sugar) and sugar-restricted (65 g sugar/150 g yeast) diets each had just over 860 calories. The control diet for the flies had equivalent amounts of sugar and yeast (150 grams), amounting to an estimated 1,203 calories.
First, the authors had to make sure the flies didn’t change their eating behavior to make up for a less nutritious diet. (They didn’t.) Reducing both nutrients increased the flies’ life spans, but yeast had a much greater effect: reducing yeast from control to dietary restriction levels increased median life span by over 60%.
But why this result?
Why might different factors promote longevity in flies and rats? It could be that the caloric-restriction/longevity paradigm needs more rigorous review—though a vast body of literature does support it. Or it may be that the animals use the same strategy for dealing with food shortages—shifting resources from reproduction to survival, for example—but have evolved different mechanisms for doing so that reflect each species’s life history, diet, and environment. Whatever explains the disparity, this study should give researchers interested in caloric restriction plenty to chew on.
Does this result upset the general rule that calorie restriction extends life expectancy? Perhaps Drosophila evolved in environments where calorie restriction always occurred at the same time that protein or fat restriction occurred. Natural selection might have selected for a detection of shortage of a single nutrient (or perhaps combination of nutrients) as a proxy for general calorie shortage. So perhaps the metabolism of Drosophila shfits gear when a shortage of protein or fat (or even some other nutrient found in yeast) occurs. Experiments using other food sources are needed to ascertain exactly what nutrient shortage (or nutrient ratio?) shifts Drosophila's metabolism into a state that slows aging.
Few people have the discipline to follow a calorie restriction diet for decades. Even if calorie restriction extends human lifespan (and that is as yet unproven) at best it will slow aging. Perhaps calorie restriction mimetic drugs will eventually provide a way to get the benefits (assuming there are any) of calorie without living with continuous hunger. However, development of treatments to reverse aging would provide more certain benefits and far greater benefits than the best case results for calorie restriction..
See the full research paper Calories Do Not Explain Extension of Life Span by Dietary Restriction in Drosophila.
Many studies have been published with conflicting and confusing results on whether long term use of assorted antioxidants is beneficial or detrimental to human health. In the latest chapter in the search for antioxidant regimens that might slow the rate of aging vitamin E supplementation has been found to raise the risk of heart failure for a coronary high risk group of older people.
Eva Lonn, M.D., of the Population Health Research Institute and McMaster University, Hamilton Health Sciences Corporation, Hamilton, Ontario, Canada, and colleagues conducted a study to evaluate whether long-term supplementation with vitamin E decreases the risk of cancer, cancer death, and major cardiovascular events. The randomized, double-blind, placebo-controlled trial ( Heart Outcomes Prevention Evaluation [HOPE] ) was initially conducted between December 21, 1993, and April 15, 1999, and included patients at least 55 years old with vascular disease or diabetes mellitus. This trial was extended ( HOPE-The Ongoing Outcomes [HOPE-TOO] ) to between April 16, 1999, and May 26, 2003.
The researchers found: "In the HOPE and HOPE-TOO trials, the daily administration of 400 IU of natural source vitamin E for a median of 7.0 years had no clear impact on fatal and nonfatal cancers, major cardiovascular events, or deaths. We observed an increase in the risk of heart failure, which is of concern. Although this adverse effect of vitamin E was unexpected and cannot be confirmed at this time by other trials, our data are internally consistent. Therefore, a meta-analysis of heart failure events including all completed large vitamin E trials is strongly recommended."
Sounds either neutral or bad for vitamin E supplementation, right? Well, this study got a lot of (mostly negative) press. However, there still tons of studies that show benefits from vitamin supplementation. Also it is very likely that there is an optimal level of dosage of vitamin E which might be lower than the 400 IU of alpha tocopherol used in this trial. For example,
Simin Nikbin Meydani of Tufts University in Boston says that lower doses of vitamin E might offer health benefits without adding risks. In her tests ... older people developed fewer respiratory infections while taking half the amount of the vitamin E they received in Lonn's study.
She notes that many of the people in the new study were on medication for heart disease. "Maybe vitamin E increases degradation of some of the drugs these people take," she suggests.
Also, from a dim faded old memory of mine I recall a study on vitamin E and old folks which found that smaller amounts of vitamin E boosted immune response whereas larger doses decreased immune response. This is not surprising. Antioxidants quench free radicals. Some free radicals are harmful and so quenching them is good. But the body also uses free radicals for intercellular and intracellular communication. Quenching those free radicals will prevent needed signals from getting through and that is certainly going to be harmful. Denman Harman MD, the guy who first proposed the free radical theory of aging way back in 1954, said in an interview (sorry, I can no longer find it on the web) that excess antioxidant supplementation will make one feel mentally and physically sluggish and that he discovered this effect on himself many years ago.
One unanswered question about antioxidant supplementation is what is the optimal dose for each antioxidant that would do more quenching of bad free radicals than it did of good free radicals? Another important question is at what absolute doses and ratios of doses of antioxidants do the antioxidants become oxidants? You see, many antioxidants neutralize free radicals by becoming free radicals themselves. Then other antioxidants quench those radicals to turn them back into antioxidants once again. In theory one could have, for example, so much vitamin E in one's body that other compounds (e.g. vitamin C) will be comparatively too rare in the body to recycle vitamin E back into its antioxidant state. So balance between antioxidants is probably very important. Does supplementation with just vitamin E upset some balance? Is one better off eating foods that have lots of different vitamins and other antioxidant compounds rather than take supplements? I wish I knew exact and detailed answers to alll these questions.
While the HOPE and HOPE-TOO trials on vitamin E, heart disease, and cancer were getting a lot of press a potentially more important study on antioxidants, genetics, and cancer risk attracted very little attention. But, hey, lucky you read me! So now pay close attention to a report with important implications for nutrigenomics. Whether selenium, vitamin E, and lycopene lower the risk of aggressive prostate cancer may depend on which genetic variation you have for the antioxidant enzyme manganese superoxide dismutatase (MnSOD).
PHILADELPHIA – Greater levels of selenium, vitamin E and the tomato nutrient lycopene have been shown to reduce prostate cancer in one out of every four Caucasian males -- those who inherit a specific genetic variation that's particularly sensitive to oxidative stress.
Conversely, if carriers of this genetic variant have low levels of these vitamins and minerals, their risk of aggressive prostate increases substantially, as great as 10-fold, over their cohorts who maintain higher levels of these nutrients.
These results, published in the March 15 issue of the journal Cancer Research, were based on the analysis of 567 men diagnosed with prostate cancer between 1982 and 1995, and 764 cancer-free men from the Physicians Health Study (PHS).
"This large prospective study provides further evidence that oxidative stress may be one of the important mechanisms for prostate cancer development and progression, and adequate intake of antioxidants, such as selenium, lycopene and vitamin E, may help prevent prostate cancer," said Haojie Li, M.D., Ph.D., a researcher at the Brigham and Women's Hospital and Harvard Medical School.
Destructive molecules known as "free radicals" have been shown to team up with oxygen in the human body resulting in oxidative stress and what some scientists believe is an assortment of age-related ailments. As a result, many believe that consumption of antioxidants can slow that process.
"Our study, as well as many other epidemiological studies, encourages dietary intake of nutrients such as lycopene from tomato products, or supplements for vitamin E and selenium to reduce risk of prostate cancer," said Li.
The initial goal of the PHS study was to assess the effect of aspirin and beta carotene on men's health. Since blood samples collected in 1982 were available from many of the study's participants, the research team decided to review variants for the gene that codes for manganese superoxide dismutatase (MnSOD), an important enzyme that works as an antioxidant in human cells to defend against disease. The MnSOD gene is passed from parents to offspring in one of three forms: VV, VA or AA.
"Compared with men with the MnSOD VV or VA genotype, people with the AA genotype seem to be more sensitive to the antioxidant status," said Li. "Men with the AA genotype are more susceptible to prostate cancer if their antioxidant levels are low."
People with the AA genotype for MnSOD will derive more benefit from antioxdant supplementation than those with other MnSOD phenotypes.
The study's results found that a quarter of the men in the study carried the MnSOD AA genotype, half carried the VA genotype, and the remaining quarter carried the VV genotype.
The results indicated that the VA and VV men were at equivalent risk for developing prostate cancer across all levels of antioxidants in their blood. Compared to MnSOD VV or VA carriers with low selenium – those men in the lowest quartile of the study group – MnSOD AA males had an 89 percent greater risk for developing aggressive prostate cancer if blood levels for selenium were low.
On the other hand, MnSOD AA carriers with high selenium – those men in the highest quartile – had a 65 percent lower risk than the MnSOD VV or VA males who maintained low levels of selenium.
"The levels of selenium in the highest quartile of these men are not abnormally high," Li said. "Our range is neither extremely high nor extremely low."
While similar trends were observed for lycopene and vitamin E when tested independently, the contrast in relative risk was most pronounced for the men who had high blood levels for all three antioxidants combined.
"Among men with the MnSOD AA genotype, we observed a 10-fold difference in risk for aggressive prostate cancer, when comparing men with high versus low levels of antioxidants combined," said Li. "In contrast, among men with the VV or VA genotype, the prostate cancer risk was only weakly altered by these antioxidant levels."
Similar interactions between dietary antioxidants and the variations in the MnSOD gene have previously been linked to risk for breast cancer.
So should you take vitamin E and selenium and eat lots of tomato products to get the lycopene? The answer probably depends on your genes. Here is a demonstration that nutrigenomics (the use of genetic information to customize diets) clearly is going to become very beneficial. Some people may derive a net harm from vitamin E supplementation whereas others may derive a net benefit. Big studies like the HOPE-TOO trial that do not examine genetic differences between study participants are going to miss the existence of genetic subgroups that are experiencing even greater harm or greater benefit than what appears to be the case when all the study participants are looked at as a single aggregate.
We need advances in gene sequencing technologies that drive down costs by orders of magnitude so that personal DNA sequencing becomes a reality. With detailed knowledge of all our genetic variations we can choose much more optimal custom diets and supplement regimens.
Never mind the tablets - heart disease could be cut by 76% and men could expect to live more than six years longer if they simply ate the right meal once a day, doctors said yesterday.
Last year the British Medical Journal ran a paper advocating the "Polypill" - combining aspirin, folic acid and cholesterol-lowering and blood-pressure drugs - for everybody over 55. But an article in the Christmas issue says a "Polymeal", containing fish, wine, dark chocolate, fruits and vegetables, garlic and almonds, would achieve roughly the same effect.
Note that the diet (assuming it works) would do this by delaying heart heart disease by an even greater number of years. A delay in the onset of heart disease would then allow time for other diseases to kill before heart disease developed to the point of being fatal.
However, a diet that reduces the risk of heart disease probably reduces the risk of a number of other diseases as well. So this diet might provide an even larger benefit than these researchers project. On the other hand, the various components of the diet may provide benefits that are not additive to the extent that these researchers assume. So the benefit could be less than they project.
Note that in order to get the benefit you would need to follow the diet for years, decades even. Also, if you already have very low cholesterol and low blood pressure I would not expect much of a benefit.
Oscar Franco, a public health scientist at the University Medical Centre in Rotterdam, The Netherlands, and his colleagues suggest the "Polymeal" as a natural alternative to the "Polypill".
This wonder pill - a cocktail of six existing drugs - was proposed in June 2003 as a preventive pill which might slash the risk of heart attack or stroke in people over 55 years old by as much as 80%. The proposal was underpinned by an analysis of over 750 trials of the existing drugs.
The polypill is made up of aspirin, folic acid (a vitamin that would lower homocysteine in the blood), a statin (to lower cholesterol; e.g. Crestor or Lipitor), and three blood pressure lowering medicines. The Polypill brings with it a number of risks including stomach bleeding from the aspirin and muscle problems from a statin.
The recommended daily "dosage" is 150 milliliters of wine, 100 grams of dark (nondairy) chocolate, 400 g. of fruits and vegetables, 2.7 g. of fresh or frozen garlic, 68 g. of almonds and 114 g. of fish four times a week.
Milk in chocolate is believed to counter the beneficial antioxidant effects of bittersweet chocolate, which is known to reduce blood pressure.
Garlic reduces cholesterol, and fresh produce cuts both that and blood pressure, the authors wrote.
My advice? I think anyone considering the Polymeal Diet ought to first consider the Ape Diet to lower cholesterol and inflammation. The Ape Diet has a fair amount of overlap with the Polymeal Diet but will probably exert a stronger cholesterol lowering effect. Though the two could probably be blended. One could eat the Ape Diet with a few of the elements from the Polymeal Diet that are not specifically called out in the Ape Diet.
The most important thing to keep in mind about diet improvements is that you should pursue sustainable improvements. If you think you will stay on a diet only for a few months before tiring of it then there isn't much point pursuing it. But if there are parts of one of these diets you think you could sustain without any feeling of constant sacrifice then certainly start doing those parts.
About the wine in the Polymeal Diet: It should be red wine in order to get the antioxidant resveratrol. My guess is that consuming dark grape juice may work just as well and using a lot of red wine vinegar may also deliver the resveratrol and other antioxidants found in red wine.
As for the chocolate: Some of the dark chocolates have a lot of their flavonoids removed during processing. The company that makes Doves chocolates has made an effort to preserve the flavonoids and it is likely that Doves Dark Promises provides more benefit than most other dark chocolates. Their point about eating dark bittersweet chocolate has to be taken seriously. One would need to eat more milk chocolate to get the same amount of chocolate as dark chocolate contains. The less sweet the chocolate the better because fewer calories would then need to be consumed to get the flavonoid compounds that are thought to be providing health benefits. However, I am still skeptical about the benefits of chocolate for the vascular system since the vasodilation effect is transitory according to accounts I've read. If anyone has more certain information about this then please post a comment.
As for the fish: Check out my favorite FDA table on fish mercury levels (and this fish mercury chart too) and avoid high mercury fish.
Update: Let me amend what I said above about grape juice and vinegar. Grape juice may not be a useful source of resveratrol.
The resveratrol content of wine is related to the length of time the grape skins are present during the fermentation process. Thus the concentration is significantly higher in red wine than in white wine, because the skins are removed earlier during white-wine production, lessening the amount that is extracted . Grape juice, which is not a fermented beverage, is not a significant source of resveratrol. A fluid ounce of red wine averages 160 µg of resveratrol, compared to peanuts, which average 73 µg per ounce . Since wine is the most notable dietary source, it is the object of much speculation and research.
Also, there are apparently at least two ways to make vinegar. One involves exposure to air and may destroy the resveratrol. I do not know which method of making vinegar is most common. But vinegar does not appear to be a reliable source of resveratrol. If you do not want to drink red wine there is at least one commercial red wine extract whose maker claims it preserves resveratrol.
Even among red wines the concentration of resveratrol can vary by more than an order of magnitude. Red grapes grown in colder conditions and for longer periods of fermentation have higher concentrations of resveratrol. If anyone comes across a table listing resveratrol concentration by wine brand and vintage please post a comment with a link to it.
When hamburgers are cooked heterocyclic amines (HCAs) are formed at high temperatures. HCAs are carcinogens and are probably one of the reasons why red meat consumption raises the incidence of cancer. Well, some new research provides evidence that addition of just 1% potato starch to hamburgers reduces carcinogen formation by an order of magnitude.
Overall, the burgers treated with potato starch developed the lowest total quantity of HCAs in their crust, just 5.5 nanograms per gram of cooked meat, Skog's team reports in an upcoming issue of the Journal of Agricultural and Food Chemistry. The next best performer was a fructose-glucose mix, which yielded roughly 8 ng/g. By contrast, the untreated burgers ended up with an HCA content of 60 ng/g, and the one laced with only salt and TPP yielded HCAs at 16 ng/g.
Lower temperature cooking by boiling meats would probably reduce HCA formation by a comparable amount and perhaps even by more.
Previous research has demonstrated that mixing cherries into hamburgers also reduces formation of heterocyclic aromatic amines (HAAs also referred to as heterocyclic amines or HCAs above) during cooking.
In the study, MSU researchers found that ground beef patties containing 15 percent fat and 11.5 percent tart cherry tissue had "significantly" fewer HAAs when pan fried, compared to patties without cherry tissue added. The overall HAA reduction ranged from nearly 69 percent to 78.5 percent. The reduction is "clearly due to cherry components functioning as inhibitors of the reaction(s) leading to HAA formation," according to the journal article. Measurements done during the study showed that the fat content of cherry patties was lower than that of regular patties, but the moisture content was greater, thereby verifying early findings.
Among food samples cooked to a well-done, non-charred state, bacon strips had almost 15-fold more mass (109.5 ng/g) than that of the beef, whereas no heterocyclic amine (HCA) was detected in the fried tempeh burgers.
The total amounts of HCAs in the smoke condensates were 3 ng/g from fried bacon, 0.37 ng/g from fried beef and 0.177 ng/g from fried soy-based food.