Damaging fat accumulation in the liver, especially common among the obese, might be reduced by eating tofu and other soy food products. Rats fed soy protein experienced less liver fat accumulation.
University of Illinois researchers will report this week that new research shows how soy protein could significantly reduce fat accumulation and triglycerides in the livers of obese patients by partially restoring the function of a key signaling pathway in the organ.
Hong Chen, an assistant professor of food science and human nutrition at the University of Illinois, will present her team's findings at 1:05 p.m. Sunday, April 22, at the annual meeting of the American Society for Biochemistry and Molecular Biology, held in conjunction with the Experimental Biology 2012 meeting in San Diego.
Fatty liver disease is amazingly common.
"Almost a third of American adults have fatty liver disease, many of them without symptoms," Chen explained. "Obesity is a key risk factor for this condition, which can lead to liver failure."
Results like these show how much foods act like drugs. They alter our metabolisms in many ways. Whether a powerful food/drug like soy is a net benefit probably depends on the risks and problems faced by each individual.
While diet had no effect on the liver profiles of lean animals, the obese rats that were fed soy showed a 20 percent reduction in triglycerides and overall fat accumulation in the liver, leading Chen to believe that soy protein could be used to alleviate the symptoms of fatty liver disease.
Soy might also reduce the incidence of benign prostatic hyperplasia (swollen prostates - which are also common with age).
At least among the overweight eating carbs that digestly slowly lowers markers for inflammation. Choose your carbohydrates for lower glycemic index.
SEATTLE – Among overweight and obese adults, a diet rich in slowly digested carbohydrates, such as whole grains, legumes and other high-fiber foods, significantly reduces markers of inflammation associated with chronic disease, according to a new study by Fred Hutchinson Cancer Research Center. Such a "low-glycemic-load" diet, which does not cause blood-glucose levels to spike, also increases a hormone that helps regulate the metabolism of fat and sugar. These findings are published online ahead of the February print issue of the Journal of Nutrition.
The controlled, randomized feeding study, which involved 80 healthy Seattle-area men and women – half of normal weight and half overweight or obese – found that among overweight and obese study participants, a low-glycemic-load diet reduced a biomarker of inflammation called C-reactive protein by about 22 percent.
"This finding is important and clinically useful since C-reactive protein is associated with an increased risk for many cancers as well as cardiovascular disease," said lead author Marian Neuhouser, Ph.D., R.D., a member of the Cancer Prevention Program in the Public Health Sciences Division at the Hutchinson Center. "Lowering inflammatory factors is important for reducing a broad range of health risks. Showing that a low-glycemic-load diet can improve health is important for the millions of Americans who are overweight or obese."
The diets had the same amounts of total carbohydrates.
Study participants completed two 28-day feeding periods in random order – one featuring high-glycemic-load carbohydrates, which typically are low-fiber, highly processed carbs such as white sugar, fruit in canned syrup and white flour; and the other featuring low-glycemic-load carbohydrates, which are typically higher in fiber, such as whole-grain breads and cereals. The diets were identical in carbohydrate content, calories and macronutrients. All food was provided by the Hutchinson Center's Human Nutrition Laboratory, and study participants maintained weight and physical activity throughout.
Check out Rick Mendosa's tables on glycemic index and glycemic load. Become familiar with higher glycemic index foods and avoid them.
Researchers at the Dana-Farber Cancer Institute in Boston find a hormone that makes a high-fat diet less damaging. The hormone has effects similar to that of exercise - but without all that effort and time spent exercising.
Mice given irisin lost a few grams in the first 10 days after treatment, the study shows, and certain genes involved in powering the cell were turned on. Irisin also appeared to reduce the damage done by a high-fat diet, protecting mice against diet-induced obesity and diabetes, according to the paper, whose first author is postdoctoral fellow Pontus Boström.
Drug delivery is a serious problem in this case. Also, it isn't clear this hormone will deliver all the benefits of exercise.
DALLAS – April 19, 2011 – Curbing carbohydrates is more effective than cutting calories for individuals who want to quickly reduce the amount of fat in their liver, report UT Southwestern Medical Center researchers.
"What this study tells us is that if your doctor says that you need to reduce the amount of fat in your liver, you can do something within a month," said Dr. Jeffrey Browning, assistant professor of internal medicine at UT Southwestern and the study's lead author.
The results, available online and in an upcoming issue of the American Journal of Clinical Nutrition, could have implications for treating numerous diseases including diabetes, insulin resistance and nonalcoholic fatty liver disease, or NAFLD. The disease, characterized by high levels of triglycerides in the liver, affects as many as one-third of American adults. It can lead to liver inflammation, cirrhosis and liver cancer.
While a high percentage of obese people develop fatty liver disease and fatty liver disease is associated with metabolic syndrome and obesity the arrows of causation are not easily discerned. One might expect obesity causes metabolic syndrome. But it could be that only when fat cells exceed their capacity to store lipids do lipids get deposited in the liver and other places where they cause metabolic syndrome and diseases. Still, if you aren't obese the odds of getting excess fat in the liver and metabolic syndrome are lower.
Since fried foods seem to boost the risk of metabolic syndrome it could be the omega 6 fatty acids in the vegetable oil used for frying is causing inflammation that leads to metabolic syndrome.
BTW, I've been pouring more olive oil on my lunches to cut my desire for carbohydrates. Seems to be working.
Update: Read the Gary Taubes article in the NY Times Magazine “Is Sugar Toxic?”. Also, see my post on fructose as a possible cause of high blood pressue and watch the video of UCSF medical school prof Robert Lustic about why fructose is the most dangerous type of sugar.
Don't drink coffee when you eat a meal at a fast food joint. Or, better yet, don't eat junk food so that you can drink coffee.
Eating a fatty fast food meal is never good for you, but washing that meal down with a coffee is even worse, according to a new University of Guelph study.
Researcher Marie-Soleil Beaudoin has discovered not only that a healthy person's blood sugar levels spike after eating a high-fat meal, but that the spike doubles after having both a fatty meal and caffeinated coffee – jumping to levels similar to those of people at risk for diabetes.
Saturated fat and caffeine interact to impair sugar removal from the blood?
"The results tell us that saturated fat interferes with the body's ability to clear sugars from the blood and, when combined with caffeinated coffee, the impact can be even worse," said Beaudoin, a PhD student who conducted the study with U of G professors Lindsay Robinson and Terry Graham. "Having sugar remain in our blood for long periods is unhealthy because it can take a toll on our body's organs."
Or even better: skip the coffee and the junk food and eat a paleo diet.
After reading more about polyphenols, and coming to understand that the prevailing hypothesis of why they work makes no sense, I decided that the whole thing is probably bunk: at best, specific polyphenols are protective in rodents at unnaturally high doses due to some drug-like effect. But-- I kept my finger on the pulse of the field just in case, and I began to notice that more sophisticated studies were emerging almost weekly that seemed to confirm that realistic amounts of certain polyphenol-rich foods (not just massive quantities of polyphenol extract) have protective effects against a variety of health problems.
Stephan then proceeds to list a sampling of recent studies showing health benefits from polyphenols. Click thru to read the details. Though if you are regular reader here you've seen similar reports such as berries cutting Parkinson's risk, red wine polyphenols to slow blood vessel aging, black raspberries to cut colon cancer risk, blueberries to also cut colon cancer risk, many posts about the glories of chocolate, and of course benefits of cherries.
Aside: I accidentally discovered some years back that eating Montmorency cherries shifted my body clock to wake up earlier. I can even tell you why: high melatonin. So foods are drugs. Cherries even attracted the (unwanted as far as I am concerned) attention of the US Food and Drug Administration.
Okay, back on point: The thrust of Stephan's first post above was that the main theory advanced for the benefits of polyphenols (antioxidant effect) does not stand up to scrutiny. Yet much to his surprise the foods that contain polyphenols really do benefit health for reasons related to their polyphenol concentrations. Why? He gives a clue in the first post:
Wait a minute... let's rewind. Eating blueberries caused mice to increase the expression level of their own antioxidant enzymes?? Why would that happen if blueberry polyphenols were themselves having a direct antioxidant effect? One would expect the opposite reaction if they were. What's going on here?
For some more biologically knowledgeable readers that clue is enough. Anyone see it? Stephan likes to set up his ideas in one post, leave his regular readers (including me btw) hanging, and then provide the answers one or two posts later. To save my own readers the agony of suspense I waited until he came out with his second post. He starts out with the observation that other known mild stressors can improve long term health by up-regulating the body's repair and protection mechanisms.
One of the more curious things that has been reported in the scientific literature is that although high-dose ionizing radiation (such as X-rays) is clearly harmful, leading to cancer, premature aging and other problems, under some conditions low-dose ionizing radiation can actually decrease cancer risk and increase resistance to other stressors (1, 2, 3, 4, 5). It does so by triggering a protective cellular response, increasing cellular defenses out of proportion to the minor threat posed by the radiation itself. The ability of mild stressors to increase stress resistance is called "hormesis." Exercise is a common example. I've written about this phenomenon in the past (6).
The ideal stressor probably would have a very low level of toxicity while eliciting a large repair and defense response. Finding out which polyphenols are best from that standpoint is not trivial though. Whatever damage they cause must be measured as well as the level of each protective response (e.g. up-regulation of each of the enzymes that break down free radicals and other toxins).
Stephan says the body's responses to polyphenols overlap with the body's responses to low level radiation.
Although it may not be obvious, radiation and polyphenols activate a cellular response that is similar in many ways. Both activate the transcription factor Nrf2, which activates genes that are involved in detoxification of chemicals and antioxidant defense**(9, 10, 11, 12). This is thought to be due to the fact that polyphenols, just like radiation, may temporarily increase the level of oxidative stress inside cells. Here's a quote from the polyphenol review article quoted above (13):We have found that [polyphenols] are potentially far more than 'just antioxidants', but that they are probably insignificant players as 'conventional' antioxidants. They appear, under most circumstances, to be just the opposite, i.e. prooxidants, that nevertheless appear to contribute strongly to protection from oxidative stress by inducing cellular endogenous enzymic protective mechanisms. They appear to be able to regulate not only antioxidant gene transcription but also numerous aspects of intracellular signaling cascades involved in the regulation of cell growth, inflammation and many other processes.It's worth noting that this is essentially the opposite of what you'll hear on the evening news, that polyphenols are direct antioxidants. The scientific cutting edge has largely discarded that hypothesis, but the mainstream has not yet caught on.
Stephan is on the scientific cutting edge. His own diet and blood lipids are unusual. Since that post is a few years old and he's made adjustments since then I'd be very curious to know exactly how he's eating today. Probably eating more polyphenol-rich food for one.
Here's yet another in a series of reports about how Deep Fat is not a health problem. The latest? Supposedly evil milk fat that we've all been taught to avoid might be good for us. Pass me the butter. Turns out a fatty acid in milk fat is associated with a substantially lower risk of type 2 insulin resistant diabetes. This study does not provide direction of causation but is highly suggestive.
Boston, MA – Scientists at the Harvard School of Public Health (HSPH) and collaborators from other institutions have identified a natural substance in dairy fat that may substantially reduce the risk of type 2 diabetes. The compound, trans-palmitoleic acid, is a fatty acid found in milk, cheese, yogurt, and butter. It is not produced by the body and so only comes from the diet.
In the United States almost almost a quarter of those over 60 years old have type 2 insulin resistant diabetes. Since type 2 diabetes accelerates the body's aging and shortens life expectancy ways to avoid it can make a big difference in longevity.
Conventional wisdom is to avoid full-fat dairy products. Could conventional wisdom be wrong?
Reporting in the December 21, 2010, issue of Annals of Internal Medicine, investigators led by Dariush Mozaffarian, associate professor in the Department of Epidemiology at HSPH and Division of Cardiovascular Medicine, Brigham and Women’s Hospital and Harvard Medical School, and Gökhan S. Hotamisligil, J.S. Simmons Professor of Genetics and Metabolism and chair of the Department of Genetics and Complex Diseases at HSPH, explain that trans-palmitoleic acid may underlie epidemiological evidence in recent years that diets rich in dairy foods are linked to lower risk of type 2 diabetes and related metabolic abnormalities. Health experts generally advise reducing full-fat dairy products, but trans-palmitoleic acid is found in dairy fat.
Many blood health indicators look better in people with high trans-palmitoleic acid.
The HSPH researchers examined 3,736 participants in the National Heart, Lung, and Blood Institute-funded Cardiovascular Health Study, who have been followed for 20 years in an observational study to evaluate risk factors for cardiovascular diseases in older adults. Metabolic risk factors such as blood glucose and insulin levels, and also levels of circulating blood fatty acids, including trans-palmitoleic acid, were measured using stored blood samples in 1992, and participants were followed for development of type 2 diabetes.
At baseline, higher circulating levels of trans-palmitoleic acid were associated with healthier levels of blood cholesterol, inflammatory markers, insulin levels, and insulin sensitivity, after adjustment for other risk factors. During follow-up, individuals with higher circulating levels of trans-palmitoleic acid had a much lower risk of developing diabetes, with about a 60% lower risk among participants in the highest quintile (fifth) of trans-palmitoleic acid levels, compared to individuals in the lowest quintile.
What's next? Steak for heart disease treatment? Pork to fight cancer?
Seriously though, what factors influence trans-palmitoleic acid levels in milk? Does range fed milk have more? Or goat's milk? Anyone know about what influences its concentration in milk?
No surprise here but a useful reminder: A meta analysis of studies on sugary beverage consumption and health finds risk of metabolic syndrome and insulin-resistant type diabetes.
Boston, MA—A new study has found that regular consumption of soda and other sugar-sweetened beverages is associated with a clear and consistently greater risk of metabolic syndrome and type 2 diabetes. According to the Harvard School of Public Health (HSPH) researchers, the study provides empirical evidence that intake of sugary beverages should be limited to reduce risk of these conditions.
Since I already only drink water and the occasional beer this does not fall into the category of News I Can Use. But surely some readers must still be drinking the demon cola drinks on a regular basis. If so, confess the heinous sin of soda gluttony. Beware of where it can take you.
Parenthetically, sugary drinks are still widely available in schools. Schools ought to just ban them.
Avoid insulin resistance and weight gain.
The findings showed that drinking one to two sugary drinks per day increased the risk of type 2 diabetes by 26% and the risk of metabolic syndrome by 20% compared with those who consumed less than one sugary drink per month. Drinking one 12-ounce serving per day increased the risk of type 2 diabetes by about 15%.
"The association that we observed between soda consumption and risk of diabetes is likely a cause-and-effect relationship because other studies have documented that sugary beverages cause weight gain, and weight gain is closely linked to the development of type 2 diabetes," said Hu.
So let me state the obvious: Bad foods really are bad for you.
Then we come to good foods. Vitamin K, found in high concentrations in kale and spinach, slows the development of insulin resistance. So good foods really are good for you too.
If you feel more motivated to improve your diet when you read research explaining mechanisms of how nutrients help your body function better then read on. The omega 3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) reduce inflammation by binding macrophage (immune cell) GPR120 receptors and, by doing so, reduce inflammation.
Researchers at the University of California, San Diego School of Medicine have identified the molecular mechanism that makes omega-3 fatty acids so effective in reducing chronic inflammation and insulin resistance.
The discovery could lead to development of a simple dietary remedy for many of the more than 23 million Americans suffering from diabetes and other conditions.
Reduced inflammation and enhanced insulin sensitivity.
The scientists conducted their research using cell cultures and mice, some of the latter genetically modified to lack the GPR120 receptor. All of the mice were fed a high-fat diet with or without omega-3 fatty acid supplementation. The supplementation treatment inhibited inflammation and enhanced insulin sensitivity in ordinary obese mice, but had no effect in GPR120 knockout mice. A chemical agonist of omega-3 fatty acids produced similar results.
Given that the oceans are overfished already and yet EPA and DHA are good for our health what we need is genetic engineering of grain crops (e.g. soy and corn) to produce EPA and DHA. Then the grains could be fed to farmed salmon.
Jane Brody of the New York Times takes a look at the evidence for benefits from raising blood vitamin D levels.
“As a species, we do not get as much sun exposure as we used to, and dietary sources of vitamin D are minimal,” Dr. Edward Giovannucci, nutrition researcher at the Harvard School of Public Health, wrote in The Archives of Internal Medicine. Previtamin D forms in sun-exposed skin, and 10 to 15 percent of the previtamin is immediately converted to vitamin D, the form found in supplements. Vitamin D, in turn, is changed in the liver to 25-hydroxyvitamin D, the main circulating form. Finally, the kidneys convert 25-hydroxyvitamin D into the nutrient’s biologically active form, 1,25-dihydroxyvitamin D, also known as vitamin D hormone.
A person’s vitamin D level is measured in the blood as 25-hydroxyvitamin D, considered the best indicator of sufficiency. A recent study showed that maximum bone density is achieved when the blood serum level of 25-hydroxyvitamin D reaches 40 nanograms per milliliter or more.
“Throughout most of human evolution,” Dr. Giovannucci wrote, “when the vitamin D system was developing, the ‘natural’ level of 25-hydroxyvitamin D was probably around 50 nanograms per milliliter or higher. In modern societies, few people attain such high levels.”
Note Giovannucci's reference to human evolution as relevant to discussions about human dietary needs. The Paleo Diet approach to looking at human nutrition is becoming mainstream. You can find knowledgeable writers on nutrition such as Stephan Guyenet basically taking an anthropological approach to identifying appropriate foods including the use of isotope ratios in predecessors to modern humans to discover how much of different food types they ate.
Brody also quotes noted vitamin D researcher Michael Holick. Worth a read to hear what he has to say about disease risks that are boosted by not getting enough vitamin D.
Health conscious consumers have long known that virgin olive oil is a good choice when it comes to preparing meals and dipping breads. Now, a team of researchers, including one with the Agricultural Research Service (ARS), has found that phenolic components in olive oil actually modify genes that are involved in the inflammatory response.
The researchers knew from other studies that consuming high-phenolic-content virgin olive oil reduces pro-inflammatory, pro-oxidant and pro-blood-clotting biomarkers when compared with consuming low-phenolic-content olive oil. But they wanted to know whether olive oil’s beneficial effects could be the result of gene activity.
Use of low phenolic olive oil controls for the fat content and suggests that phenolic compounds deliver at least some of the health benefits from consuming olive oil.
Some of the turned down genes are linked to obesity. Would high phenolic olive oil reduce weight gain?
One of the experimental breakfasts contained virgin olive oil with high-content phenolic compounds (398 parts per million) and the other breakfast contained olive oil with low-content phenolic compounds (70 parts per million). All volunteers consumed the same low-fat, carbohydrate rich “background” diet during both study phases.
The researchers tracked the expression of more than 15,000 human genes in blood cells during the after-meal period. The results indicated that 79 genes are turned down and 19 are turned up by the high-phenolic-content olive oil. Many of those genes have been linked to obesity, high blood-fat levels, type 2 diabetes and heart disease. Importantly, several of the turned-down genes are known promoters of inflammation, so those genes may be involved in “cooling off” inflammation that often accompanies metabolic syndrome.
I'm thinking whole olives would deliver a bigger benefit since the ratio of phenolics to oil would likely be higher in whole olives.
Anyone know whether phenolics are stable in the presence of the oil that is used to turn some olives black?
While some rats might want to opt for the health promoting benefits of grape in rat chow another study finds that the overweight rat should give serious consideration to cherry in the diet. Anthocyanins in cherries are suspected by the scientists as the causative agents for the measured benefits.
ANAHEIM, CA, April 27, 2010 – There's more evidence of tart cherries' powerful anti-inflammatory benefits, according to a new study presented by a team of Michigan researchers today at the Experimental Biology annual meeting. Using a "whole food" approach, researchers found that a cherry-enriched diet not only reduced overall body inflammation, but also reduced inflammation at key sites (belly fat, heart) known to affect heart disease risk in obese, at-risk rats.
At-risk obese rats were fed a cherry-enriched "Western Diet," characterized by high fat and moderate carbohydrate – in line with the typical American diet – for 90 days. Cherry-enriched diets, which consisted of whole tart cherry powder as 1 percent of the diet, reduced risk factors for heart disease including cholesterol, body weight, fat mass and known markers of inflammation. While inflammation is a normal process the body uses to fight off infection or injury, according to recent science, a chronic state of inflammation increases the risk for diseases.
"Chronic inflammation is a whole body condition that can affect overall health, especially when it comes to the heart," said study co-author Mitch Seymour, PhD, at the University of Michigan. "This study offers further promise that foods rich in antioxidants, such as cherries, could potentially reduce inflammation and have the potential to lower disease risk."
Rats have very short lives compared to humans. I'm sure many rats will be excited by this result.
Even humans appear to derive a similar benefit from drinking tart cherry juice.
A second pilot study found similar results in humans. Ten overweight or obese adults drank eight ounces of tart cherry juice daily for four weeks. At the end of the trial, there were significant reductions in several markers of inflammation, in addition to lower levels of triglycerides, another key risk factors for heart disease.
Grapes help rats in the rat race of life. Powdered grapes made up 3% of their diets.
Researchers studied the effect of regular table grapes (a blend of green, red and black grapes) that were mixed into a powdered form and integrated into the diets of laboratory rats as part of a high-fat, American style diet. All of the rats used were from a research breed that is prone to being overweight.
They performed many comparisons between the rats consuming a grape-enriched diet and the control rats receiving no grape powder. Researchers added calories and sugars to the control group to balance the extra calories and sugars gained from getting the grape powder.
Lower blood pressure and improved glucose tolerance were among the indicators pointing at benefits from eating grapes.
After three months, the rats that received the grape-enriched diet had lower blood pressure, better heart function, and reduced indicators of inflammation in the heart and the blood than rats who received no grape powder. Rats also had lower triglycerides and improved glucose tolerance.
The effects were seen even though the grape-fed animals had no change in body weight.
So there you have it. Eat some grapes or raisins. My guess is that assorted berries rich in phytonutrients will deliver many of the same benefits. Try to get the various types of phytonutrients in your diet.
Stanford and Interleukin Genetics researchers find that the best way to lose weight depends on your genes. Low carbo or low fat? It depends on your genes.
Key Stanford findings from the study include:
- Individuals on genotype-appropriate diets lost 5.3 percent of body weight compared to individuals on diets not matched to their genotype, who experienced only 2.3 percent weight loss (p=0.005);
- The weight loss differences were even stronger when considering the individuals who were trying to follow the lowest carbohydrate (Atkins) and the lowest fat (Ornish) diets: 6.8% weight loss for those whose genotype matched the diet they were following vs. 1.4% for those not matched to their genotype (p=0.03);
- The statistical significance of the findings increased when taking into account the actual diet habits reported by study participants (rather than just the specific diet they were asked to follow);
- Improvements in clinical measures related to weight loss (e.g., blood triglyceride levels) paralleled the weight loss differences.
“The differentiation in weight loss observed for individuals who followed a diet matched to their genotype versus one that was not matched to their genotype is highly significant in numerous categories and represents an approach to weight loss that has not been previously reported in the literature,” said Christopher Gardner, Ph.D., Director of Nutrition Studies at the Stanford Prevention Research Center and an Associate Professor of Medicine at Stanford University. “The potential of using genetic information to achieve this magnitude of weight loss without pharmaceutical intervention would be important in helping to solve the pervasive problem of excessive weight in our society. We are eager to follow-up on this study and to determine the magnitude of health benefits that may result from following a diet that is matched to one’s genotype.”
Once more genes are discovered that influence how you metabolize food we can find out what we ought to eat. What I'm wondering: Does anyone have a metabolism that functions best on chocolate ice cream? Or cheese burgers? "Oh sorry, my genetic profile says I shouldn't eat vegetables".
Increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria, according to research being published online this week by Science magazine.
The finding strengthens the case that intestinal bacteria can contribute to human obesity and metabolic disease, since previous research has shown that intestinal bacterial populations differ between obese and lean humans.
So eat special yogurt to give yourself weight loss bacteria?
Tea and coffee reduce the risk of insulin-resistant diabetes that many develop in middle age and later.
Drinking more coffee (regular or decaffeinated) or tea appears to lower the risk of developing type 2 diabetes, according to an analysis of previous studies reported in the December 14/28 issue of Archives of Internal Medicine, JAMA (1).
By the year 2025, approximately 380 million individuals worldwide will be affected by type 2 diabetes (1).
Despite considerable research attention, the role of specific dietary and lifestyle factors remains uncertain, although obesity and physical inactivity have consistently been reported to raise the risk of diabetes mellitus. A previously published meta-analysis suggested drinking more coffee may be linked with a reduced risk, but the amount of available information has more than doubled since.
Decaffeinated coffee appears to cut risks the most while tea cuts risks the least. This makes caffeine unlikely to be the protective agent.
When the authors combined and analyzed the data, they found that each additional cup of coffee consumed in a day was associated with a 7 percent reduction in the excess risk of diabetes.
Individuals who drank three to four cups per day had an approximately 25 percent lower risk than those who drank between zero and two cups per day.
In addition, in the studies that assessed decaffeinated coffee consumption, those who drank more than three to four cups per day had about a one-third lower risk of diabetes than those who drank none. Those who drank more than three to four cups of tea had a one-fifth lower risk than those who drank no tea.
Magnesium and some antioxidants might offer protection.
Other compounds in coffee and tea including magnesium, antioxidants known as lignans or chlorogenic acids may be involved, the authors note.
Okay, so is magnesium a plausible protective agent? First off, let us look at how much magnesium is in a cup of coffee. A real cup is 8 ounces though people frequently drink less than 8 ounces at a time. But let us assume 3 8 ounce cups or 24 ounces per day. That's at least in the ballpark since some people drink 4 smaller servings. Well, each ounce of coffee contains 24 mg of magnesium and 34.5 mg of potassium. It also provides 1.6 mg of niacin. 24 ounces times 24 mg equals 576 mg of magnesium - a quite substantial amount.
Over the age of 30 the recommended daily dose of magnesium for males is 420 mg and for females 320 mg. So a 4 cup coffee drinker is going to get more than the recommended daily dose of magnesium.
But tea only contains .3 mg of magnesium per ounce. So tea's protective effect must not be due to magnesium. Tea's lack of magnesium does not mean that the magnesium in coffee isn't helping however. A number of studies have found that magnesium lowers type 2 diabetes risk and risk of metabolic syndrome.
If you want to get more magnesium without drinking coffee then nuts, green leafy vegetables, beans, and whole grains will help.
Eating chocolate might be good for people whose metabolisms show up as stressed in blood tests. Though I have to wonder whether attacking the underlying causes of high stress hormones would be more likely to deliver a real benefit.
The "chocolate cure" for emotional stress is getting new support from a clinical trial published online in ACS' Journal of Proteome Research. It found that eating about an ounce and a half of dark chocolate a day for two weeks reduced levels of stress hormones in the bodies of people feeling highly stressed. Everyone's favorite treat also partially corrected other stress-related biochemical imbalances.
One big problem with research on benefits of food on health: research that turns up a positive result is more likely to get published than research that turns up a negative result. So the body of all published research has a bias toward showing benefits.
Another big problem: short term effects do not always translate into long term reduction of illness or death. We end up with lots of promising studies that suggest dietary practices which are unproven or disproved many years later. Long term research takes too long and is so expensive that the number of hypotheses that get tested by long term research ends up being pretty short.
This study reminds me of a third problem: Some studies produce positive results because they happen to use experimental subjects most likely to benefit. Subsets of people who have more stress, a lousier diet to start with, or other problems are probably more likely to benefit from a diet change. Should you eat chocolate? The answer might depend on your levels of stress hormones.
In the study, scientists identified reductions in stress hormones and other stress-related biochemical changes in volunteers who rated themselves as highly stressed and ate dark chocolate for two weeks. "The study provides strong evidence that a daily consumption of 40 grams [1.4 ounces] during a period of 2 weeks is sufficient to modify the metabolism of healthy human volunteers," the scientists say
So does eating chocolate deliver a benefit? I'm still not convinced. But at least with chocolate my taste buds think I ought to lower my standard of evidence.
Update: Big population studies of diet and health will become a lot more useful once it becomes affordable to genetically sequence each person. My guess is that in some of the studies that find a benefit from a dietary practice for some of the people in that study their genomes were well matched to the dietary practice under study. The inability to control for genetic endowment is one of the causes of positive results that fail to generalize to hold up in other studies.
Similarly, if we all had implanted nanosensors reporting our metabolic condition our cell phones could query our nanosensors, report the results to a web site, and then get back recommendations for, say, exercise or chocolate or cruciferous vegetables.
The team, led by Assistant Clinical Professor of Public Health at Warwick Medical School Dr Oscar Franco, has discovered that simultaneously having obesity, high blood pressure and high blood sugar are the most dangerous combination of health factors when developing metabolic syndrome.
How dangerous are these factors? Way more.
In his study, published in the American Heart Association journal Circulation, Dr Franco has identified the most dangerous combination of these conditions to be central obesity, high blood pressure and high blood sugar. People who have all three of these conditions are twice as likely to have a heart attack and three times more likely to die earlier than the general population.
His team looked at 3,078 people to track the prevalence and progress of Metabolic Syndrome as part of the Framingham Offspring Study.
What to do about it? Exercise and a better diet of course.
Intensive lifestyle changes aimed at modest weight loss reduced the rate of developing type 2 diabetes by 34 percent over 10 years in people at high risk for the disease.
My own advice: eat lots and lots of vegetables, drug no sweet drinks, and avoid food that has high fructose corn syrup or sugar in it. Start reading labels.
I suspect the benefit of frequent interaction with health-care professionals mainly came in the form of repetitive encouragement to lose weight and eat better and less food.
The DPP results showed that intensive lifestyle changes, including exercise, reducing calories and fat intake and frequent interaction with health-care professionals, reduced the development of type 2 diabetes by 58 percent after three years. Those assigned to two daily doses of metformin but no lifestyle changes reduced the development of the disease by 31 percent over the same period.
Of course you could just take the drug. It'll only deliver about half the benefit but with much less effort.
We've all heard about the damage that reactive oxygen species (ROS) – aka free radicals – can do to our bodies and the sales pitches for antioxidant vitamins, skin creams or "superfoods" that can stop them. In fact, there is considerable scientific evidence that chronic ROS production within cells can contribute to human diseases, including insulin resistance and type 2 diabetes.
But a new report in the October 7th Cell Metabolism, a Cell Press publication, adds to evidence that it might not be as simple as all that. The researchers show that low levels of ROS – and hydrogen peroxide in particular -- might actually protect us from diabetes, by improving our ability to respond to insulin signals.
Unfortunately, toxins are essential elements of human metabolism. We use reactive oxygen species to perform essential functions at the expense of aging more rapidly. This is why we need to develop the ability to do repairs: Fix cells, replace cells, and replace whole organs.
There really is too much of a good thing. At least when it comes to food. I still haven't come across an equivalent report for sex.
"Our studies indicate that 'physiological' low levels of ROS may promote the insulin response and attenuate insulin resistance early in the progression of type 2 diabetes, prior to overt obesity and hyperglycemia," said Tony Tiganis of Monash University in Australia. "In a way, we think there is a delicate balance and that too much of a good thing - surprise, surprise - might be bad."
Tiganis' team found that mice with a deficiency that prevented them from eliminating physiological ROS didn't become insulin resistant on a high-fat diet as they otherwise would have. They showed that those health benefits could be attributed to insulin-induced signals and the uptake of glucose into their muscles. When those animals were given an antioxidant, those benefits were lost, leaving the mice with more signs of diabetes.
About 5 months ago some Harvard, Leipzig and Jena University researchers also reported vitamins C and E reduce exercise benefits and interfere with glucose metabolism in ways might boost diabetes risk. Also see my 2004 post Excessive Antioxidant Activity Risk Factor For Type II Diabetes. Vitamins are not a panacea. Stem cell therapies, gene therapies, and nanobot repair machines - they are the panacea!
Carnitine might help reduce insulin-resistant diabetes in humans if the results with rats translate well to humans.
DURHAM, N.C. – Supplementing obese rats with the nutrient carnitine helps the animals to clear the extra sugar in their blood, something they had trouble doing on their own, researchers at Duke University Medical Center report.
A team led by Deborah Muoio (Moo-ee-oo), Ph.D., of the Duke Sarah W. Stedman Nutrition and Metabolism Center, also performed tests on human muscle cells that showed supplementing with carnitine might help older people with prediabetes, diabetes, and other disorders that make glucose (sugar) metabolism difficult.
Carnitine is made in the liver and recycled by the kidney, but in some cases when this is insufficient, dietary carnitine from red meat and other animal foods can compensate for the shortfall.
After just eight weeks of supplementation with carnitine, the obese rats restored their cells' fuel- burning capacity (which was shut down by a lack of natural carnitine) and improved their glucose tolerance, a health outcome that indicates a lower risk of diabetes.
No guarantee here that carnitine will help you if you have blood glucose that is too high and possible early stage insulin-resistant adult onset diabetes. If you are obese then weight loss is a more sure way to improve your lipids, sugar levels, and other aspects of your health.
Low carnitine limits the ability of sugar to enter mitochondria and get broken down for energy.
Carnitine is a natural compound known for helping fatty acids enter the mitochondria, the powerhouses of cells, where fatty acids are "burned" to give cells energy for their various tasks. Carnitine also helps move excess fuel from cells into the circulating blood, which then redistributes this energy source to needier organs or to the kidneys for removal. These processes occur through the formation of acylcarnitine molecules, energy molecules that can cross membrane barriers that encase all cells.
Researchers at Duke had observed that skeletal muscle of obese rats produced high amounts of the acylcarnitines, which requires free carnitine. As these molecules started to accumulate, the availability of free, unprocessed carnitine decreased. This imbalance was linked to fuel-burning problems, that is, impairments in the cells' combustion of both fat and glucose fuel.
So does carnitine lower blood sugar level in humans with elevated blood sugar? Does it work as well for humans who normally eat a lot of red meat (and hence normally get more carnitine in their diet)?
While I'm asking questions: Do any other compounds have similar effect to carnitine in enhancing glucose transport and lowering unhealthily elevated blood glucose?