Why restrict your calories when you can just cut back on carbs a couple of days a week.
SAN ANTONIO — An intermittent, low-carbohydrate diet was superior to a standard, daily calorie-restricted diet for reducing weight and lowering blood levels of insulin, a cancer-promoting hormone, according to recent findings.
Researchers at Genesis Prevention Center at University Hospital in South Manchester, England, found that restricting carbohydrates two days per week may be a better dietary approach than a standard, daily calorie-restricted diet for preventing breast cancer and other diseases, but they said further study is needed.
"Weight loss and reduced insulin levels are required for breast cancer prevention, but [these levels] are difficult to achieve and maintain with conventional dietary approaches," said Michelle Harvie, Ph.D., SRD, a research dietician at the Genesis Prevention Center, who presented the findings at the 2011 CTRC-AACR San Antonio Breast Cancer Symposium, held Dec. 6-10, 2011.
It is not reasonable to expect the vast majority of people to sustain a lower calorie diet. The mental pull to eat more is just too strong. Sustained weight loss requires ways to cut appetite. The "ad lib" here means ad libitum which means "at pleasure": eat as much as you want. So an ad libitum low carbohydrate diet involves eating as much as you want as long as its only fat or protein or very low carb high fiber foods such as many vegetables (e.g. cauliflower).
Harvie and her colleagues compared three diets during four months for effects on weight loss and blood markers of breast cancer risk among 115 women with a family history of breast cancer. They randomly assigned patients to one of the following diets: a calorie-restricted, low-carbohydrate diet for two days per week; an "ad lib" low-carbohydrate diet in which patients were permitted to eat unlimited protein and healthy fats, such as lean meats, olives and nuts, also for two days per week; and a standard, calorie-restricted daily Mediterranean diet for seven days per week.
Eating something close to a Mediterranean diet with low carbohydrate is probably close to ideal.
Cutting calories along with cutting carbs improved insulin resistance better than just cutting carbs. But carb cutting alone delivered most of the benefit.
Data revealed that both intermittent, low-carbohydrate diets were superior to the standard, daily Mediterranean diet in reducing weight, body fat and insulin resistance. Mean reduction in weight and body fat was roughly 4 kilograms (about 9 pounds) with the intermittent approaches compared with 2.4 kilograms (about 5 pounds) with the standard dietary approach. Insulin resistance reduced by 22 percent with the restricted low-carbohydrate diet and by 14 percent with the "ad lib" low-carbohydrate diet compared with 4 percent with the standard Mediterranean diet.
The low carb diet probably cut appetite more. Hence the better result. An ideal diet should be ad libitum (no constant willpower fight) but only foods that do not stimulate the appetite.
Does cutting the size of the stomach thru bariatric surgery cause weight loss by cutting the appeal of fatty foods?
Bethesda, Md. (July 27, 2011)—Roux-en-Y gastric bypass, the most common type of bariatric surgery in the United States, is currently considered the most effective therapy for morbid obesity. Patients who undergo this procedure, in which the stomach is reduced to a small pouch and connected to the middle of the small intestine, often lose massive amounts of weight. However, the reasons behind this surgery’s success have been unclear. Shedding more light on why this procedure prompts such dramatic weight loss, a team of researchers has found, in a study using both humans and rats, that Roux-en-Y appears to lead patients to significantly reduce their intake of dietary fat. This effect, which was present for both solid and liquid dietary fat, lingered for up to 200 days after surgery in the animals. Further experiments suggest that this fat avoidance is triggered through digestive consequences, rather than just altered taste, and may be the result of an excess of hormones previously linked to food avoidance.
Unpleasant gastrointestinal sensations as a consequence of fat consumption might play a role in causing an aversion to fat after gastric bypass surgery.
What mechanism causes this aversion to fat? One hormone linked with reduced appetite, glucagon-like peptide-1 (GLP-1), was found to be higher in those who have undergone gastric bypass surgery. Perhaps injections of GLP-1 and/or other appetite-suppressing hormones could some day emulate at least some of the effects of gastric bypass surgery. Or perhaps a messenger RNA drug or a gene therapy could adjust the stomach to secrete more GLP-1 or Peptide YY in response to a meal. Turn up the body's sensitivity to food to more quickly and intensely suppress appetite when food hits the stomach or intestines.
Some Caltech researchers found that the dorsolateral prefrontal cortex (dlPFC) in the brain exerts self control to make people make healthier decisions and it is possible to make the dlPFC more active to improve your food choices.
When you decide what to eat, not only does your brain need to figure out how it feels about a food's taste versus its health benefits versus its size or even its packaging, but it needs to decide the importance of each of those attributes relative to the others. And it needs to do all of this more-or-less instantaneously.
Antonio Rangel, professor of economics and neuroscience at Caltech, has been studying this value-deriving and decision-making process for years now. Along with Todd Hare—a former postdoc at Caltech who is now an assistant professor of neuroeconomics at the University of Zurich in Switzerland—he published a paper in Science in 2009 describing differences in the brains of people who are better at exercising self-control than others. What they found was that while everyone uses the same area of the brain—the ventral medial prefrontal cortex, or vmPFC—to make value-laden decisions like what to munch on, there's a second brain area—the dorsolateral prefrontal cortex, or dlPFC—that seems to come to life when a person is using self-control during the decision-making process.
In other words, when the dlPFC is active, it allows the vmPFC to take into account health benefits as well as taste when it assigns a value to a particular food.
Imagine a gene therapy or cell therapy that long term boosts the level of dlPFC activity to basically change your preferences for food and likely for other things as well.
Before showing series of pictures of food to say yes or no to the researchers showed one of the messages "consider the healthiness," "consider the tastiness," or "make decisions naturally." The "consider the healthiness" image caused subjects to choose healthier foods and that image made their dorsolateral prefrontal cortex more active.
Things got interesting when the researchers looked at the other three categories, however. Among their findings:
- When thinking about healthiness, subjects were less likely to eat unhealthy foods, whether or not they deemed them to be tasty, and more likely to eat healthy-untasty foods.
- Being asked to think about healthiness led subjects to say "no" to foods more often than they did when asked to make decisions naturally.
- There were no real differences between the choices made during the "consider the tastiness" and "make decisions naturally" portions of the experiment.
When the researchers turned to the fMRI results, they found that the vmPFC was, as predicted, "more responsive to the healthiness of food in the presence of health cues," says Rangel. And, as they'd seen previously, the robustness of that response was due to the influence of the dlPFC—that bastion of self-control—which was much quieter when the study's subjects were thinking about taste or their own personal choice than when they were asked to throw healthiness into the equation.
How about "consider the healthiness" pasted in your refrigerator door? Where its really needed: on the entrance of fast food joints.
Smoking really does suppress appetite and some researchers at Yale and Baylor College of Medicine have narrowed down the appetite suppression mechanism to a particular class of neural receptors in the hypothalamus. This discovery opens up a target for drug development for both smokers and non-smoking folks with weight problems.
Smokers tend to die young, but they tend to die thinner than non-smokers. A team of scientists led by Yale School of Medicine has discovered exactly how nicotine suppresses appetite – findings that suggest that it might be possible to develop a drug that would help smokers, and non-smokers, stay thin.
Nicotine activates a small set of neurons in a section of the hypothalamus that signals the body has had enough to eat, the researchers report in the June 10 issue of the journal Science. Nicotine accomplishes this trick by activating a different set of receptors on the surface of neurons than those that trigger a craving for tobacco.
"Unfortunately, smoking does keep weight off," said Marina Picciotto, the Charles B.G. Murphy Professor of Psychiatry, professor of neurobiology and pharmacology and senior author of the paper. "Many people say they won't quit smoking because they'll gain weight. Ultimately, we would like to help people maintain their body weight when they kick the habit and perhaps help non-smokers who are struggling with obesity."
In the study, lead investigator Dr. Marian Picciotto, Yale University School of Medicine, and her research team focused on nicotine receptors expressed in the hypothalamic neurons that control the motivation to eat. In mice, they were able to determine that a particular nicotinic receptor subtype, the α3β4 nicotinic receptor, can influence how much a subject eats. They found that when nicotine binds to this receptor, pro-opiomelanocortin (POMC) neurons are activated, beginning the process that leads to appetite suppression.
From identification of a drug target to availability of a drug on the market can easily take 10 years. So this is good news for smokers overweight people in the 2020s.
An important question. Do you eat dirt? Sera Young and other researchers at Cornell asked the question of why do people eat dirt? While at first glance micronutrient deficiencies might seem a plausible guess in reality the clay most often eaten is not a good source of minerals.
The nutrition hypothesis was also a poor fit to the data. The database shows that the kind of earth people eat most often is a type of clay that contains low amounts of nutrients like iron, zinc, and calcium. Plus, if calcium deficiency drove people to eat dirt, one would expect them to do it most often at life stages when they need calcium the most—adolescence or old age. But that isn't the case, according to the database. Reports do indicate that geophagy is often associated with anemia, but several studies have shown that cravings for earth continue even after people are given iron supplements. What's more, some research suggests that clay can bind to nutrients in the stomach, making them hard to digest. If that's true, it's not a lack of nutrients that causes geophagy; rather it could be the other way around.
So what is it? The dirt might be killing parasites and pathogens.
Overall, the protection hypothesis fits the data best, the Cornell researchers found. The database shows that geophagy is documented most commonly in women in the early stages of pregnancy and in pre-adolescent children. Both categories of people are especially sensitive to parasites and pathogens, according to Young and her colleagues. In addition, geophagy is most common in tropical climates where foodborne microbes are abundant. Finally, the database shows that people often eat earth during episodes of gastrointestinal stress. It's unlikely the intestinal problems are caused by the dirt itself because the type of clay people usually eat comes from deep in the ground, where pathogens and parasites are unlikely to contaminate it. Plus, people usually boil the clay before eating it.
Boiled clay? So there's a whole gastronomic tradition around clay eating.
So the thought crossed my mind: Are there clay diet cookbooks? Didn't find anything promising. But turns out Sera Young has written a Kindle book on why people have cravings for clay and a few other items.Craving Earth: Understanding Pica--the Urge to Eat Clay, Starch, Ice, and Chalk.
Any closet chalk-eaters out there? Do you eat it for calcium? To save money on Tums? Turns out the calcium carbonate in chalk comes from coccolith plankton. Ring a bell? See my recent post on the advantage that coccolith will have other other plankton as higher atmospheric CO2 increases ocean acidity.
One of the competing theories to explain the obesity epidemic is a rise in fructose consumption causing alterations in hormone levels that increase appetite. UCSF med school prof Robert Lustig has a pretty good rant-lecture on the evils of fructose. Well, here's another study on part of the mechanism in the brain of how fructose might be causing increased obesity.
PORTLAND, Ore. – The dietary concerns of too much fructose is well documented. High-fructose corn syrup has become the sweetener most commonly added to processed foods. Many dietary experts believe this increase directly correlates to the nation's growing obesity epidemic. Now, new research at Oregon Health & Science University demonstrates that the brain – which serves as a master control for body weight – reacts differently to fructose compared with another common sweetener, glucose. The research is published in the online edition of the journal Diabetes, Obesity and Metabolism and will appear in the March print edition.
In humans the cortical brain control areas of the brain were inhibited by the influx of fructose.
Functional MRI allows researchers to watch brain activity in real time. To conduct the research, nine normal-weight human study subjects were imaged as they received an infusion of fructose, glucose or a saline solution. When the resulting brain scans from these three groups were compared, the scientists observed distinct differences.
Brain activity in the hypothalamus, one brain area involved in regulating food intake, was not affected by either fructose or glucose. However, activity in the cortical brain control areas showed the opposite response during infusions of the sugars. Activity in these areas was inhibited when fructose was given but activated during glucose infusion.
This is an important finding because these control brain areas included sites that are thought to be important in determining how we respond to food taste, smells, and pictures, which the American public is bombarded with daily.
The result increases the plausibility of fructose as a causal agent.
"This study provides evidence in humans that fructose and glucose elicits opposite responses in the brain. It supports the animal research that shows similar findings and links fructose with obesity," added Purnell.
There is now another good reason to exercise. Besides burning calories, exercise restores the sensitivity of neurons involved in the control of satiety (feeling full), which in turn contributes to reduced food intake and consequently weight loss. This is the conclusion of a study led by Brazilian researchers at the University of Campinas, and the findings will be published next week in the online, open access journal PLoS Biology. This disclosure may bring hope to over 40% of the population that suffers from weight problems and obesity around the world.
Exercise might make weight loss easier to do by reducing appetite.
The group led by José Barreto C. Carvalheira demonstrated that exercising obese rodents showed signals of restored satiety in hypothalamic neurons and decreased food intake. "In obese animals, exercise increased IL-6 and IL-10 protein levels in the hypothalamus, and these molecules were crucial for increasing the sensitivity of the most important hormones, insulin and leptin, which control appetite," Carvalheira explained. Physical activity contributes to the prevention and treatment of obesity, not only by increasing energy expenditure but also by modulating the signals of satiety and reducing food intake.
Eric Stice, Cara Bohon, and other researchers find that as a group of women gained weight their brains showed less signs of pleasure under a brain scan when eating sweet foods.
In a new study published Sept. 29 in the Journal of Neuroscience, Bohon fed milkshakes to a group of overweight women and monitored their brains' response to the combination of Häagen Dazs ice cream and Hershey's chocolate syrup. She used functional magnetic resonance imaging, or fMRI, to measure changes in brain blood flow and found that the sugary treat stimulated activity in the striatum. The striatum, located deep inside the brain, is a primitive mass of brain cells that, among other things, release feelings of pleasure when we eat foods we like.
Six months later, the women returned and repeated the experience. Some had gained a few pounds. The more weight they had gained during those months, the less their brains responded to the second milkshake, as compared to the first.
You can see a vicious cycle here that the researchers liken to cocaine addiction: The need for a bigger dose to get the same pleasure. In this case the need for the bigger dose causes weight gain which causes the deadening of taste response.
So how to restore taste sensitivity? I'd like to see a study done on whether weight loss alone fully restores taste sensitivity.
The big Firestone beer I tried at dinner tonight has me in the right frame of mind to write this post. Scientists investigate an important topic.
In an advance that may give brewers powerful new ability to engineer the flavor and aroma of beer — the world's favorite alcoholic beverage — scientists are publishing the most comprehensive deciphering of the beer's "proteome" ever reported. Their report on the proteome (the set of proteins that make beer "beer") appears in ACS' monthly Journal of Proteome Research.
This sort of research will inevitably lead to genetic engineering of barley, yeast, and corn to produce the ideal beer. Or, rather, the ideal pale ale, the ideal lager, and so on. Then European beers will fall behind in taste as the EU will probably ban the genetically engineered grains.
I expect we'll eventually see beers classified by their proteome pattern as well as other chemical fingerprints. You'll be able to web surf to a site that has all that data and it'll tell you that if you like a certain Dutch beer then which German or Japanese or American beer you ought to try. It'll be like Pandora for music but for beer.
Pier Giorgio Righetti and colleagues say they were inspired to do the research by a popular Belgian story, Les Maîtres de l'Orge (The Brew Masters), which chronicles the fortunes of a family of brewers over 150 years. They realized that beer ranks behind only water and tea as the world's most popular beverage, and yet little research had been done to identify the full set of proteins that make up beer. Those proteins, they note, play a key role in the formation, texture, and stability of the foamy "head" that drinkers value so highly. Nevertheless, scientists had identified only a dozen beer proteins, including seven from the barley used to make beer and two from yeast.
They identified 20 barley proteins, 40 proteins from yeast, and two proteins from corn, representing the largest-ever portrait of the beer proteome. "These findings might help brewers in devising fermentation processes in which the release of yeast proteins could be minimized, if such components could alter the flavor of beer, or maximized in case of species improving beer's aroma," the report notes.
Jeffrey B. Schwimmer, MD, associate professor of clinical pediatrics at UC San Diego, and colleagues examined 124 children, ages 8 to 18, for the presence of antibodies specific to adenovirus 36 (AD36), one of more than 50 strains of adenovirus known to infect humans and cause a variety of respiratory, gastrointestinal and other infections. AD36 is the only human adenovirus currently linked to human obesity.
Slightly more than half of the children in the study (67) were considered obese, based on a Body Mass Index or BMI in the 95th percentile or greater. The researchers detected neutralizing antibodies specific to AD36 in 19 of the children (15 percent). The majority of these AD36-positive children (78 percent) were obese, with AD36 antibodies much more frequent in obese children (15 of 67) than in non-obese children (4 of 57).
Children who were AD36-positive weighed almost 50 pounds more, on average, than children who were AD36-negative. Within the group of obese children, those with evidence of AD36 infection weighed an average of 35 pounds more than obese children who were AD36-negative.
So then does the virus integrate into host cell genomes of cells in fat layers and send out signals to replicate? If so, the virus would have to do this to many cells through out the body with lasting results in a great many cells. Otherwise the obesity would feature a very uneven distribution of fat. Do the obese kids with AD36 antibodies have fat distribution similar to that of obese kids who lack AD36 antibodies?
The virus might cause progenitors to fat cells to replicate more rapidly.
In cell cultures, Schwimmer said, the virus infects pre-adipocytes or immature fat cells, prompting them to develop more quickly and proliferate in greater numbers than normal. “This might be the mechanism for obesity,” Schwimmer said, “but more work needs to be done.”
Cells that replicate totally out of control are popularly known as cancer. Viruses cause some forms of cancer. So it seems at least plausible that a virus could cause a more limited proliferation of fat cells. Some obese people might need a treatment roughly equivalent to anti-cancer therapies - though preferably an anti-cancer therapy of the future that does not cause large scale damage and death of normal cells.
In this study, researchers evaluated a group of 104 obese or overweight men and women during an 8-week low-calorie diet and again 32 weeks after treatment. Researchers measured body weight as well as plasma fasting ghrelin, leptin and insulin concentrations before, during and after dieting. They found that subjects with higher plasma leptin and lower ghrelin levels before dieting were more prone to regain weight lost after dieting and that these hormone levels could be proposed as biomarkers for predicting obesity-treatment outcomes.
"We believe this research is of foremost relevance in clinical terms as it may indicate that the outcome of weight therapy may be pre-conditioned," said Crujeiras. "Furthermore, our findings may provide endocrinology and nutrition professionals a tool to identify individuals in need of specialized weight-loss programs that first target appetite hormone levels before beginning conventional dietary treatment."
Ghrelin increases appetite while leptin reduces it. Correction: So why does a person with lower ghrelin and higher leptin have a weight problem in the first place? See my update below. One possibility: Leptin insensitivity. So once they lose weight and go off their diet their appetites drive them to put on too much weight again. Ghrelin might also cause abdominal fat accumulation.
So any way to adjust your hormone levels in order to keep weight off? Not sure. But Byron J. Richards, author of The Leptin Diet: How Fit Is Your Fat?, argues that snacking is a major cause of low leptin and therefore of weight gain.
No snacks, high protein breakfast, and low carb. A high protein, low carb breakfast is pretty easily doable.
Update: As someone points out in the comments, the study subjects who regained the most weight had higher leptin levels - which one might expect would help them suppress appetite. So what gives? Leptin and ghrelin levels are hard to interpret because some people might have brain insensitivity to leptin (which reminds of type II diabetes which is characterized by insulin insensitivity and higher insulin levels). The result above might really indicate that people gain weight because leptin no longer suppresses their appetite. A high fat diet decreased mouse leptin sensitivity in one study and estrogen deficiency caused leptin sensitivity in rats. A diet that increases leptin sensitivity might be the key to weight loss.
Thinking about living with your girlfriend? For the sake of her health and your own esthetic experience put some emotional distance between you and the special lady.
After adjusting for other variables, the 10-year weight gain for an average 140-pound woman was 20 pounds if she had a baby and a partner, 15 if she had a partner but no baby, and only 11 pounds if she was childless with no partner. The number of women with a baby but no partner was too small to draw statistically significant conclusions.
Nature really doesn't want us thrilled and happy. Nature just wants us to reproduce. Once we are deeply hooked up the thrills get taken away. Obviously humans are in need of some serious amounts of genetic engineering.
Blocking the hormone ghrelin in mice reduced how hard they'd try to get food. Mice with added ghrelin were more drawn to food.
The premise that hunger makes food look more appealing is a widely held belief – just ask those who cruise grocery store aisles on an empty stomach, only to go home with a full basket and an empty wallet.
Prior research studies have suggested that the so-called hunger hormone ghrelin, which the body produces when it's hungry, might act on the brain to trigger this behavior. New research in mice by UT Southwestern Medical Center scientists suggest that ghrelin might also work in the brain to make some people keep eating "pleasurable" foods when they're already full.
"What we show is that there may be situations where we are driven to seek out and eat very rewarding foods, even if we're full, for no other reason than our brain tells us to," said Dr. Jeffrey Zigman, assistant professor of internal medicine and psychiatry at UT Southwestern and co-senior author of the study appearing online and in a future edition of Biological Psychiatry.
Scientists previously have linked increased levels of ghrelin to intensifying the rewarding or pleasurable feelings one gets from cocaine or alcohol. Dr. Zigman said his team speculated that ghrelin might also increase specific rewarding aspects of eating.
Drugs that block ghrelin production might make weight loss, drug addiction, and alcoholism easier to control.
Would added ghrelin help dangerously skinny people who have anorexia?
Women in heat eat less food with guys around. I bet this doesn't hold true for married women eating with their husbands.
Hamilton, ON. August 5, 2009 – If you are a woman who dines with a man, chances are you choose food with fewer calories than if you dine with a woman. That is one of the findings in a study conducted by researchers at McMaster University.
The results appear in the online version of the international journal Appetite.
Meredith Young, PhD candidate in the Department of Psychology, Neuroscience & Behaviour, found that what a person chooses to eat at lunch or dinner is influenced by who they eat with and the gender make-up of the group.
You can probably measure the decline of a woman's romantic attraction for her mate by how much she eats with him around. At least in college settings (mostly single women) the presence of men restrains female wolfing of food.
By observing students in naturalistic settings in three large university cafeterias with a wide choice of food options and dining companions, Young found that women who ate with a male companion chose foods of significantly lower caloric value than did women who were observed eating with another woman.
The more men the less the women eat.
What's more, when women ate in mixed-gender groups their food choices were at the lower end of the caloric scale; the more men in the group the fewer the calories. When women ate in all-female groups, their food was significantly higher in calories.
I wonder how women eating alone compare.
June 26, 2009 - (BRONX, NY) - A variation in a gene that is active in the central nervous system is associated with increased risk for obesity, according to an international study in which Albert Einstein College of Medicine of Yeshiva University played a major role. The research adds to evidence that genes influence appetite and that the brain plays a key role in obesity.
Robert Kaplan, Ph.D., associate professor of epidemiology & population health, helped direct the international study, which involved 34 research institutions and is published online in PLoS Genetics. Dr. Kaplan and his U.S. and European colleagues found that people who have inherited the gene variant NRXN3 have a 10-15 percent increased risk of being obese compared with people who do not have the variant.
The researchers examined data from eight studies involving genes and body weight. These studies included more than 31,000 people of European origin, ages 45 to 76, representing a broad range of dietary habits and health behaviors.
After analyzing more than two million regions of the human genome, the researchers found that the NRXN3 gene variant ─ previously associated with alcohol dependence, cocaine addiction, and illegal substance abuse ─ also predicts the tendency to become obese. Altogether, researchers found the gene variant in 20 percent of the people studied.
NRXN3 has also been implicated in addiction.
Since NRXN3 is active in the brain and also implicated in addiction, these traits may share some neurologic underpinnings.
Central abdominal fat is a strong risk factor for diabetes and cardiovascular disease. To identify common variants influencing central abdominal fat, we conducted a two-stage genome-wide association analysis for waist circumference (WC). In total, three loci reached genome-wide significance. In stage 1, 31,373 individuals of Caucasian descent from eight cohort studies confirmed the role of FTO and MC4R and identified one novel locus associated with WC in the neurexin 3 gene [NRXN3 (rs10146997, p = 6.4×10−7)]. The association with NRXN3 was confirmed in stage 2 by combining stage 1 results with those from 38,641 participants in the GIANT consortium (p = 0.009 in GIANT only, p = 5.3×10−8 for combined analysis, n = 70,014). Mean WC increase per copy of the G allele was 0.0498 z-score units (0.65 cm). This SNP was also associated with body mass index (BMI) [p = 7.4×10−6, 0.024 z-score units (0.10 kg/m2) per copy of the G allele] and the risk of obesity (odds ratio 1.13, 95% CI 1.07–1.19; p = 3.2×10−5 per copy of the G allele). The NRXN3 gene has been previously implicated in addiction and reward behavior, lending further evidence that common forms of obesity may be a central nervous system-mediated disorder. Our findings establish that common variants in NRXN3 are associated with WC, BMI, and obesity.
Another paper from the same issue of Plos Genetics finds still more genes that influence obesity and fat distribution.
Here, we describe a meta-analysis of genome-wide association data from 38,580 individuals, followed by large-scale replication (in up to 70,689 individuals) designed to uncover variants influencing anthropometric measures of central obesity and fat distribution, namely waist circumference (WC) and waist–hip ratio (WHR). This work complements parallel efforts that have been successful in defining variants impacting overall adiposity and focuses on the visceral fat accumulation which has particularly strong relationships to metabolic and cardiovascular disease. Our analyses have identified two loci (TFAP2B and MSRA) associated with WC, and a further locus, near LYPLAL1, which shows gender-specific relationships with WHR (all to levels of genome-wide significance). These loci vary in the strength of their associations with overall adiposity, and LYPLAL1 in particular appears to have a specific effect on patterns of fat distribution. All in all, these three loci provide novel insights into human physiology and the development of obesity.
Expect to see a continued acceleration of the rate of gene searches looking for genetic variants that cause behavioral and health differences. Genetic sequencing and genetic testing costs have fallen so fast that the full effect of the price drops hasn't filtered through to published papers. The price drops continue because the technology continues to advance rapidly. So the amount of data available for gene searches keeps going up faster. This flood of data is going to lead to a flood of findings. The most dramatic consequence will be a big acceleration in human evolution.
Sooner or later scientists will discover compounds that will make human appetite easily controllable. But once again mice get the cool new treatments first.
Researchers at Imperial College London have identified a new appetite suppressant for promoting weight loss that they say works in rodents and may one day be used to develop an effective anti-obesity treatment. Results of the new study were presented at The Endocrine Society's 91st Annual Meeting in Washington, D.C.
The experimental treatment, prokineticin 2, is a recently discovered signaling molecule that occurs naturally in the part of the brain that helps control hunger. Both lean and obese mice treated with PK2 for 5 days lost almost 5 percent of their body weight, the authors reported.
"This is a greater weight loss than people achieve with current nonsurgical weight loss therapies," said study co-author Waljit Dhillo, a clinical senior lecturer at Imperial College London.
The researchers first dissolved a commercially available form of PK2 (from PeproTech Ltd.) in saline and injected it into the brain of 12 rats, which were allowed to eat as much as they wanted for 24 hours. Compared with 12 control rats that received only saline injections, the treated rats ate much less food; in the first hour alone, their food intake was 86 percent less.
The brain injection part isn't exactly appealing. But surely some appetite-cutting compounds will be able to travel via the blood. After all, appetite is influenced by the hormone ghrelin (secreted epsilon cells of the pancreas and P/D1 cells of the stomach) and leptin (secreted by adipose tissues). So the blood does contain compounds that make it into the brain.
While we are living in an era with a high prevalence of obesity we are nearing the end of that era. 20 years from now I expect obesity to be rare in developed countries as drugs that suppress appetite hit the market.
WESTCHESTER, Ill. – According to a research abstract that will be presented on Monday, June 8 at SLEEP 2009, the 23rd Annual Meeting of the Associated Professional Sleep Societies, in the presence of free access to food, sleep restricted subjects reported decrease in appetite, food cravings and food consumption; however, they gained weight over the course of the study. Thus, the finding suggests that energy intake exceeded energy expenditure during the sleep restriction
Results indicate that people whose sleep was restricted experienced an average weight gain of 1.31 kilograms over the 11 days of the study. Of the subjects with restricted sleep who reported a change in their appetite and food consumption, more than 70 percent said that it decreased by day 5 of the study. A group of well rested control subjects did not experience the weight gain.
According to lead investigator Siobhan Banks, PhD, a research fellow at the University of South Australia and former assistant research professor at the University of Pennsylvania School of Medicine, it was surprising that participants did not crave foods rich in carbohydrates after sleep restriction, as previous research suggested they might. Results indicate that even though physiologically the desire to eat was not increased by sleep loss in participants, other factors such as the sedentary environment of the laboratory and the ability to snack for longer due to reduction in time spent asleep might have influenced the weight gain.
This result is consistent with other research which finds a link between lack of sleep and weight gain. This relationship might be due to the simple result that if you are awake more hours you have more time to think about food and eat. However, the lack of sleep could be boosting appetite by increasing levels of the hormone ghrelin while lowering the hormone leptin.
Could sleep be a critical component to maintaining a healthy body weight? According to new research to be presented on Sunday, May 17, at the American Thoracic Society’s 105th International Conference in San Diego, body mass index (BMI) is linked to length and quality of sleep in a surprisingly consistent fashion.
As part of the Integrative Cardiac Health Project at Walter Reed Army Medical Center, researchers analyzed the sleep, activity and energy expenditures of 14 nurses who had volunteered for a heart-health program at the Walter Reed, where the nurses were employed. The program included nutritional counseling, exercise training, stress management and sleep improvement.
Each participant wore an actigraphy armband that measured total activity, body temperature, body position and other indices of activity and rest.
“When we analyzed our data by splitting our subjects into ‘short sleepers’ and ‘long sleepers,’ we found that short sleepers tended to have a higher BMI, 28.3 kg/m2, compared to long sleepers, who had an average BMI of 24.5. Short sleepers also had lower sleep efficiency, experienced as greater difficulty getting to sleep and staying asleep,” said lead investigator Arn Eliasson, M.D.
Are we too busy to get enough sleep and hence we weigh more?
In this study overweight people burn more calories but still weigh more.
Surprisingly, overweight individuals tended to be more active than their normal weight counterparts, taking significantly more steps than normal weight individuals: 14,000 compared to 11,300, a nearly 25 percent difference, and expending nearly 1,000 more calories a day—3,064 versus 2,080.
However, those additional energy expenditures did not manifest in reduced weight.
A wearable patch that you replace once a week monitors heart rate, respiration, body temperature, and other indicators to calculate your calorie consumption and burning rates. Then a cell phone or PC can get the information via Bluetooth and advise you about whether you need to eat less or exercise more.
The calorie monitor, which is being developed by biotech incubator PhiloMetron, uses a combination of sensors, electrodes, and accelerometers that--together with a unique algorithm--measure the number of calories eaten, the number of calories burned, and the net gain or loss over a 24-hour period. The patch sends this data via a Bluetooth wireless connection to a dieter's cell phone, where an application tracks the totals and provides support. "You missed your goal for today, but you can make it up tomorrow by taking a 15-minute walk or having a salad for dinner," it might suggest.
I have no idea how well this generation of device works. But it is a step in an inevitable direction. We will wear external sensors as patches and as sensor nets built into clothing, jewelry, and watches. Diabetics and heart patients can benefit from real time warnings. Athletes can get warnings of overheating and dehydration.
The monitoring systems will eventually get integrated with embedded drug releasing systems that will act much like endocrine organs adjusting our metabolism when it gets out of desirable operating ranges.
Some CalTech scientists think that using brain scans and food choices they have been able to identify the part of the brain that allows people control their desires and refrain from making harmful decisions. If you can say no to unhealthy food you probably have a fairly strong dorsolateral prefrontal cortex (DLPFC) in your brain
After all the choices had been made, the researchers were able to pick out 19 volunteers who showed a significant amount of dietary self-control in their choices, picking mostly healthy foods, regardless of taste. They were also able to identify 18 additional volunteers who showed very little self-control, picking what they believed to be the tastier food most of the time, regardless of its nutritional value.
When they looked at the brain scans of the participants, they found significant differences in the brain activity of the self-control group as compared to the non-self-controllers.
Previous studies have shown that value-based decisions--like what kind of food to eat--are reflected in the activity of a region in the brain called the ventromedial prefrontal cortex, or vmPFC. If activity in the vmPFC goes down, explains Todd Hare, a postdoctoral scholar in neuroeconomics and the first author on the Science paper, "it means the person is probably going to say no to that item; if it goes up, they're likely to choose that item."
In the non-self-controllers, Rangel notes, the vmPFC seemed to only take the taste of the food into consideration in making a decision. "In the case of good self-controllers, however, another area of the brain--called the dorsolateral prefrontal cortex [DLPFC]--becomes active, and modulates the basic value signals so that the self-controllers can also incorporate health considerations into their decisions," he explains. In other words, the DLPFC allows the vmPFC to weigh both taste and health benefits at the same time.
"The vmPFC works during every decision," says Hare. "The DLPFC, on the other hand, is more active when you're employing self-control."
"This, ultimately, is one reason why self-controllers can make better choices," Rangel adds.
Still, the DLPFC can only do so much. For instance, it can't override a truly negative reaction to a food, notes Hare. "We rarely got people to say they'd eat cauliflower if they didn't like cauliflower," he says. "But they would choose not to eat ice cream or candy bars, knowing they could eat the healthier index food instead."
Suppose neural stem cell therapy could boost the power of your dorsolateral prefrontal cortex. Would opt for the cell therapy that would do this?
I expect future prospective parents will gain the option of boosting and dampening various brain genes. I expect most prospective parents will opt for genetic twiddling that will boost the power of the dorsolateral prefrontal cortex. So people of the future will be more self-controlled.
DURHAM, N.C. –- Just seeing a salad on the menu seems to push some consumers to make a less healthy meal choice, according a Duke University researcher.
It's an effect called "vicarious goal fulfillment," in which a person can feel a goal has been met if they have taken some small action, like considering the salad without ordering it, said Gavan Fitzsimons, professor of marketing and psychology at Duke's Fuqua School of Business, who led the research.
In a lab experiment, participants possessing high levels of self-control related to food choices (as assessed by a pre-test) avoided french fries, the least healthy item on a menu, when presented with only unhealthy choices. But when a side salad was added to this menu, they became much more likely to take the fries.
The team's findings are available in the online version of the Journal of Consumer Research, and will appear in its October 2009 print edition.
Natural selection created some pretty strange cognitive biases in human minds. Methinks if you want to ensure you eat healthy food you should go to places that only offer healthy food.
Québec City, March 12, 2009 – Boosting calcium consumption spurs weight loss, according to a study published in the most recent issue of the British Journal of Nutrition, but only in people whose diets are calcium deficient.
Angelo Tremblay and his team at Université Laval's Faculty of Medicine made the discovery in a 15-week weight loss program they conducted on obese women. The participants consumed on average less than 600 mg of calcium per day, whereas recommended daily intake is 1000 mg. In addition to following a low calorie diet, the women were instructed to take two tablets a day containing either a total of 1200 mg of calcium or a placebo. Those who took the calcium tablets lost nearly 6 kg over the course of the program, the researchers found, compared to 1 kg for women in the control group.
"Our hypothesis is that the brain can detect the lack of calcium and seeks to compensate by spurring food intake, which obviously works against the goals of any weight loss program," said Angelo Tremblay, holder of the Canada Research Chair in Environment and Energy Balance. "Sufficient calcium intake seems to stifle the desire to eat more," he added.
Maybe the study is flawed and doesn't prove their result. Don't know. But getting enough calcium when you are deficient will help you even if it doesn't help you lose weight.
COLUMBUS, Ohio – With obesity reaching epidemic levels, researchers at the Ohio State University Medical Center are studying a potentially long-term treatment that involves injecting a gene directly into one of the critical feeding and weight control centers of the brain.
"Obesity significantly increases the risk for diabetes, cardiovascular disease, stroke and some cancers," says Dr. Matthew During, senior author and professor in Ohio State Medical Center's department of molecular virology, immunology and medical genetics. "Our findings represent a promising new treatment for obesity that could ultimately provide a much safer and more effective approach than some conventional therapies."
Scientists have discovered that a particular gene, BDNF, can result in improved insulin sensitivity, reduced fat mass and weight loss when active in the hypothalamus. The findings are published online in the journal Nature Medicine.
According to first author Lei Cao, assistant professor in the department of molecular virology, immunology and medical genetics, the study involved injecting the BDNF gene in normal mice, diabetic mice and mice fed with a high fat diet, to determine how the gene transfer would affect their weight. "The gene was active in the overweight mice, but as they lost weight the gene expression was essentially 'dialed down,' using a novel RNA interference approach, thus stopping the weight from continuing to decrease and allowing a stable target weight to be reached," she says.
You know where this is going: Will we choose our own brain gene therapy? Or will governments choose how our brains get reprogrammed? I figure some governments will reprogram brains of criminals at a minimum. If genetic reprogramming of, for example, pedophiles would work would you support reprogramming of brains as a condition of parole from prison?
A new study in the January 7th issue of Cell Metabolism, a Cell Press publication, helps to explain why obese people and animals fail to respond to leptin, a hormone produced by fat that signals the brain to stop eating. What's more, they show that two FDA-approved drugs might restore leptin sensitivity, offering a novel treatment for obesity.
" Most importantly, our study is the first success in sensitizing obese mice on a high-fat diet to leptin," said Umut Ozcan of Harvard Medical School. "If it works in humans, it could treat obesity."
When leptin was first discovered some 13 years ago, it led to great excitement in the field, Ozcan said. Studies showed that leptin administered to obese mice that lacked the hormone lost weight. The buzz over leptin's potential as an obesity therapy soon waned, however, because obese animals and people don't respond to the hormone. Efforts to find drugs that act as leptin sensitizers over the years have also failed.
A part of cells known as the endoplasmic reticulum (ER) is involved in many cellular processes including protein manufacturing, lipid and carbohydrate synthesis, and other functions. Stress in the ER appears to play a role in a metabolic disorder linked to obesity. These researchers decided that perhaps ER stress played a role in reduced response of the brain's hypothalamus to leptin.
Recent studies by him and his colleagues showed that a condition known as endoplasmic reticulum (ER) stress in peripheral organs plays an important role in obesity-induced insulin resistance and type 2 diabetes. Ozcan describes ERs as protein factories within cells. Within those cellular components, molecular chaperones, which serve as the factory workers, facilitate the folding and transport of proteins. When the chaperones can't keep up, it triggers a stress response known as the unfolded protein response (UPR).
The researchers went looking for drugs that could reduce ER stress in hopes that ER stress reduction would make the hypothalamus more sensitive to leptin and thereby reduce appetite. Turns out, ER stress reduction caused mouse weight loss.
The question then became whether the animals could be resensitized by treating them with either of two pre-existing drugs (4-Phenyl Butyric Acid [PBA] and Tauroursodeoxycholic acid [TUDCA]) that act as ER stress reducers. And the answer, they report, is yes.
" It was very exciting," Ozcan said of the discovery. "Normal mice treated with the drugs dropped some weight and quickly rebounded, but the knockout mice [that were genetically predisposed to ER stress in the brain] continued to lose weight. It shows that ER stress relievers are leptin sensitizers."
This research does not prove that ER stress reducer drugs will reduce appetite in overweight humans. Also, ER stress reduction in humans might turn out to be very difficult to do without undesirable side effects. Development of drugs which have only very specific effects is usually a difficult and problematic undertaking.
ER stress probably increases with age as cells malfunction due to accumulated damage. So rejuvenation therapies will probably, as a side effect, make us skinnier. But this study underlines the need to rejuvenate the brain - which is by far the most difficult organ in the body to rejuvenate.
If you can't keep your weight down at a healthy level then you've got an increasing cast of genetic actors to blame for your excess fat. The 6 latest discoveries all are active in the brain.
The international GIANT (Genetic Investigation of Anthropometric Parameters) consortium works on the discovery of obesity genes. So far, the scientists have analyzed two million DNA variations in 15 genome-wide association studies with a total of more than 32,000 participants. The hereby identified candidate genes were validated in 14 further studies including 59,000 participants. In addition to the FTO and MC4R genes already known, it was now possible for six more obesity genes to be identified: TMEM18, KCTD15, GNPDA2, SH2B1, MTCH2, and NEGR1.
Gene expression analyses have shown that all six genes are active in brain cells. Also the previously known two obesity genes, FTO and MC4R, show a similar expression pattern; in case of the MC4R gene, a genotype-dependant influence on the behavior of appetite is already established. Scientists of the German National Genome Research Network (NGFN), Prof. H.-Erich Wichmann and Dr. Iris Heid from the Helmholtz Zentrum München, Institute of Epidemiology, who lead the German participation of this consortium, emphasize: "Definitely, the two main causes for obesity are poor nutrition and lack of physical activity. But the biology of these genes suggests genetic factors underlying the different reaction of people to lifestyle and environmental conditions."
With the exception of the SH2B1 gene, which plays a role in the leptin signalling and thus in the regulation of appetite, none of the other five genes was hitherto discussed as obesity genes. Iris Heid and her collegue Claudia Lamina from the Ludwigs-Maximilians-Universität München are enthused: "The purely statistical approach of the genome-wide association analysis can depict new aspects of the biology of weight regulation, which were previously unanticipated."
As a next step, the scientists evaluate other anthropometric measures, in order to shed light on different aspects of obesity. In addition, they will expand and include further studies into their analysis as they have realized that the individual studies are all too small, and only by means of collaboration, is it possible to achieve further success here.
This project was financed by the German National Genome Research Network (NGFN, head of the Obesity Network: Prof. Johannes Hebebrand, University of Duisburg-Essen; Project Leader Helmholtz Zentrum München: PD Dr. Thomas Illig), the National Institutes of Health, USA, and the Munich Center of Health Sciences of the LMU Munich. The genotyping was carried out at the Institute for Human Genetics of the Helmholtz Zentrum München under the leadership of Prof. Thomas Meitinger.
What I would like to know: How many of these genes regulate appetite? My guess is that most or all play roles in appetite. But maybe some of them control our propensity to exercise by, for example, controlling how much pleasure we experience when exercising or by making us more or less fidgety.
You hear people argue that legalizing chocolate truffles will not lead to use of more powerful food drugs. But the evidence says otherwise. Truffles are the gateway to indulgence and food abuse.
Indulging in just one small chocolate truffle can induce cravings for more sugary and fatty foods—and even awaken a desire for high-end status products, according to a new study in the Journal of Consumer Research.
Truffles even awaken a desire for high-end status products? First you eat a truffle. Then you eat a pizza. Before you know it you find yourself shopping for a Rolls Royce or maybe a Patek Philippe watch. Just say no.
In a study that examined goals and behavior in consumers, authors Juliano Laran (University of Miami) and Chris Janiszewski (University of Florida) found that study participants who consumed a chocolate truffle desired ice cream, pizza, and potato chips more than people who were told to resist eating a truffle.
When participants were allowed eat a truffle, they unconsciously activated a goal of indulgence, the authors explain. Likewise, those who were asked to resist the treat activated health goals. Once people felt their goals were met, they tended to reverse their behaviors. For example, when people who resisted the truffle were told they did a good job, they indicated that they desired fatty foods more than healthy foods.
"Once people feel like they have achieved a certain goal, they tend to pursue the opposing goal. When asked about their behaviors, no participant related their desires to the initial chocolate consumption, indicating the operation of a non-conscious system that guides people's behaviors," write the authors.
Truffles even awaken a desire for high-end status products? How rapidly has truffle consumption grown in recent years? Does this account the unsustainable US trade deficit, excessive personal indebtedness, and government budget deficits? Are truffles handed out by lobbyists?
6 genetic variants variants have been identified as possible contributing factors for obesity. 5 of them are expressed in the brain.
A genetic study of more than 90,000 people has identified six new genetic variants that are associated with increased Body Mass Index (BMI), the most commonly used measure of obesity. Five of the genes are known to be active in the brain, suggesting that many genetic variants implicated in obesity might affect behaviour, rather than the chemical processes of energy or fat metabolism.
Obesity is an increasing problem that results in individual risk to health as well as increasing burdens on health care systems. By identifying genetic variants that affect obesity, researchers hope to understand better the mechanisms regulating energy balance, which will guide the development of new therapies and help to develop improved diagnosis.
These genes reduce the human capacity to exercise free will. People who want to lose weight but find themselves compelled to eat do not have free will over the amount of food they consume.
For example, one of the genes, NEGR1, controls how your brain is wired as it is developing by regulating neuronal growth, Abecasis said.
"In younger children, ages 5-10, we found that with three of (the genes) the children were already heavier at that young age, and with the other three genes, we saw that there was no effect on children," he said. "For those, we only saw an effect in much older individuals. This points to different mechanisms influencing your weight at different ages."
Another example is SH2B1, which was first discovered by U-M researchers studying mice, Abecasis said. Researchers created an obese mouse then returned it to its normal weight by turning on the SH2B1 gene in the brain.
We are going to hear about many more genetic variants that influence behavior every year. The cost of genetic testing has dropped so far that studies search through large amounts of genetic data are becoming cheaper and more feasible to do. Costs of genetic testing and genetic sequencing will continue to plummet and the rate of discovery will continue to rise.
News you can use: Dark chocolate, which basically is the purer stronger chocolate with more flavonoids and other chocolate compounds, cuts appetite as compared to milk chocolate.
To compare the effects of dark and milk chocolate on both appetite and subsequent calorie intake, 16 young and healthy men of normal weight who all liked both dark and milk chocolate took part in a so-called crossover experiment. This meant that they reported for two separate sessions, the first time testing the dark chocolate, and the second time the milk chocolate.
They had all fasted for 12 hours beforehand and were offered 100g of chocolate, which they consumed in the course of 15 minutes. The calorific content was virtually the same for the milk and dark chocolate.
During the following 5 hours, participants were asked to register their appetite every half hour, i.e. their hunger, satiety, craving for special foods and how they liked the chocolate.
Two and a half hours after eating the chocolate, participants were offered pizza ad lib.
They were instructed to eat until they felt comfortably satiated. After the meal, the individuals’ calorie intake was registered.
The results were significant. The calorie intake at the subsequent meal where they could eat as much pizza as they liked was 15 per cent lower when they had eaten dark chocolate beforehand.
The participants also stated that the plain chocolate made them feel less like eating sweet, salty or fatty foods.
So if you are trying to cut back on your pizza eating then dark chocolate might help.
Why this result? What in chocolate cuts appetite? Anyone know of any clues?
The brain is very sensitive to blood sugar level. The brain also craves carbo and sugars. Not coincidentally, women who go on a low carb diet perform more poorly at some cognitive tasks than women who go on low calorie diets which cut all types of calories.
MEDFORD/SOMERVILLE, Mass. -- A new study from the psychology department at Tufts University shows that when dieters eliminate carbohydrates from their meals, they performed more poorly on memory-based tasks than when they reduce calories, but maintain carbohydrates. When carbohydrates were reintroduced, cognition skills returned to normal.
The more general lower calorie diet has more carbs in it than the low carb diet. The sugars in those carbs probably helps feed the brain and cause higher brain performance.
Low-carb dieters showed a gradual decrease on the memory-related tasks compared with the low-calorie dieters. Reaction time for those on the low-carb diet was slower and their visuospatial memory was not as good as those on the low-calorie diet. However, low-carb dieters actually responded better than low-calorie dieters during the attention vigilance task. Researchers note that past studies have shown that diets high in protein or fat can improve a person's attention in the short-term, which is consistent with the results in this study.
Participants were also asked about their hunger levels and mood during each session. The hunger-rating did not vary between participants on a low-carb diet and those on a low-calorie diet. The only mood difference between dieters was confusion, which was higher for low-calorie dieters during the middle of the study.
This was only a 3 week study. Possibly on a longer diet the result would be different. A diet with severe carbo restriction which drives the body to make ketones might performance higher cognitive performance than the low-carb diet used above.
A vigorous 60-minute workout on a treadmill affects the release of two key appetite hormones, ghrelin and peptide YY, while 90 minutes of weight lifting affects the level of only ghrelin, according to a new study. Taken together, the research shows that aerobic exercise is better at suppressing appetite than non-aerobic exercise and provides a possible explanation for how that happens.
This line of research may eventually lead to more effective ways to use exercise to help control weight, according to the senior author, David J. Stensel of Loughborough University in the United Kingdom.
Ghrelin and peptide YY have opposite effects on appetite.
There are several hormones that help regulate appetite, but the researchers looked at two of the major ones, ghrelin and peptide YY. Ghrelin is the only hormone known to stimulate appetite. Peptide YY suppresses appetite.
Think of this research as part of a drive to simulate the effects of exercise as a substitute for real exercise. By discovering all the changes that exercise causes in the body scientists can pinpoint all signaling systems in the body that will have to be tweaked in order to emulate the effects of exercise. Want the weight-losing effects of exercise? You'll need to boost peptide YY and lower ghrelin for starters.
A Yale researcher has discovered that the lipid NAPE—N-acylphosphatidylethanolamine, excreted by the small intestine, travels to the brain,concentrates in the hypothalamus, and suppresses hunger in rats and mice. Rats wearing an IV vest that delivers NAPE for days ate less than controls and lost weight.
Howard Hughes Medical Institute investigator Gerald Shulman at Yale School of Medicine led the research team, which reported its findings in the November 26, 2008, issue of the journal Cell. Shulman's research group is well known for its work on understanding how insulin resistance develops and leads to diabetes. In the course of that research, his team developed a sensitive system to identify and measure lipids in tissue samples. After seeing the power of that system in his diabetes research, Shulman was eager to see if it might also be applied to understanding obesity.
Note that a low fat and high carbo diet might set you up for more hunger (this is obviously not an original thought). Only fat causes NAPE release and appetite suppression in rats.
They found only low levels of NAPE in the blood of rats that had fasted for 12 hours. The level of NAPE shot up 40 to 50 percent in animals that had dined on high-fat chow. Furthermore, NAPE didn't increase in rodents that ate only protein or carbohydrate, suggesting that NAPE levels reflect the amount of fat eaten in a meal.
The researchers found that when they injected synthetic NAPE into the abdominal cavity or blood, the rodents' appetites diminished substantially. The more NAPE they received, the less food they ate. "It's really quite effective," Shulman says. "At the highest doses, it keeps the animals from eating for up to 12 hours." At a low dose—comparable to the spike in NAPE that occurs naturally after a meal—the rodents still ate 25 percent less than controls. They even acted full, going into "siesta mode" as if they had just eaten, Shulman says, noting that additional tests confirmed that the animals were only lethargic, not ill or incapacitated.
The scientists are going to study NAPE in primates and humans with the hope of finding evidence to justify clinical trials.
If periodic injections or some other method of delivery could work for humans then NAPE might serve as an effective compound for weight loss. Though I'm concerned how the clinical trials would get funding. NAPE occurs naturally in the body. Can a drug company get a patent on it for weight loss so that an incentive would exist to spend the hundreds of millions of dollars needed to go through the clinical trials and drug application process?
Human appetite, like many other basic human desires, is going to become very manipulable with pharmaceuticals. Which basic desire do you most want to increase or decrease?
Obesity gradually numbs the taste sensation of rats to sweet foods and drives them to consume larger and ever-sweeter meals, according to neuroscientists. Findings from the Penn State study could uncover a critical link between taste and body weight, and reveal how flab hooks the brain on sugary food.
"When you have a reduced sensitivity to palatable foods, you tend to consume it in higher amounts," said Andras Hajnal, associate professor of neural and behavioral sciences at Penn State College of Medicine. "It is a vicious circle."
Previous studies have suggested that obese persons are less sensitive to sweet taste and crave sweet foods more than lean people. However, little is known about the specific differences between obese and lean individuals in their sense of taste and the pleasure they derive from sweet foods.
Hajnal and his Penn State colleague Peter Kovacs, a post-doctoral fellow, investigated these differences by studying the taste responses of two strains -- OLETF and LETO rats.
Compared to the lean and healthy LETO rats, the taste responses in OLETF rats mirror those in obese humans. These rats have normal body weight at first, but they tend to chronically overeat due to a missing satiety signal, become obese and develop diabetes. The obese rats also show an increased preference for sweet foods and also are willing to work harder to obtain sweet solutions as a reward for their learning.
Obese rats react less to weaker concentrations of sucrose sugar but more to stronger concentrations - as compared to non-obese rats.
The researchers implanted electrodes in the rodents' brains to record the firing of nerve cells when the rats' tongues were exposed to various tastes -- salt, citric acid, plain water and six different concentrations of sucrose.
Hajnal and Kovacs specifically looked at differences in processing taste in the pontine parabrachial nucleus (PBN), a part of the brain that uses nerve cells to relay information from the surface of the tongue to the brain.
"We found that compared to the LETO rats, the OLETF rats had about 50 percent fewer neurons firing when their tongues were exposed to sucrose, suggesting that obese rats are overall less sensitive to sucrose," explained Hajnal, whose findings appeared in a recent issue of the Journal of Neurophysiology. The response to salt was the same for both strains.
However, when the obese rats were fed a stronger concentration of sucrose, their nerve cells fired more vigorously than in the lean rats. In other words, obese rats have a weaker response to weak concentrations and a stronger response to strong concentrations.
This probably at least partially explains human obesity. If one could increase the neural response to less sugary foods while dampening the neural response to stronger sugar concentrations one could make it much easier for people to eat less food.
A new study in the November issue of the journal Appetite finds that obese women display significantly weaker impulse control than normal-weight women, but between obese and normal-weight men, the impulsivity levels are nearly the same. The study was conducted by researchers in the University of Alabama at Birmingham (UAB) Department of Psychology.
UAB researchers conducted the study to see how obese and normal-weight men and women differed in their decision-making skills, specifically in delay discounting, the measure of how much an individual is driven by immediate gratification versus the willingness to wait for delayed but greater rewards.
In the study of 95 men and women, UAB researchers gave the participants the choice of receiving varying hypothetical amounts of money immediately or fixed hypothetical amounts of money to be received after delays of two weeks, one month, six months or one, three, five or 10 years. The hypothetical rewards ranged from $1,000 to $50,000.
The researchers found that obese women discounted the value of future rewards at a rate three-to-four times greater than that of normal-weight women, suggesting greater impulsivity. Obese men, however, and the male and female control subjects all showed similar levels of delay discounting. The results were the same even when the researchers controlled for differences in IQ and income, both of which have been found to be related to measures of impulsivity.
First off, what's the evolutionary explanation for this result? Are the women more obese because they were selected for to be more obese in order to avoid starvation? Or is the obesity a modern side effect of selection for impulsivity which provided a reproductive fitness advantage some other way?
Also, why the difference between men and women? Also, if impulsivity doesn't contribute to male obesity then what other factor does? In the United States the prevalence of obesity is higher among females than among males. But the difference isn't large.
Among men, the prevalence of obesity increased significantly between 1999-2000 (27.5%) and 2003-2004 (31.1%). Among women, no significant increase in obesity was observed between 1999-2000 (33.4%) and 2003-2004 (33.2%). The prevalence of extreme obesity (body mass index > or =40) in 2003-2004 was 2.8% in men and 6.9% in women.
CHICAGO, IL, October 26 – New research continues to link tart cherries, one of today's hottest "Super Fruits," to lowering risk factors for heart disease. In addition to lowering cholesterol and reducing inflammation, the study being presented by University of Michigan researchers at next week's American Dietetic Association annual meeting, found that a cherry-enriched diet lowered body weight and fat – major risk factors for heart disease.
Maybe the inflammation reduction causes a change in signaling that reduces body weight.
In the study, at-risk, obese rats that were fed a cherry-enriched diet saw significant decreases in body weight and fat (especially the important "belly" fat with known risk for heart disease) while maintaining lean muscle mass. After twelve weeks, the cherry-fed rats had 14 percent lower body fat compared to the other rats who did not consume cherries (cherry-fed rats were approximately 54% body fat; rats eating the Western diet alone were 63% body fat). The researchers suggested cherry consumption could have an effect on important fat genes and genetic expression. According to the American Heart Association, being overweight or obese, in particular when the weight is concentrated in the middle, is a major risk factor for heart disease . Nearly two out of three Americans are overweight.
The animals were fed a "Western diet," characterized by high fat and moderate carbohydrate – in line with the typical American diet – with or without added whole tart cherry powder, as 1 percent of the diet. The study was funded by the Cherry Marketing Institute, which provided an unrestricted grant to the University of Michigan to conduct the research and was not directly involved in the design, conduct or analysis of the project.
Would blueberries or cranberries deliver the same benefit? Would this work in humans?
Not only are fat people cursed with less physical attractiveness, greater health risks, and greater difficulty in getting around. Obese people get less pleasure out of eating food.
AUSTIN, Texas—Obese individuals may overeat because they experience less satisfaction from eating food due to a reduced response in their brains' reward circuitry, according to a new study by Eric Stice, psychology researcher at The University of Texas at Austin.
While eating, the body releases dopamine, a neurotransmitter in the reward centers of the brain, but Stice found obese people show less activation in the striatum relative to lean people. He also found individuals with a blunted response were more likely to show unhealthy weight gain, particularly if they had a gene associated with compromised dopamine signaling in the brain's reward circuitry.
Stice and a team of researchers have published their findings in the Science article, "Relation Between Obesity and Blunted Striatal Response to Food is Moderated by TaqIA A1 Allele."
A genetic variation that lowers the number of dopamine neurotransmitter receptors reduces one's ability to enjoy a chocolate milkshake. Nature is cruel. Some people have a handicapped ability to excite their brain's dorsal striatum.
Using Functional Magnetic Resonance Imaging (fMRI), Stice's team measured how the dorsal striatum was activated in response to the taste of a chocolate milkshake (versus a tasteless solution). The researchers also tested participants for the presence of a genetic variation linked to a lower number of dopamine D2 receptors, the Taq1A1 allele.
So if you are skinny you probably can better enjoy food than fat people can.
So the overweight aren't overweight because they've enjoyed food more. They are overweight because they need more stimulation to feel pleasure from food.
The results, drawn from two studies using functional magnetic resonance imaging (fMRI) at the University of Oregon's Lewis Center for Neuroimaging, appear in the Oct. 17 issue of the journal Science. The first-of-its-kind approach unveiled blunted activation in the brain's dorsal stratium when subjects were given milkshakes, which may reflect less-than-normal dopamine output.
"Although recent findings suggested that obese individuals may experience less pleasure when eating, and therefore eat more to compensate, this is the first prospective evidence for this relationship," said Eric Stice, lead author and senior researcher at the Oregon Research Institute (ORI) in Eugene. "The evidence of temporal precedence suggests it is a true vulnerability factor that predates obesity onset. In addition, the evidence that this relation is even stronger for individuals at genetic risk for compromised signaling in these brain regions points to an important biological factor that appears to increase risk for obesity onset."
The researchers focused on a variant of the TaqlA1 gene, which is associated with increased body mass as well as a reduction of dopamine signaling in the dorsal striatum. The blunted response to tasty food was particularly pronounced in women with the variant. In addition, women with the variant were much more likely to gain weight after a year.
Prior work had shown that obese people tend to have fewer dopamine receptors in the brain and suggested that they overeat to compensate for this reward deficit. The current findings are consistent with the theory that the blunted response to food represents a vulnerability factor for obesity but it does not conclusively rule out the possibility that the finding reflects an adaptation to over-eating, Small cautioned.
How wide ranging is this genetically caused diminished capacity for pleasure? Does it reduce pleasure from most aspects of life?
Using Functional Magnetic Resonance Imaging (fMRI), Stice’s team measured the extent to which a certain area of the brain (the dorsal striatum) was activated in response to the individual’s receipt of a taste of chocolate milkshake (versus a tasteless solution). Participants in the studies were also tested for the presence of a genetic variation linked to a lower number of dopamine D2 receptors, the Taq1A1 allele. Researchers tracked participants’ changes in body mass index (BMI) over a 1-year follow up. Results showed that those participants with decreased striatal activation in response to milkshake receipt and those with the A1 allele were more likely to gain weight over time.
“These results suggest that individuals with hypofunctioning reward circuitry are at increased risk for unhealthy weight gain,” said Stice. “Thus, it is possible that behavioral or pharmacological interventions that correct this reward deficit may help prevent and treat obesity – an avenue we are currently pursuing in our research.”
This puts a whole new spin on the idea of "appetite for life". You'll be healthier if you can get more enjoyment from less experience.
Imagine a future treatment for obesity: Gene therapy or stem cell therapy that increases your concentration of dopamine D2 receptors in the dorsal striatum of the brain. Such a therapy would alter how a person experiences life.
A fatty acid found in abundance in olive oil and other "healthy" unsaturated fats has yet another benefit: it helps keep the body satisfied to prolong the time between meals.
A new study in the October Cell Metabolism, a publication of Cell Press, reveals that once this type of fat, known as oleic acid, reaches the intestine, it is converted into a lipid hormone (oleoylethanolamide, or OEA) that wards off the next round of hunger pangs. The researchers said it may be the first description of an ingredient in food that directly provides the raw materials for a hormone's production.
The findings in rats may yield insight into the precise dietary makeup of fat and protein for optimal hunger control, the researchers said. (Protein plays in important role in limiting hunger as well, but by different means.) The newly discovered signaling pathway might also be tapped into with drugs designed to control appetite by supplementing OEA levels or blocking its breakdown. Similarly, in conditions where people don't eat enough, the researchers speculate that treatments targeting this system might improve the appetite.
Importantly, diets high in processed foods that are riddled with saturated fats might throw a wrench into this system of metabolic control, the researchers said.
Olive oil also contains phenolic compounds which are suspected of providing additional health benefits.
Destruction of a blood vessel that feeds the top part of the stomach cuts ghrelin hunger hormone production. The expectation is that ghrelin reduction via this technique can reduce hunger and obesity.
Johns Hopkins scientists report success in significantly suppressing levels of the "hunger hormone" ghrelin in pigs using a minimally invasive means of chemically vaporizing the main vessel carrying blood to the top section, or fundus, of the stomach. An estimated 90 percent of the body's ghrelin originates in the fundus, which can't make the hormone without a good blood supply.
"With gastric artery chemical embolization, called GACE, there's no major surgery," says Aravind Arepally, M.D., clinical director of the Center for Bioengineering Innovation and Design and associate professor of radiology and surgery at the John Hopkins University School of Medicine. "In our study in pigs, this procedure produced an effect similar to bariatric surgery by suppressing ghrelin levels and subsequently lowering appetite."
The problem with this approach is that it is not easily reversible or tunable. Suppose your appetite gets cut too far. Well, you could end up like an anorexic.
Using X-ray for guidance, members of the research team threaded a thin tube up through a large blood vessel near the pigs' groins and then into the gastric arteries supplying blood to the stomachs. There, they administered one-time injections of saline in the left gastric arteries of five control pigs, and in the other five, one-time injections of sodium morrhuate, a chemical that destroys the blood vessels.
The team then sampled the pigs' blood for one month to monitor ghrelin values. The levels of the hormone in GACE-treated pigs were suppressed up to 60 percent from baseline.
We need researchers to do appetite studies to show that pigs treated with this procedure experience the expected reduction in appetite.
We need dynamic finer granularity ways to control appetite. But for someone who is morbidly obese this procedure could potentially deliver substantial benefits.
Thinking makes you hungry. So if you want to lose weight become vacuous and shallow? "Sorry I was so inconsiderate and thoughtless dear. You know my diet requires it."
Quebec City, September 4, 2008—A Université Laval research team has demonstrated that intellectual work induces a substantial increase in calorie intake. The details of this discovery, which could go some way to explaining the current obesity epidemic, are published in the most recent issue of Psychosomatic Medicine.
The research team, supervised by Dr. Angelo Tremblay, measured the spontaneous food intake of 14 students after each of three tasks: relaxing in a sitting position, reading and summarizing a text, and completing a series of memory, attention, and vigilance tests on the computer. After 45 minutes at each activity, participants were invited to eat as much as they wanted from a buffet.
The researchers had already shown that each session of intellectual work requires only three calories more than the rest period. However, despite the low energy cost of mental work, the students spontaneously consumed 203 more calories after summarizing a text and 253 more calories after the computer tests. This represents a 23.6% and 29.4 % increase, respectively, compared with the rest period.
Blood samples taken before, during, and after each session revealed that intellectual work causes much bigger fluctuations in glucose and insulin levels than rest periods. "These fluctuations may be caused by the stress of intellectual work, or also reflect a biological adaptation during glucose combustion," hypothesized Jean-Philippe Chaput, the study's main author. The body could be reacting to these fluctuations by spurring food intake in order to restore its glucose balance, the only fuel used by the brain.
"Caloric overcompensation following intellectual work, combined with the fact that we are less physically active when doing intellectual tasks, could contribute to the obesity epidemic currently observed in industrialized countries," said Mr. Chaput. "This is a factor that should not be ignored, considering that more and more people hold jobs of an intellectual nature," the researcher concluded.
Maybe the mental work uses up glucose in the brain and causes the brain cells that control appetite to sense this and drive up appetite to compensate?
A study on humans with a genetic disorder confirms animal studies: low brain derived neurotrophic factor (BDNF) causes unusually strong appetites and obesity.
A brain chemical that plays a role in long term memory also appears to be involved in regulating how much people eat and their likelihood of becoming obese, according to a National Institutes of Health study of a rare genetic condition.
Brain derived neurotrophic factor (BDNF) is, as its name implies, produced in the brain. Studies of laboratory animals have suggested it also helps control appetite and weight. The NIH study, appearing in the August 28 New England Journal of Medicine, provides the first strong evidence that BDNF is important for body weight in human beings as well.
The NIH researchers studied children and adults with WAGR syndrome, a rare genetic condition. The researchers found that some of the people with this syndrome lack a gene for BDNF and have correspondingly low blood levels of the substance. The people in this subgroup also have unusually large appetites and a strong tendency towards obesity.
"This is a promising new lead in the search for biological pathways that contribute to obesity," said Duane Alexander, M.D., director of the NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development. "This finding may eventually lead to the development of new drugs to regulate appetite in people who have not had success with other treatments."
Not all adults with WAGR syndome have the BDNF deletion. Those with WAGR without the deletion do not have a higher rate of obesity.
In the current study, the NIH researchers conducted analyses of chromosome 11 in 33 patients with WAGR syndrome. A total of 19 patients (58 percent) had deletions of all or a major proportion of one copy of the gene for BDNF. By age 10, all of the 19 were obese and were reported to have a strong tendency to overeat. Moreover, all of the 19 had blood levels of BDNF that were roughly 50 percent lower than those of patients who had two working copies of the BDNF gene. The patients who had two working copies of the BDNF gene were no more likely to develop childhood onset obesity than the general population, and did not report unusually high levels of overeating.
Leptin, a known appetite regulator, might work by controlling release of BDNF by the hypothalamus. Perhaps BDNF injections could suppress appetite in obese people.
Dr. Yanovski explained that BDNF is believed to work in combination with a variety of other substances that regulate appetite and body weight. Chief among these is leptin, a hormone found to be involved in signaling hunger. Dr. Yanovski added that release of BDNF in the hypothalamus, a part of the brain involved in controlling eating, is believed to be indirectly triggered by leptin. Studies of the relationship between the two, and of BDNF's action on tissues, may lead to the development of new drugs to treat obesity in some individuals.
If the BDNF release by the hypothalamus then reaches the rest of the brain by the bloodstream that opens up the possibility of injecting BDNF into the bloodstream as a treatment to reduce appetite. Injection has obvious downsides such as that you have to do it in the first place. Diabetics already carry this burden. Poking a needle into yourself one or more times a day is a painful and potentially dangerous chore and need to store the BDNF in a refrigerator are all downsides. Plus, the injection regime would tend to cause larger and less frequent bursts of blood BDNF than natural hypothalamus release. What we need: embeddable reservoirs that would gradually release the BDNF. Another possibility: Use gene therapy to convert some cells in the body into BDNF producers.
As the cost of genetic testing and other biological testing comes down the rate of discoveries such as this one will only go faster and faster until most of the biological mechanisms in the human body are understood. With these discoveries will come a big shrinkage of our perceived ability to act with free will. So many genes will be found to have variants that influence behavior that a growing portion of all that we do will be attributed at least partially to genetic causes.
On more than one occasion I've found myself defending drug addicts while arguing with someone who is obese. Basically I argued that their own inability to ignore their hunger is very similar to a drug addict's inabilty to ignore the craving for another dose. Each person who I made this argument to responded like I was insulting them. But the evidence strongly suggests common mechanisms involved in food and drug cravings. Now a new study finds that a drug under development against cocaine and meth causes weight loss in rats.
UPTON, NY -- Vigabatrin, a medication proposed as a potential treatment for drug addiction by scientists at the U.S. Department of Energy's (DOE) Brookhaven National Laboratory, also leads to rapid weight loss and reduced food intake according to a new animal study from the same research group. The study will be published online August 20, 2008, by the journal Synapse. Vigabatrin is currently undergoing U.S. Food and Drug Administration (FDA)-approved Phase II clinical trials against cocaine and methamphetamine addiction across the U.S.
In the current study, animals genetically bred to be obese experienced a loss of up to 19 percent of their total weight while non-obese animals lost 12 to 20 percent following short-term vigabatrin administration.
This might seem like good news for people who weigh too much. But it might also be bad news for coke and meth addicts. Will they eat enough while on this drug? Maybe so. Then again, if the drug works and they stop their drug addiction then that's a huge benefit.
"Our results appear to demonstrate that vigabatrin induced satiety in these animals," said Amy DeMarco, who led the study, working in the laboratory of Brookhaven Lab senior scientist Stephen Dewey. Dewey first identified vigabatrin as a potential addiction treatment and has conducted more than 20 years of preclinical research with this promising medication.
Earlier studies at Brookhaven Lab found a strong connection between obesity and addiction, including similar changes in the brains of the obese and those addicted to drugs like cocaine. Based on these connections, Dewey hypothesized that vigabatrin would quench food cravings in the lab rats.
This drug alters people's basic desires. If our desires can be altered so easily do we really have free will?
ROCHESTER, Minn. -- A new implantable medical device, developed in collaboration with Mayo Clinic researchers, shows promise as a reversible and less extreme alternative to existing bariatric surgeries, according to findings published in the current issue of the journal Surgery.
Laparoscopic surgery places electrodes into the abdomen. The control unit is under the skin. This treatment is much more reversible than gastric bypass. People who had the therapy done lost weight.
In a six-month open label trial involving three medical centers in Australia, Mexico and Norway, the 31 obese participants who received the vagal nerve blocking device, also called VBLOCTM vagal blocking therapy, lost an average of nearly 15 percent of their excess weight. A quarter of the participants lost more than 25 percent, and three patients lost more than 30 percent.
15% of one's excess weight doesn't sound like so much. But without knowing the absolute amount of weight loss it is hard to judge. Also, will the weight loss continue?
The interesting thing about this approach is that it amounts to playing games to fool one's nervous system.
Michael Camilleri, M.D., is a gastroenterologist who helped design the study and one of the Mayo Clinic researchers whose previous work and know-how contributed to development of the device in collaboration with EnteroMedics, Inc. Dr. Camilleri says the goal is to find a less drastic alternative to bariatric surgery that will still yield significant weight loss. Bariatric surgery techniques include "banding" -- placement of a band around the top part of the stomach to reduce its capacity -- or bypass procedures which reroute food and remove part of the stomach.
"For this study, we wanted to get an initial assessment of whether blocking the vagus nerve electrically could cause obese patients to feel full after a normal-sized meal," Dr. Camilleri explains. "Patients were not put on any restricted diets or given counseling that typically accompanies gastric banding or bypass. We wanted to determine how much weight loss could be attributed to the device alone."
Dr. Camilleri says VBLOC therapy is similar to a heart pacemaker, but instead of stimulating a normal, regular heartbeat, it uses high-frequency electricity to block the nerve impulses between the brain and the stomach and pancreas. A pacemaker continuously monitors the heart and regulates its beating. But the patient flips a switch to activate the VBLOC device when the system is worn during the daytime hours so that the blocking signal can influence how the stomach functions and food is digested following a meal.
With conventional stomach bypass some of the weight loss comes from a reduction in the level of the hunger hormone ghrelin. Does this VBLOC therapy reduce the amount of ghrelin in the bloodstream? If so, does it reduce ghrelin as much as bypass surgery does? A method short of surgery that reduced the amount of ghrelin in the bloodstream would offer a lot of advantages in terms of avoided sometimes deadly complications from surgery and also avoided costs of surgery and recovery.
DALLAS – June 15, 2008 – New research at UT Southwestern Medical Center may explain why some people who are stressed or depressed overeat.
While levels of the so-called "hunger hormone" ghrelin are known to increase when a person doesn't eat, findings by UT Southwestern scientists suggest that the hormone might also help defend against symptoms of stress-induced depression and anxiety.
"Our findings in mice suggest that chronic stress causes ghrelin levels to go up and that behaviors associated with depression and anxiety decrease when ghrelin levels rise. An unfortunate side effect, however, is increased food intake and body weight," said Dr. Jeffrey Zigman, assistant professor of internal medicine and psychiatry at UT Southwestern and senior author of a study appearing online today and in a future print edition of Nature Neuroscience.
Dr. Michael Lutter, instructor of psychiatry at UT Southwestern and lead author of the study, said, "Our findings support the idea that these hunger hormones don't do just one thing; rather, they coordinate an entire behavioral response to stress and probably affect mood, stress and energy levels."
What I wonder: If you are under stress and ghrelin goes up then do you get more stress-reduction benefit from ghrelin if you manage to refrain from eating more? Does weight gain cause a decrease in ghrelin and therefore less stress-reduction benefit from ghrelin?
Ghrelin reduces the stress reaction from getting bullied.
To test whether ghrelin could regulate depressive symptoms brought on by chronic stress, the researchers subjected mice to daily bouts of social stress, using a standard laboratory technique that induces stress by exposing normal mice to very aggressive "bully" mice. Such animals have been shown to be good models for studying depression in humans.
The researchers stressed both wild-type mice and altered mice that were unable to respond to ghrelin. They found that after experiencing stress, both types of mice had significantly elevated levels of ghrelin that persisted at least four weeks after their last defeat encounter. The altered mice, however, displayed significantly greater social avoidance than their wild-type counterparts, indicating an exacerbation of depression-like symptoms. They also ate less than the wild-type mice.
Avoid the alpha male bullies. Or beat them up. The health costs of being a beta male are very real.
The extra fat we carry around our middle could be making us hungrier, so we eat more, which in turn leads to even more belly fat. Dr. Yaiping Yang and his colleagues at the Lawson Health Research Institute affiliated with The University of Western Ontario found abdominal fat tissue can reproduce a hormone that stimulates fat cell production. The researchers hope this discovery will change in the way we think about and treat abdominal obesity.
So then does liposuction done to the belly reduce the amount of future weight gain? After all, belly liposuction removes fat cells that secrete Neuropeptide Y.
Yang identified that the hormone Neuropeptide Y (NPY) is reproduced by abdominal fat tissue. Previously, it was believed to only be produced by the brain. Yang believes this novel finding may lead to new therapeutic targets for combating obesity. Their findings were reported in a recent issue of The FASEB Journal.
The traditional view is that one of the main reasons why overweight people eat more food is because their brains produce the hormone NPY in excessive amounts. NPY is the most potent appetite stimulating hormone known, sending signals to the individual that they are constantly hungry. However, Yang, a Professor in the Departments of Obstetrics & Gynaecology and Physiology & Pharmacology at the Schulich School of Medicine & Dentistry at The University of Western Ontario, has provided evidence that in obese rat models NPY is also produced locally by abdominal fat.
A fat cell cannot replicate itself. But the researchers found NPY increases fat cell number by stimulating the replication of fat cell precursor cells, which then change into fat cells.
Yang says “this may lead to a vicious cycle where NPY produced in the brain causes you to eat more and therefore gain more fat around your middle, and then that fat produces more NPY hormone which leads to even more fat cells.”
If you can't lose weight blame it on NPY.
University at Buffalo researchers now have shown in a randomized trial that by using a device that automatically restricted video-viewing time, parents reduced their children's video time by an average of 17.5 hours a week and lowered their body-mass index (BMI) significantly by the end of the 2-year study.
In contrast, children in the control group, whose video time was monitored, but not restricted, reduced their viewing time by only 5 hours per week.
By the end of the study, children with no time limits reduced their TV and computer use by an average of 5.2 hours per week, compared with an average reduction of 17.5 hours per week among children whose time was restricted. BMI as adjusted for age and sex and calorie intake also were lower among the group with restrictions on viewing than among the control group. No difference between the two groups was observed in the amount of physical activity.
University of Minnesota School of Public Health Project Eating Among Teens (EAT) researchers have found further evidence to support the importance of encouraging youth to eat breakfast regularly. Researchers examined the association between breakfast frequency and five-year body weight change in more than 2,200 adolescents, and the results indicate that daily breakfast eaters consumed a healthier diet and were more physically active than breakfast skippers during adolescence. Five years later, the daily breakfast eaters also tended to gain less weight and have lower body mass index levels – an indicator of obesity risk – compared with those who had skipped breakfast as adolescents.
Mark Pereira, Ph.D., corresponding author on the study, points out that this study extends the literature on the topic of breakfast habits and obesity risk because of the size and duration of the study. “The dose-response findings between breakfast frequency and obesity risk, even after taking into account physical activity and other dietary factors, suggests that eating breakfast may have important effects on overall diet and obesity risk, but experimental studies are needed to confirm these observations,” he added.
On the other hand, the teenagers who ate breakfast less frequently were the ones who were most likely to smoke, drink alcohol, and use dieting and other ways to control their weight.
If you feel inspired to start eating a grain-based breakfast then make sure you eat a whole grain.
Over the 12-week study period, all participants received the same dietary advice on weight loss, and encouragement to participate in moderate physical activity. Researchers also asked participants to consume five daily servings of fruits and vegetables, three servings of low-fat dairy products, and two servings of lean meat, fish or poultry.
The study's findings are published in the January 2008 issue of the American Journal of Clinical Nutrition.
Results from the study showed that waist circumference and body weight decreased significantly in both groups – between 8-11 pounds on average – but weight loss in the abdominal region was significantly greater in the whole grain group.
According to Katcher, the whole grain group experienced a 38 percent decrease in C-reactive protein levels in their blood. A high level of this inflammatory marker is thought to place patients at a higher risk for diabetes, hypertension and cardiovascular disease.
"Typically you would expect weight loss to be associated with a decrease in C-reactive protein, but the refined grain group showed no decrease in this marker of inflammation even though they lost weight," said Kris-Etherton.
The Penn State researcher suggests that the finding is because the consumption of refined grains has been linked to increased levels of the protein. So even though people in the refined grain group lost weight, the fact that they ate so many refined grains probably negated the beneficial effect of weight loss on C-reactive protein levels.
WASHINGTON — Want to lose weight" It might help to pour that diet soda down the drain. Researchers have laboratory evidence that the widespread use of no-calorie sweeteners may actually make it harder for people to control their intake and body weight. The findings appear in the February issue of Behavioral Neuroscience, which is published by the American Psychological Association (APA).
Psychologists at Purdue University’s Ingestive Behavior Research Center reported that relative to rats that ate yogurt sweetened with glucose (a simple sugar with 15 calories/teaspoon, the same as table sugar), rats given yogurt sweetened with zero-calorie saccharin later consumed more calories, gained more weight, put on more body fat, and didn’t make up for it by cutting back later, all at levels of statistical significance.
Appetite regulatory mechanisms in the body might get confused by the taste of sweetness followed by a lack of blood sugar rise and perhaps the mechanisms respond by upping appetite?
Artificial sweeteners in diet soda might be behind the results from a recent paper in Circulation which found diet soda as amount the dietary factors associated with a higher incidence metabolic syndrome (which includes higher weight, higher blood pressure, and higher blood sugar).
“This is interesting,” said Lyn M. Steffen, an associate professor of epidemiology at the University of Minnesota and a co-author of the paper, which was posted online in the journal Circulation on Jan. 22. “Why is it happening? Is it some kind of chemical in the diet soda, or something about the behavior of diet soda drinkers?”
Less sleep can increase a child’s risk of being overweight or obese, according to a study by researchers at the Johns Hopkins Bloomberg School of Public Health. Their analysis of epidemiological studies found that with each additional hour of sleep, the risk of a child being overweight or obese dropped by 9 percent. The results are published in the February 2008 edition Obesity, the journal of The Obesity Society.
“Our analysis of the data shows a clear association between sleep duration and the risk for overweight or obesity in children. The risk declined with more sleep,” said Youfa Wang, MD, PhD, senior author of the study and associate professor with the Bloomberg School’s Center for Human Nutrition. “Desirable sleep behavior may be an important low cost means for preventing childhood obesity and should be considered in future intervention studies. Our findings may also have important implications in societies where children do not have adequate sleep due to the pressure for academic excellence and where the prevalence of obesity is rising, such as in many East Asian countries.”
Sleep well and stay skinny. You'll also get sick less often.
Some people think women need to go on diets after giving birth in order to take off weight gained while pregnant. But the weight gained while pregnant might not be the biggest problem. Time taken to care for babies might cause a state of sleep deficiency that causes weight gain.
Mothers who reported sleeping five hours or less per day when their babies were six months old had a threefold higher risk for substantial weight retention (11 pounds or more) at their baby’s first birthday than moms who slept seven hours per day, according to a new study by Kaiser Permanente and Harvard Medical School / Harvard Pilgrim Health Care.
The study, published in the November issue of the American Journal of Epidemiology, is the first to look at the impact of sleep deprivation on postpartum weight retention. Previous studies have looked at the effect of early postpartum sleep deprivation on mothers’ cognitive and emotional health but never associated weight gain.
“We’ve known for some time that sleep deprivation is associated with weight gain and obesity in the general population, but this study shows that getting enough sleep – even just two hours more – may be as important as a healthy diet and exercise for new mothers to return to their pre-pregnancy weight,” said Erica P. Gunderson, PhD, an investigator at the Kaiser Permanente Division of Research in Oakland and the lead author of the study.
This result is consistent with other studies which find sleep deficiency promotes weight gain. The interesting twist on this study is that the stereotype of women losing their figures when they have kids might be explained by lack of sleep rather than by a permanent change in their metabolism caused by pregnancy.
What to do about it? Babies are oblivious to the needs of their mothers and some babies wake up a lot in the middle of the night.
The study also found that mothers who slept fewer hours at one year postpartum than they did at six months postpartum had twice the risk of substantial weight retention. Other studies have shown that persistent sleep deprivation causes hormonal changes that may stimulate appetite. Shorter sleep duration has not only been linked to obesity in women, but coronary artery disease and diabetes as well.
Mothers who learn to let their babies cry themselves to sleep have better nights and suffer less postnatal depression, research suggests.
A report in the British Medical Journal found that teaching mothers "controlled crying" techniques significantly reduced sleep problems.
The researchers found that women who were asked to suppress their thoughts about chocolate consumed 50 per cent more when offered it, compared with women who were told to express their feelings about chocolate.
James Erskine, a psychologist at the University of Hertfordshire, believes his findings may help people who are struggling to give up unhealthy foods or smoking.
By contrast, when men were told to express their feelings about chocolate they ate more of it.
Men who took part in the study were less prone to the effect, instead eating more when told to express their feelings about chocolate.
Hey, maybe the act of expressing their feelings about anything makes guys more anxious and this made them eat more chocolate. I'm only half joking about that.
WASHINGTON, Oct. 12, 2007 — For the first time, scientists have linked the all-too-human preference for a food — chocolate — to a specific, chemical signature that may be programmed into the metabolic system and is detectable by laboratory tests. The signature reads ‘chocolate lover’ in some people and indifference to the popular sweet in others, the researchers say.
The study by Swiss and British scientists breaks new ground in a rapidly emerging field that may eventually classify individuals on the basis of their metabolic type, or metabotype, which can ultimately be used to design healthier diets that are customized to an individual’s needs. The study is scheduled for publication in the Nov. 2 issue of American Chemical Society’s Journal of Proteome Research, a monthly publication.
Sunil Kochhar and colleagues studied 11 volunteers who classified themselves as ‘chocolate desiring’ and 11 volunteers who were ‘chocolate indifferent.’ In a controlled clinical study, each subject — all men — ate chocolate or placebo over a five day period while their blood and urine samples were analyzed. The ‘chocolate lovers’ had a hallmark metabolic profile that involved low levels of LDL-cholesterol (so-called ‘bad’ cholesterol) and marginally elevated levels of albumin, a beneficial protein, the scientists say.
The chocolate lovers expressed this profile even when they ate no chocolate, the researchers note. The activity of the gut microbes in the chocolate lovers was also distinctively different from the other subjects, they add.
If people who dislike chocolate take cholesterol-lowering statins then will that increase their desire for chocolate? Or does the chain of cause and effect flow in some different direction?
Does this difference have a genetic cause? Just how many of our preferences and desires have genetic causes?
If we turned on a gene that increases longevity and causes cholesterol to get expelled would we crave more chocolate as a result? At least we'd live longer and therefore would gain more time to each chocolate.
The study focused on a gene called SIRT1, which the researchers found prevents cholesterol buildup by activating a cellular pathway that expels cholesterol from the body via HDL (high density lipoprotein or “good cholesterol”).
“SIRT1 is an important mediator of cholesterol efflux, and as such it's predicted to play a role in the development of age-associated diseases where cholesterol is a contributing factor,” said Leonard Guarente, MIT professor of biology and senior author of a paper on the work to be published in the Oct. 12 issue of Molecular Cell.
Drugs that enhance the effects of SIRT1 could lower the risk of cholesterol-related diseases, Guarente said. Potential drugs could be based on polyphenols, which are found in red wine and have been shown to enhance SIRT1. However, the quantities naturally found in red wine are not large enough to have a significant impact on cholesterol levels.
In earlier studies, Guarente has shown that high levels of SIRT1 can be achieved with extreme calorie restriction, but that is unappealing for most people.
Would taking resveratrol increase one's desire for chocolate?
But there is a downside to tuning your metabolism to crave chocolate. Chocolate lovers can be bribed with chocolate.
"Student evaluations of a professor have major influence on what happens to the professor's career - whether a university or college chooses to retain him, give him tenure and even teaching assignments," Youmans said. "We began wondering if outside influences could affect how students rated a professor. People pride themselves in being fair and objective when they are asked to give an assessment of someone else's performance, such as evaluating a professor. But what if they really aren't being objective? What if something else could influence their judgments?"
To test their theory, Youmans visited undergraduate classes with laboratory sections, study sections led by a teaching assistant that drew students from a larger lecture into two smaller groups. In one group, Youmans passed out the evaluations and collected them when the students were finished. In the second group, when it was time for the students to assess their professor's performance, Youmans repeated what was done in the first class, except he offered the students chocolate, saying it was leftover from a prior event, while passing out the evaluations.
Youmans and Jee repeated the experiment in three different classes, and each time the result was the same: The groups that received the offer of chocolate gave their professors higher ratings than the groups that were not offered candy, even though students from either group were rating a class and instructor that they had experienced together.
"I should point out that not everyone in the classes offered chocolate took the candy. Also, we made it clear in all the classes that we were not affiliated with the professor, just 'strangers' asked to pass out and retrieve the evaluations," Youmans said. "But we found that the good feelings brought on by the offer of chocolate from a complete stranger, even in those students who didn't accept the candy, affected the professors' evaluations in a positive way."
So if you need someone to maintain their objectivity be aware of the danger chocolate poses to the human capacity to render objective judgments.
In mouse studies, Valerie Compan from the University of Montpellier, and her colleagues, found that by directly stimulating so-called 5HT-4 receptors in the nucleus accumbens, an area of the brain associated with feelings of reward, they could mimic the effects of anorexia - reducing the animals' desire to eat.
This reduction in appetite is also a well-recognised side effect of ecstasy or MDMA. When the researchers injected MDMA into mice genetically engineered to lack 5HT-4 receptors, it did not cause the reduction in appetite seen in normal mice - suggesting ecstasy's appetite-suppressing effect is mediated by the same receptors.
This discovery could help lead to a treatment for anorexia and also for obesity.
Compan says that ecstasy and anorexia may have more in common than we think. Her study suggests that starving yourself can be addictive, and is further evidence that anorexia may be related to neurological defects.
The findings may also highlight targets for drug treatment. "Our studies over seven years open the possibility that the 5-HT4 receptor would represent an important therapeutic target to treat patients suffering from these disorders," Compan says.
Fat people and anorexics are living testaments to the limits on human free will. Chemicals and receptors in our brains create desires in our minds that are at war with our conscious mind's preferences. Biotechnology is going to strengthen the power of the conscious mind to impose its will in the rest of the brain. Neurological science and neurotechnology are weapons in the war that the conscious mind is waging with other parts of the brain. But in some cases I'm thinking the other parts of the brain are winning by making the conscious mind figure out ways to give the rest of the mind what it wants (e.g. more sex with the help of Levitra, Cialis, and Viagra).
“From worms to mammals, this gene controls fat formation,” said Dr. Jonathan Graff, associate professor of developmental biology and internal medicine at UT Southwestern and senior author of a study appearing in the Sept. 5 issue of Cell Metabolism. “It could explain why so many people struggle to lose weight and suggests an entirely new direction for developing medical treatments that address the current epidemic of diabetes and obesity.
In the current study, the UT Southwestern researchers examined how adipose works by analyzing fruit flies, tiny worms called C. elegans, cultured cells, and genetically engineered mice, as well as by exploiting sophisticated molecular techniques. Using several methods, they manipulated adipose in the various animals, turning the gene on and off at different stages in the animals’ lives and in various parts of their bodies.
It was discovered that the gene, which is also present in humans, is likely to be a high-level master switch that tells the body whether to accumulate or burn fat.
In the mice, the researchers found that increasing adipose activity improved the animals’ health in many ways. Mice with experimentally increased adipose activity ate as much or more than normal mice; however, they were leaner, had diabetes-resistant fat cells, and were better able to control insulin and blood-sugar metabolism.
In contrast, animals with reduced adipose activity were fatter, less healthy and had diabetes.
Scientists might be able to find a drug that turns up the expression of adipose. Such a drug might cause weight loss.
To explore Adp’s function even further, Graff and his colleagues produced a strain of mutant flies like those that Doane had found years earlier. They found that the mutant flies were indeed fat and also had trouble getting around. Flies with only one copy of the Adp mutation fell somewhere in between the fat and normal flies, evidence that the gene’s effects are “dose dependent,” they reported.
Treatments that increased Adp in the insects’ fat tissue led them to lose weight, evidence that the gene operates within fat cells themselves. In mice that expressed the gene in fat-storing tissues, the same patterns emerged.
“We made mice that expressed Adp in fat-storing tissues, and lo and behold, what happened"” Graff said. “They were skinny—weighed less with markedly less fat—and their fat cells were smaller.” Smaller fat cells usually translate into better metabolic function, he said, including better blood sugar control.
Imagine the selective use of gene therapy to turn up the adipose gene in some tissue and turn down adipose in other parts of the body. It could be used to sculpt desired body shapes.
If you think you can trust your intuition you probably are making a mistake. Our intuitive judgments about food cause us to eat too much. We let our guards down in what we perceive as safer territory. People who eat at supposedly healthier restaurants consume more calories than those prudent people who wisely choose to eat at places with unhealthy food.
An important new study from the Journal of Consumer Research explains the “American obesity paradox”: the parallel rise in obesity rates and the popularity of healthier food. In a series of four studies, the researchers reveal that we over-generalize “healthy” claims. In fact, consumers chose beverages, side dishes, and desserts containing up to 131% more calories when the main dish was positioned as “healthy”.
“In our black and white view, most food is good or not good,” explain Pierre Chandon (INSEAD, France) and Brian Wansink (Cornell University). “When we see a fast-food restaurant like Subway advertising its low-calorie sandwiches, we think, ‘It’s OK: I can eat a sandwich there and then have a high-calorie dessert,’ when, in fact, some Subway sandwiches contain more calories than a Big Mac.”
In one study, Chandon and Wansink had consumers guess how many calories are in sandwiches from two restaurants. They estimated that sandwiches contain 35% fewer calories when they come from restaurants claiming to be healthy than when they are from restaurants not making this claim.
The result of this calorie underestimation: Consumers then chose beverages, side dishes, and desserts containing up to 131% more calories when the main course was positioned as “healthy” compared to when it was not—even though, in the study, the “healthy” main course already contained 50% more calories than the “unhealthy” one.
Do you need to lose weight? I'm sorry, you are going to have to shift your tastes toward thoroughly unhealthy restaurants so that you don't delude yourself about how many calories you are consuming. Eat unhealthy to be healthy.
A man of science might argue there must be a more rational option. The more rational option (know exactly how many calories are in what you are ordering) requires better information availability. Therein lies the problem. Marketers don't want to give you reasons to order fewer items on the menu. But if we had an automated way to know as we order how many calories we've racked up so far then we could pick and choose to lower calorie counts.
Here's yet another reason why people should stay home from work when they are sick. That wheezing and coughing guy over in the next cubicle might make you fat.
BOSTON, Aug. 20, 2007 — Scientists today reported new evidence that infection with a common virus may be a contributing factor to the obesity epidemic sweeping through the United States and other countries. In laboratory experiments they showed that infection with human adenovirus-36 (Ad-36), long recognized as a cause of respiratory and eye infections in humans, transforms adult stem cells obtained from fat tissue into fat cells. Stem cells not exposed to the virus, in contrast, were unchanged.
Vaccination against obesity. What a concept.
In addition, the study reported identification of a specific gene in the virus that appears to be involved in this obesity-promoting effect. The findings, which could lead to a vaccine or antiviral medication to help fight viral obesity in the future, were presented at the 234th national meeting of the American Chemical Society.
“We’re not saying that a virus is the only cause of obesity, but this study provides stronger evidence that some obesity cases may involve viral infections,” says study presenter Magdalena Pasarica, M.D., Ph.D., of the Pennington Biomedical Research Center, a campus of the Louisiana State University system.
Virus infection by itself is not sufficient to cause obesity.
“Not all infected people will develop obesity,” she notes. “We would ultimately like to identify the underlying factors that predispose some obese people to develop this virus and eventually find a way to treat it.”
Pasarica was part of the original research group which demonstrated that the Ad-36 virus was capable of causing animals infected with the virus to accumulate fat. Led by Nikhil Dhurandhar, Ph.D., now an associate professor at Pennington Biomedical Research Center, the group also conducted a noted epidemiologic study — the first to associate a virus with human obesity — showing 30 percent of obese people were infected with the Ad-36 virus in comparison to 11 percent of lean individuals. But evidence that the virus could actually cause fat levels to increase in human cells was lacking until now, Pasarica says.
This is more evidence for the argument of Paul Ewald and Greg Cochran that infections cause many more diseases than those historically thought to have infectious causes.
12 people in the whole world are known to lack the appetite regulation hormone leptin. 2 leptin deficient teens were found to rate even broccoli as very tasty.
Without leptin, the two teens wanted to eat non-stop. The boy weighed 103 kilograms by age 14 and the girl weighed 128 kilograms at 19 years old. As part of the study, the researchers asked them to rate how much they liked various foods, ranging from chocolate cake to broccoli, and discovered that they rated bland foods unusually highly.
These teens had unusual activation patterns in an area of the brain called the nucleus accumbens. Leptin therapy caused their appetites to become more normal. They also lost their appetite for broccoli.
Farooqi then began treating the two leptin-deficient teens with the hormone and tested their brain response to various foods one week later. After receiving leptin therapy, the nucleus accumbens of the subjects only became activated by foods when they had not eaten for several hours.
If you can't keep your weight down then blame it on your genes.
Studies suggest that genetics accounts for 40 to 70 percent of adult body weight, but researchers don't know all the culprits. Four years ago, Farooqi's group discovered that a separate mutation in the gene for melanocortin-4 receptor shows up in 1 percent of obese people and 5 to 6 percent of severely obese children.
Offspring genetic engineering will eventually make obesity very rare. Even before then better appetite control drugs will greatly reduce problems with excess weight. This study suggests that a leptin mimic drug might reduce appetite and make weight control much easier.
Using over 12,000 people studied over 32 years as part of the Framingham Heart Study Harvard and UCSD researchers find that people are more likely to become obese if people they are close to become obese.
Are your friends making you fat? Or keeping you slender? According to new research from Harvard and the University of California, San Diego, the short answer on both counts is “yes.”
Appearing in the July 26 issue of the New England Journal of Medicine, a study coauthored by Nicholas Christakis of Harvard Medical School and James Fowler of UC San Diego suggests that obesity is “socially contagious,” spreading from person to person in a social network.
The study – the first to examine this phenomenon – finds that if one person becomes obese, those closely connected to them have a greater chance of becoming obese themselves. Surprisingly, the greatest effect is seen not among people sharing the same genes or the same household but among friends.
If a person you consider a friend becomes obese, the researchers found, your own chances of becoming obese go up 57 percent. Among mutual friends, the effect is even stronger, with chances increasing 171 percent.
Christakis and Fowler also looked at the influence of siblings, spouses and neighbors. Among siblings, if one becomes obese, the likelihood for the other to become obese increases 40 percent; among spouses, 37 percent. There was no effect among neighbors, unless they were also friends.
“What we see here is that one person’s obesity can influence numerous others to whom he or she is connected both directly and indirectly,” says Nicholas Christakis, MD, PhD, a professor in Harvard Medical School’s Department of Health Care Policy. “In other words, it’s not that obese or non-obese people simply find other similar people to hang out with. Rather, there is a direct, causal relationship.”
Over the last 25 years, the incidence of obesity among U.S. adults has more than doubled, shooting from 15 to 32 percent. In addition, roughly 66 percent of U.S. adults are considered overweight.
In a way this makes sense. You do not feel as strong a need to maintain some form of appearance if the people around you let go.
The guys are less likely to follow their fat friends into fatness than the gals are.
Gender played an important role in how these statistics broke down. In same-sex friendships, individuals experienced a 71 percent increased risk if a friend of theirs became obese. This pattern was also observed in siblings. Here, if a man’s brother became obese, his chances of becoming obese increased by 44 percent. Among sisters, the risk was 67 percent. Friends and siblings of opposite genders showed no increased risk. While the researchers note that correlations among siblings provide evidence for a biological, and possibly even a genetic, component to obesity, patterns seen among friends indicate that there’s more than biology at work.
So if you are going to have fat friends make sure they are of opposite sex.
What to do with this information if it is true? Maybe virtual reality will help. See all your friends as skinny in virtual reality and you'll become more likely to keep off the pounds. Any other ideas?
Do people who are obsessed with skinny celebrities stay skinnier than those who do not suffer such obessions?
A Cochrane Review meta-analysis of high and low glycemic index diets found that weight loss is greater and easier on low glycemic index diets.
Put aside the white bread and pick up an apple. A diet of foods less likely to spike blood sugar levels helps dieters lose more weight, according to a new systematic review from Australia.
“Losing weight is very difficult and many people are unable to sustain a weight-loss diet. The low glycemic index diet is satisfying and has proven benefits,” said review co-author Elizabeth Elliott, Ph.D., professor at the University of Sydney, The Children’s Hospital at Westmead.
It is disappointing that they could find only 6 suitable trials with a total of 202 adults.
Researchers evaluated randomized controlled trials that compared weight loss in people eating foods low on the glycemic index to weight loss in people on higher GI diets or other types of weight loss plans.
Six trials, involving 202 adults from Australia, France, South Africa, Denmark and the United States were included in the review. The diets lasted from five weeks to six months.
While the average low glycemic index dieter lost 2.2 pounds more the weight loss was even greater for obese dieters.
The review found that dieters focused on eating low GI foods dropped significantly more weight — about 2.2 pounds more — than participants on other diets. Low GI dieters also experienced greater decreases in body fat measurements and body mass index.
None of the studies reported adverse effects associated with consuming a low glycemic index diet.
“Compared to other diets, the low GI diet is more satisfying — people are less inclined to feel hungry. One advantage of this type of diet is that it is more likely to be maintained than other strict diets on which people feel hungry,” Elliott said.
Low glycemic diets appear to be effective even in obese people who need to lose considerable amounts of weight, the authors said.
In the two studies that evaluated only obese participants, low GI dieters lost about 9.2 pounds, compared with about 2.2 pounds shed by other dieters.
These results are not surprising. The higher blood sugar spikes after a meal the more insulin that pancreatic cells will release into the blood to bring it down. The insulin will make the blood sugar go down and all the food will get absorbed pretty quickly. Then you'll feel the need for more food.
High blood sugar spikes cause bad blood lipid profiles. So again it is not surprising that the lower glycemic index diets yield better blood cholesterol levels.
In the three studies that measured cardiovascular risk factors, people eating low GI foods experienced greater improvements in total blood cholesterol and low-density lipoprotein (LDL) — sometimes called “bad” cholesterol. High levels of total cholesterol and LDL cholesterol increase the risks for heart disease.
A professor at John Hopkins' public health school notes the paucity of good research on the weight effects of low glycemic index diets.
After reviewing the findings, Lawrence Cheskin, M.D. said, “There’s surprisingly little in the way of studies to draw any hard and fast conclusions.” Cheskin is director of the Johns Hopkins Weight Management Center and associate professor at Johns Hopkins Bloomberg School of Public Health in Baltimore. He was not involved with the review.
Most vegetables are very low glycemic index foods. But most people do not want to eat large quantities of vegetables every day.
Low glycemic index diets can be effective for weight management, Cheskin said, but the success of low glycemic diets lies with an individual’s willingness to comply with its nutritional principles.
“There aren’t many people who need to lose weight who are willing to eat lots of vegetables and whole grains. If they did, they wouldn’t have a weight problem in the first place,” Cheskin said.
A lot of people want to know what constitutes the ideal diet. The problem is that they've heard many times about the benefits of vegetables and filtered out that information as basically an unacceptable answer. They don't want to hear that the ideal diet involves eating 5 or 10 servings of vegetables each day. There aren't a few super high nutrient yummy foods that can substitute for low glycemic index vegetables. You have to eat more veggies.
Washington, D.C. − In what they call a “stunning research advance,” investigators at Georgetown University Medical Center have been able to use simple, non-toxic chemical injections to add and remove fat in targeted areas on the bodies of laboratory animals. They say the discovery, published online in Nature Medicine on July 1, could revolutionize human cosmetic and reconstructive plastic surgery and treatment of diseases associated with human obesity.
While the ability to lose fat has obvious value for everyone fighting a bulging wasteline the ability to gain fat in specific locations has cosmetic value for women especially.
Investigators say these findings may also, over the long-term, lead to better control of metabolic syndrome, which is a collection of risk factors that increase a patient’s chances of developing heart disease, stroke, and diabetes. Sixty million Americans were estimated to be affected by metabolic syndrome in 2000, according to a study funded by the Centers for Disease Control in 2004.
In the paper, the Georgetown researchers describe a mechanism they found by which stress activates weight gain in mice, and they say this pathway − which they were able to manipulate − may explain why people who are chronically stressed gain more weight than they should based on the calories they consume.
This pathway involves two players − a neurotransmitter (neuropeptide Y, or NPY) and the receptor (neuropeptide Y2 receptor, or Y2R) it activates in two types of cells in the fat tissue: endothelial cells lining blood vessels and fat cells themselves. In order to add fat selectively to the mice they tested, researchers injected NPY into a specific area. The researchers found that both NPY and Y2R are activated during stress, leading to apple-shape obesity and metabolic syndrome. Both the weight gain and metabolic syndrome, however, were prevented by administration of Y2R blocker into the abdominal fat.
In the future most body sculpting will not require plastic surgery. Injections of hormones, gene therapies, and bioengineered cells will become the biosculpting equivalents of a sculpting artist's drills and saws. Cells will get ordered to divide or kill themselves or change the color of pigment they produce. Gene therapies will deliver genes to make enzymes that repair aged cells. The therapies will make you look younger and will also make your body parts operate at a more youthful level of performance.
Time for another chapter in the on-going saga on which diet - if any - works to lose and keep off weight. Foods that provide lots of weight but few calories probably make weight loss easier.
Eating smart, not eating less, may be the key to losing weight. A year-long clinical trial by Penn State researchers shows that diets focusing on foods that are low in calorie density can promote healthy weight loss while helping people to control hunger.
Foods that are high in water and low in fat – such as fruits, vegetables, soup, lean meat, and low-fat dairy products – are low in calorie density and provide few calories per bite.
“Eating a diet that is low in calorie density allows people to eat satisfying portions of food, and this may decrease feelings of hunger and deprivation while reducing calories” said Dr. Julia A. Ello-Martin, who conducted the study as part of her doctoral dissertation in the College of Health and Human Development at Penn State. Previously, little was known about the influence of diets low in calorie density on body weight.
Whole grains lower calorie density because they have more fiber. Ditto lots of vegetables. These foods which are already considered better for other reasons are also better for weight loss.
The researchers compared the effects of two diets – one reduced in fat, the other high in water-rich foods as well as reduced in fat – in 71 obese women aged 22 to 60. The participants were taught by dietitians to make appropriate food choices for a diet low in calorie density, but unlike most diets, they were not assigned daily limits for calories.
At the end of one year, women in both groups showed significant weight loss as well as a decrease in the calorie density of their diets. However, women who added water-rich foods to their diets lost more weight during the first six months of the study than those who only reduced fat in their diets – 19.6 pounds compared to 14.7 pounds. Weight loss was well maintained by subjects in both groups during the second six months of the study.
I am guessing fiber will work as well or better than water as a substance to increase the weight of what you eat. The water-rich food eaters ate 25% more food by weight.
Records kept by the women showed that those who included more water-rich foods ate 25 percent more food by weight and felt less hungry than those who followed the reduced-fat diet. “By eating more fruits and vegetables they were able to eat more food, and this probably helped them to stick to their diet and lose more weight,” said Ello-Martin.
Yet another reason to eat more fruits and vegetables in place of other foods.
Scientists have identified the most clear genetic link yet to obesity in the general population as part of a major study of diseases funded by the Wellcome Trust, the UK's largest medical research charity. People with two copies of a particular gene variant have a 70 per cent higher risk of being obese than those with no copies.
We can probably expect discovery of more genetic variations that contribute to obesity. They all serve as clues for how the brain and body regulate weight. All these clues will lead to the development of drugs and other treatments that make obesity rare in developed countries. 20 years from now I expect obesity to be rare.
A variation of the gene FTO makes a big weight difference.
Scientists from the Peninsula Medical School, Exeter, and the University of Oxford first identified a genetic link to obesity through a genome-wide study of 2000 people with type 2 diabetes and 3000 controls. This study was part of the Wellcome Trust Case Control Consortium, one of the biggest projects ever undertaken to identify the genetic variations that may predispose people to or protect them from major diseases. Through this genome-wide study, the researchers identified a strong association between an increase in BMI and a variation, or 'allele', of the gene FTO. Their findings are published online today in the journal 'Science'.
The researchers then tested a further 37 000 samples for this gene from Bristol, Dundee and Exeter as well as a number of other regions in the UK and Finland.
Carrying 2 copies of the FTO allele brings with it about 3 kg or 6.6 lb more weight.
The study found that people carrying one copy of the FTO allele have a 30 per cent increased risk of being obese compared to a person with no copies. However, a person carrying two copies of the allele has a 70 per cent increased risk of being obese, being on average 3 kg heavier than a similar person with no copies. Among white Europeans, approximately one in six people carries both copies of the allele.
The existence of genetic variations that cause weight gain is not surprising. Calorie malnutrition was probably the biggest cause of death for most of human history. So genetic variations that cause weight gain during good times would have conferred survival advantages. But why don't all people have the same strongest tendency to weight gain? To put it another way: what diadvantages of this FTO allele prevented it from becoming the only version of the FTO gene in humans?
A continued decline in the cost of DNA testing will accelerate the rate of discovery of important genetic variations. In the next decade we are going to find out in enormous detail most of the genetic variations that control many aspects of who we are.
Teens who are most physically active and consume the most calories are the leanest, researchers say.
“The take-home message would be to encourage your child to do as much vigorous physical activity as possible, including at least one hour of moderate to vigorous physical activity on a daily basis,” says Dr. Paule Barbeau, exercise physiologist at the Medical College of Georgia and corresponding author on the paper in the April issue of The International Journal of Obesity. “This allows your child to eat more calories, which encourages more healthy eating habits while remaining in energy balance.”
The kids who ate the least were the fattest:
Also interestingly, some teens who ate the least – they also moved the least and tended to be female – had the highest percent body fat. “If you think about teenagers trying to restrict their energy intake, they usually are not going to be doing a lot of physical activity to stay at that energy balance because they will be tired,” Ms. Stallmann-Jorgensen says. “We really expected the energy intake to be lower in kids who were leaner but when we started thinking about it we realized the leaner kids were at a different energy balance than the others,” Dr. Barbeau notes.
We need easier ways to mix exercise into our work schedules. I will repeat what I most want to see: Businesses should add exercise bicycles and stair stepper machines to meeting rooms. Then people called into status meetings, design meetings, and training classes could get exercise while doing meetings.
Boston — Research published in the Journal of Molecular Medicine examines how calories from fat, carbohydrate, and protein might interact with genes to affect body mass index (BMI), or body weight-for-height, and risk of obesity among adults in the Framingham Heart Study. Jose Ordovas, PhD, director of the Nutrition and Genomics Laboratory at the Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University, and colleagues analyzed several common gene variants known as single nucleotide polymorphisms (SNPs) of the apolipoprotein A5 gene (APOA5), which produces a protein (APOA5) involved in the metabolism of fats in the body. For 13 percent of people in the study with a specific SNP (-1131T>C), dietary fat intake was not significantly associated with BMI and risk of obesity.
Genetic testing will eventually allow us each to choose an optimal diet for our own genetic profiles. This report illustrates how nutritional genomics will enable us to customize our diets so that we each eat the diet that best works for our personal genetic profile.
For the people who carry this genetic variation the consumption of monounsaturated fats actually appears to keep weight off.
Ordovas determined that the interaction between the specific SNP (-1131T>C) and dietary fat was strongest for monounsaturated fatty acids (MUFAs), found in foods such as olive oil and canola oil. People with the specific SNP who consumed 11 percent or more of total calories as MUFAs had a lower likelihood of obesity. “Basically, it appeared that the interaction of the specific SNP with MUFAs was the reason that fat intake did not affect BMI for this group,” says Ordovas. “This interaction between APOA5 and dietary MUFA intake may explain why the Mediterranean diet, which is rich in MUFAs, is not generally associated with an increase in body weight. However, more studies are needed to confirm this.
Yes, if you have this genetic variation you might need to pour more olive oil on your food in order to stay skinny! Science sure can be fun.
Researchers at the Oregon National Primate Research Center at the Oregon Health & Science University have found that in mice on high fat diets their brain region called the arcuate nucleus changes to make the brain insensitive to leptin. Leptin is secreted by fat cells and normally signals the brain to have a lower appetite for food.
The research was conducted in mice and involved two separate groups that were fed high-fat and low-fat diets. Over time, the high-fat diet group developed symptoms of diabetes and obesity, as is often the case in humans. The low-fat diet group did not develop these health problems.
"This research demonstrates how a portion of the hypothalamus of the brain, called the arcuate nucleus, is negatively impacted by an overabundance of leptin," explained Michael Cowley, Ph.D., an associate scientist in the Division of Neuroscience at ONPRC. "By developing a special test of neuronal function, we were able to witness the breakdown in this group of specialized cells. Eventually the cells behaved as if there was no leptin present, even though levels were 40-times higher than in normal animals. We were also able to witness the eventual repair of this important system which occurs as the mice lost weight when returned to a low fat diet."
More specifically, the scientists determined that leptin resistance prevented the arcuate nucleus from taking part in an important signaling function that regulates appetite and body weight. Meanwhile, other portions of the weight regulation system remained intact and in fact became more responsive, thereby suggesting that arcuate nucleus function is the point of breakdown during leptin deficiency.
Finally the research highlighted a key gene called SOCS-3 involved in leptin deficiency. By targeting the gene with therapeutics, scientists may be able to repair leptin deficiency, aiding in weight loss.
What I'd like to know: Does a high fat diet also shrink the arcuate nucleus in humans? Also, do all types of fats equally shrink the arcuate nucleus
If leptin resistance in the arcuate nucleus is the major cause of human obesity then it will become a major target for drug development. We now need to know the chain of events in the neurons that cause them to become insensitive to signals of excess weight in one's body.
Premenopausal women who were assigned to follow the Atkins diet for one year lost more weight when compared to women who were assigned to follow the Zone, Ornish and LEARN diets, according to a study in the March 7 issue of JAMA.
Overweight and obesity are well-documented problems in the United States. National dietary weight loss guidelines (a diet low in calories and fat, high in carbohydrates) have been challenged, particularly by supporters of low-carbohydrate diets. However, limited evidence has been available to effectively evaluate other diets, according to background information in the article.
Christopher D. Gardner, Ph.D., of Stanford University Medical School, Stanford, Calif., and colleagues examined the effects of four diets-3 popular and substantially different diets and 1 diet based on national guidelines-representing a spectrum of carbohydrate intake, on weight loss and related metabolic variables in overweight and obese premenopausal women. The diets were Atkins (very low in carbohydrate), Zone (low in carbohydrate), LEARN (Lifestyle, Exercise, Attitudes, Relationships, and Nutrition; low in fat, high in carbohydrate, based on national guidelines), and Ornish (high in carbohydrate). The study, which included 311 overweight/obese (body mass index, 27-40) nondiabetic, premenopausal women, was conducted from February 2003 to October 2005. Participants were randomly assigned to follow for 12 months the Atkins (n = 77), Zone (n = 79), LEARN (n = 79), or Ornish (n = 76) diets and received weekly instruction for 2 months, then an additional 10-month follow-up.
The high protein Atkins and low carbo Zone diets both beat the low fat and high carbo Ornish diet in weight loss. Note this does not tell us how long people will live on average under each diet.
The researchers found that weight loss was greater for women in the Atkins diet group compared with the other diet groups at one year. Average 12-month weight loss was 10.4 lbs for Atkins, 3.5 lbs. for Zone, 5.7 lbs. for LEARN, and 4.8 lbs. for Ornish. At 12 months, measurements for lipids and levels of insulin, glucose and blood pressure for the Atkins group were comparable with or more favorable than the other diet groups.
Dean Ornish's diet is modelled on Nathan Pritikin's low fat diet and the Ornish diet is 10% fat, 20% protein, and 70% carbohydrate. So the Ornish diet is a low fat diet. Therefore these results do not provide evidence that a low fat diet will reduce appetite and promote weight loss by making human brains more sensitive to leptin.
What I'd like to see: Compare diets based on what they do to blood levels of leptin, ghrelin, and other hormones the body makes to regulate weight and appetite. Does the Ornish diet make the brain more sensitive to leptin while also decreasing the amount of leptin in the blood? That might explain why the Atkins diet works better. Maybe the Atkins diet keeps leptin higher than does the Ornish diet.
Also, the Ornish diet's use of carbohydrate as the major calorie source is problematic in one respect: Different carbohydrates vary greatly in how rapidly they get broken down and absorbed. Lower glycemic index foods might work far better than higher glycemic index foods to promote weight loss.
Previously, Rui and his team have shown that mice that lack the gene for SH2B1 -- called knockout mice -- become obese, diabetic, and unable to stop eating. Their bodies lose the ability to sense the signals sent by leptin and insulin that tell the brain to slow down food intake and fat storage.
For the new paper, they looked at not only normal mice and mice that didn’t have the SH2B1 gene, but also at mice that made SH2B1 only in brain cells, either in normal or larger-than-normal amounts. They found that restoring SH2B1 just in the brain completely corrected the metabolic disorders that the knockout mice had developed, but also improved the brain cells’ ability to respond to leptin signals and produce further signals that regulate eating.
What’s more, the mice that were treated to make extra SH2B1 didn’t become obese or lose their ability to respond to leptin signals even after being fed a high-fat diet that caused those effects in other mice.
More SH2B1 means less obesity. So any drug or gene therapy that would increase SH2B1 will probably decrease hunger and cause weight loss.
“Obesity, whether in mice or humans, is the product of an altered balance between energy intake and energy use. The imbalance is linked to alterations in leptin and insulin signaling that lead to excess weight gain and Type 2 diabetes, respectively,” says Rui, an assistant professor of molecular and integrative physiology at U-M. “SH2B1 appears to play a key regulatory role in this system, through its direct influence on the processing of leptin and insulin signals in cells of the brain’s hypothalamus.”
Do people who are naturally skinny have genetic variations that causes their brain cells to make more SH2B1?
SH2B1 binds to an enzyme called a kinase that places phosphate groups onto other proteins. The kinases typically activate and deactivate other proteins. So SH2B1 changes whether tyrosine kinase regulates other proteins.
The team and other researchers have found that SH2B1, which was previously called SH2-B, is a kind of jack-of-all-trades in the world of cell signaling. Able to shuttle between the area just beneath the cell membrane and the nucleus, it can bind to many different molecules and facilitate signaling.
Specifically, it can bind to a variety of molecules called tyrosine kinases, including ones that serve as receptors for insulin and growth factors that circulate in the brain and body. One of its most important binding partners is JAK2, which is activated every time a leptin molecule binds to a cell.
Since leptin is the body’s messenger boy to the brain for “stop eating, we’re full” messages, and JAK2 helps receive those messages as they arrive, SH2B1’s partnership with JAK2 is an important one. In a previous paper, Rui and his former mentor and current colleague Christin Carter-Su, Ph.D., showed that SH2B1 encourages the action and production of JAK2, unlike two other proteins that have been shown by other teams to reduce its activity. Carter-Su is a professor of molecular and integrative physiology and heads the biomedical research division of the Michigan Diabetes Research and Training Center.
These scientists and many others are gradually piecing together a very detailed model of how the feeling of hunger is regulated in the brain. With better understanding of a complex systems comes better ability to manipulate it. The identification and study of every piece eventually leads to candidate targets for drug development and ideas for how to alter the environment of cells to cause them to act differently.
During periods of fasting, brain cells responsible for stimulating the appetite make sure that you stay hungry. Now, a new study of mice reported in the January issue of the journal Cell Metabolism, published by Cell Press, reveals the complex series of molecular events that keep those neurons active.
The researchers revealed a link between active thyroid hormone in the brain and increases in an "uncoupling" protein (UCP2) that boosts the number of power-generating mitochondria in neurons that drive hunger. The increase in mitochondria, in turn, allows the brain's hunger center to remain active when periods of food scarcity result in a "negative energy balance," said Sabrina Diano of Yale University School of Medicine, who led the study.
Indeed, the researchers found, animals lacking either UCP2 or an enzyme that stimulates thyroid hormone's production ate less than normal after a period of food deprivation.
"This shows the key importance of UCP in the brain and its effect on neuronal activity," Diano said. "It's how neurons 'learn' that food is missing, and it keeps them ready to eat when food is introduced."
A drug that targets this mechanism would make fasting much easier.
Appetite-stimulating neurons get more mitochondria made in them. Those mitochondria produce more energy molecules that drive the appetite-stimulating neurons to send out more signals to produce a stronger desire to eat.
Now, the researchers found that support cells in the hypothalamus producing an enzyme that catalyzes active thyroid hormone production are side by side with appetite-stimulating neurons that express UCP2. In mice that were fasted for 24 hours, the arcuate nucleus showed an increase in the "DII" enzyme's activity and local thyroid production, in parallel with increased UCP2 activity.
This fasting-induced, T3-mediated UCP2 activation resulted in mitochondrial proliferation in the neurons, an event that was critical for the brain cells' increased excitability and consequent rebound feeding by the animals following food deprivation.
"Our results indicate that this mechanism is critical in sustaining an increased firing rate in these [hunger-stimulating] cells so that appetite remains elevated during fasting," Diano's group concluded. "Overall, our study provides strong evidence for an interplay between local T3 production and UCP2 during fasting and reveals a central thermogenic-like mechanism in the regulation of food intake."
Strong genetically driven mechanisms to make us eat are the product of selective pressures going back millions of years. Food shortages were a very common problem. Hence we have neural mechanisms that make us eat too much in an era of plenty. We need to develop biotechnologies that let us control our instincts for food.
Soaring levels of obesity might be linked to children sleeping fewer hours at night than they used to, claims Dr Shahrad Taheri of the University of Bristol.
Dr Taheri, reporting in the Archives of Disease in Childhood, blames the increasing availability of computers, mobile phones, TVs and other such gadgets on the diminishing nightly quota of sleep, and suggests they should be banned from children's bedrooms.
Dr Taheri cites the emerging body of research on the impact on the body of a fall in the nightly quota of sleep, which reflects circumstances in real life, rather than sustained sleep deprivation, which tends to be more extreme.
This research shows that shorter sleep duration disturbs normal metabolism, which may contribute to obesity, insulin resistance, diabetes, and cardiovascular disease. Even two to three nights of shortened sleep can have profound effects, the laboratory data suggest.
One study indicated that insufficient sleep at the age of 30 months was associated with obesity at the age of seven, suggesting that this could programme the part of the brain regulating appetite and energy expenditure, says Dr Taheri.
But it is also a problem for teenagers in whom the need for sleep increases during this critical developmental period, he says.
Another piece of research shows that levels of leptin, a hormone produced by fat tissue when energy stores are low, were more than 15% lower in those sleeping five hours compared with those clocking up eight.
Similarly, ghrelin, a hormone released by the stomach to signal hunger was almost 15% higher in those with a five hour sleep quota.
We did not evolve in the modern environments which we have created. Just because we can put gadgets in our environment and on the surface those gadgets seem harmless that does not mean we can handle the presence of those gadgets without cost to our good health and well being. We need to adapt our technological environments to the needs of our minds and bodies.
Some day we'll be able to use genetic engineering and gene therapies to adapt humanity to our technological environments. But that day is still a long way off. We need to better adapt our environments to our needs as we exist today until we gain the ability to reengineer our bodies and minds.
In their latest finding on the brain's role in controlling appetite and weight, researchers at the Albert Einstein College of Medicine have shown that reducing levels of fatty acids in the hypothalamus causes rats to overeat and become obese. Their results suggest that restoring fatty-acid levels in the brain may be a promising way to treat obesity. The study, published in the January 15th on-line edition of Nature Neuroscience, was led by Dr. Luciano Rossetti, director of the Diabetes Research Center at Einstein. (The paper will appear in print in the February issue.)
Consumption of fats causes a boost in malonyl CoA in the hypothalamus. Reduction in malonyl CoA boosts appetite.
The study focused on malonyl CoA, a molecule suspected of being one of the critical nutrients influencing hypothalamic regulation of eating behavior. Previous studies had shown that hypothalamic levels of malonyl CoA increase markedly after meals and are suppressed by fasting.
The Einstein researchers wanted to know whether sustained suppression of this nutrient within the hypothalamus could result in obesity. To find out, they piggybacked an enzyme known to degrade malonyl CoA onto an adeno-associated virus and injected the virus into the hypothalamus of rats. The injections caused a chronic decrease in malonyl CoA levels, which dramatically increased the rats' food intake and led to obesity that was maintained for at least four months.
"We showed in this study that disrupting malonyl-CoA levels in this region of the brain impairs the nutrient-sensing mechanism by which the hypothalamus modulates food intake to maintain normal weight," says Dr. Rossetti, who is also the Judy R. and Alfred A. Rosenberg Professor of Diabetes Research at Einstein. "Figuring out a way to re-adjust malonyl-CoA levels in the human hypothalamus could lead to innovative therapies not only to treat obesity but to help prevent diabetes and other consequences of being overweight."
If drugs can be found that either boost malonyl CoA levels in the hypothalamus such drugs might decrease appetite. Alternatively, malonyl CoA binds somewhere to cause the appetite suppression effect. Another option is to look for where it binds and develop drugs that bind at the same place. A malonyl CoA substitute migh also suppress appetite.
Another possibility: Would slow consumption of small amounts of a fat all day reduce total calories consumed? If so, would all fats work equally well for this purpose? Or do particular fats do a better job of suppressing appetite? If so, which fats best suppress appetite?
Gainesville, Fla. -- Nearly 6 percent of morbidly obese children and adults have a genetic defect that keeps them feeling like their stomach is running on empty, no matter how much they have eaten.
The press release refers to genetic defects. The term "defect" implies an error or mistake. But a type of mutation that occurs in 6% of the population (correction: oops, 6% of the morbidly obese - gotta read more carefully) surely occurs at too high a frequency to be a mistake. The ancestors of the carriers of these mutations gained selective advantage and left more surviving offspring due to the mutations that made them more hungry.
The problem humans face today is that in industrialized countries mutations which increase the desire for food are now more a burden than a benefit. But the mutations are only defects if you use modern conditions as a reference to come up with standards for how humans should function.
Once you cross the bridge of defining modern civilization as the standard by which to decide which genetic variations are defects you've crossed a much larger bridge than most people appreciate. Consider the fight-or-flight reflex where someone feels adrenaline flowing and feels the urge to either run or attack. Since this reflex gets triggered totally inappropriately in arguments in office building meetings (few will start beating up co-workers or running for their lives down aisles of cubicles) it is hard to see the fight-or-flight reflex as adaptive at this point. If anything, the stress from adrenaline rush probably accelerates your aging.
If the fight-or-flight response and other counter-productive responses we have in modern situations are defects because they are counter-productive in modern conditions then all humans are full of defects and humanity is in need of a genetic redesign. I happen to think that, yes, we are in need of a massive redesign to adapt us to the technological and urban environments which we live in and to make it easier for us to live longer. But that will not become the majority view until we develop a far more detailed understanding of many genetic variations and how they govern the way we function.
These University of Florida scientists identified 11 mutations that make a receptor involved in hunger regulation to behave in ways that they consider to be abnormal.
Mutations of the melanocortin-4 receptor, a gene found in brain cells that play a role in regulating hunger, are the most common cause of genetic obesity. Now University of Florida researchers have determined how some of these mutations cause the receptor to miss signals from molecules that tell the body when to eat and when to put down the fork, placing scientists one step closer to finding a way to correct these defects.
In a side-by-side comparison of 40 genetic mutations, UF medicinal chemists found that 11 caused the receptor to behave abnormally, according to findings recently published in the online edition of the journal Biochemistry.
The goal is to discover the molecular glitch that causes the receptor to malfunction so chemists can make drugs to treat it, said Carrie Haskell-Luevano, Ph.D., a UF associate professor of medicinal chemistry and the study's lead author. UF researchers have already found a molecule that seems to correct one of the mutations, keeping the hunger-signaling pathway running smoothly, Haskell-Luevano said.
The collection of melanocortin-4 receptor gene mutations for obesity has been building up for years. See these papers from 1999 and 2004 for examples of earlier work on obesity and the melanocortin-4 receptor.
The discovery of more genetic variations that influence some behavior or metabolic processs opens up targets for drug development and also makes it easy to study the causes of differences in behaviors and metabolic processes.
Dallas -- July 31, 2006 -- Giving up your regular late-night snack may be hard, and not just because it's a routine. The habit may genetically change an area of the brain to expect the food at that time, researchers at UT Southwestern Medical Center have discovered.
By training mice to eat at a time when they normally wouldn't, the researchers found that food turns on body-clock genes in a particular area of the brain. Even when the food stopped coming, the genes continued to activate at the expected mealtime.
"This might be an entrance to the whole mysterious arena of how metabolic conditions in an animal can synchronize themselves with a body clock," said Dr. Masashi Yanagisawa, professor of molecular genetics and senior author of the study.
Maybe when people get older their brains get programmed to be hungry at more times of the day?
Research by Warwick Medical School at the University of Warwick has found that sleep deprivation is associated with an almost a two-fold increased risk of being obese for both children and adults.
Early results of a study by Professor Francesco Cappuccio of the University of Warwick's Warwick Medical School were presented to the International AC21 Research Festival hosted this month by the University of Warwick.
The research reviewed current evidence in over 28,000 children and 15,000 adults. For both groups Professor Cappuccio found that shorter sleep duration is associated with almost a two-fold increased risk of being obese.
The research also suggests that those who sleep less have a greater increase in body mass index and waist circumference over time and a greater chance of becoming obese over time.
This result is consistent with other studies. See my previous posts Lack Of Sleep Linked To High Blood Pressure, Other Risks and Sleep A Lot To Avoid Burn-Out From Stress And To Stay Skinny.
In the new work, the researchers studied the influence of sleep on declarative memory in healthy, college-aged adults. The results demonstrated a robust effect: Compared to participants who did not sleep during the trials, those who slept between learning and testing were able to recall more of the original words they had learned earlier. The beneficial influence of sleep was particularly marked when participants were presented with the challenge of "interference"--competing word-pair information--just prior to testing. A follow-up group further demonstrated that this sleep benefit for memory persists over the subsequent waking day. This work clarifies and extends previous study of sleep and memory by demonstrating that sleep does not just passively and transiently protect memories; rather, sleep plays an active role in memory consolidation.
I wonder whether people could learn more if they napped a few times a day between learning exercises.
CINCINNATI--A cell-signaling pathway in the brain that is linked to the development of cancer and diabetes is also a key part of networks that regulate food intake, say University of Cincinnati (UC) researchers.
The finding might one day lead to new ways of helping obese people lose weight, either with new drugs or by carefully designing diets that can activate this pathway.
Scientists from UC's Genome Research Institute demonstrated that the signaling pathway mTOR--activated by nutrient and hormonal signals--plays a role in the brain's ability to sense how much energy the body has available.
As more biochemical pathways by which appetite gets regulated become identified and understood in greater detail they become obvious targets for appetite suppressing drug development.
This finding, the researchers say, suggests that very specific micronutrients may drive these pathways in the brain and could lead to a more scientific approach to diet design to help regulate body weight.
The study, led by Randy Seeley, PhD, professor in UC's psychiatry department, appears in the May 12, 2006 issue of the journal Science.
One caveat: These researchers used rats, not humans.
Another caveat: The method of leucine delivery was injection, not diet. They injected it into a specific area of the brain no less. So that's a big caveat. Will it produce the same effect when consumed?
The mTOR pathway is very sensitive to "branched-chain" amino acids, particularly leucine, Dr. Seeley explains. In laboratory studies, he and his team found that when they administered leucine directly to the hypothalamus, a brain region that controls a number of metabolic processes, animals ate less.
Other, similar amino acids did not give the same results.
This animal study, says Dr. Seeley, could eventually have implications for human obesity.
"Rather than basing our diets only on macronutrients like fat or carbohydrates, we might one day be designing diets based on micronutrients like amino acids," he says.
To see whether the mTOR pathway in the hypothalamus responds to amino acids, Seeley injected 1 microgram of leucine directly into the brains of rodents, near the hypothalamus. Over the next day, the rats that received the injection consumed 25 grams of food on average while the control rats consumed 30 g of food.
A reduction in calories consumed by a sixth per day would prevent weight gain in most people. It would also allow for a slow weight loss.
They saw an even larger reduction in calories consumed when leucine was delivered after a 24 hour fast. But to do 24 hour fasts would probably require a far more effective appetite suppressant. If we had such a powerful appetite suppressant we wouldn't need leucine.
You can buy L-Leucine as a powder or capsule. The powder form would be cheaper. I'm not encouraging anyone to try this. Also, if you do try it I would suggest you do so in moderation. Amino acids compete with each other for absorption in a few transport mechanisms that bring amino acids into cells. You don't want to starve your cells of other amino acids by saturating one of those transport mechanisms. Though I'm not sure that's a real problem.
New Haven, Conn. - Nearly half of the people responding to an online survey about obesity said they would give up a year of their life rather than be fat, according to a study by the Rudd Center for Food Policy and Obesity at Yale.
The 4,000 respondents in varying numbers between 15% and 30% also said they would rather walk away from their marriage, give up the possibility of having children, be depressed, or become alcoholic rather than be obese. Five percent and four percent, respectively, said they would rather lose a limb or be blind than be overweight.
"We were surprised by the sheer number of people who reported they would be willing to make major sacrifices to avoid being obese. It drives home the message that weight bias is powerful and pervasive," said Marlene Schwartz, associate director of the Rudd Center and lead author of the study in Obesity, which was issued this month.
15 percent said they would trim a decade off their lives for a thinner waistline.
Whatever company comes up with a really powerful yet safe appetite suppressant is going to make billions of dollars in profits. Mind you, such a treatment has to test as safe chiefly for the benefit of regulatory agencies. Many of the potential customers are willing to run bigger risks.
Do not judge anorexics harshly. Their genes make them do it.
CHAPEL HILL – A new study led by University of North Carolina at Chapel Hill researchers estimates that 56 percent of the liability for developing anorexia nervosa is determined by genetics.
In addition, the study found that the personality trait of "neuroticism" (a tendency to be anxious and depressed) earlier in life is a significant factor associated with development of the eating disorder later.
Anorexia nervosa is a psychiatric illness characterized by an individual’s refusal to maintain a minimally acceptable body weight, intense fear of weight gain and a distorted body image. It occurs primarily among females in adolescence and young adulthood and is associated with the highest mortality rate of any mental disorder.
People prone to depression and anxiety are more prone to anorexia nervosa. So would anti-depressants and/or anti-anxiety drugs reduce the incidence of anorexia?
This study is the first published in the medical literature to estimate how much liability for developing anorexia nervosa is due to genetics, and the first to find a statistically significant association between the prospective risk factor of neuroticism and later development of anorexia, said Dr. Cynthia M. Bulik, lead author of the study, published in the March issue of the Archives of General Psychiatry.
"What this study shows is that anorexia nervosa is moderately heritable and may be predicted by the presence of early neuroticism, which reflects proneness to depression and anxiety," Bulik said. "Fifty-six percent heritability – that’s a fairly large contribution of genes. The remaining liability is due to environmental factors."
Bulik is the William R. and Jeanne H. Jordan distinguished professor of eating disorders in UNC’s School of Medicine and director of the UNC Eating Disorders Program at UNC Hospitals. She also is a professor of nutrition, a department housed in the schools of public health and medicine, and holds the only endowed professorship in eating disorders nationwide.
The reason she and her co-authors reached these conclusions where previous studies could not, Bulik said, is that their study was based on data obtained from screening a very large sample of twins. Their sample, from the Swedish Twin Registry, consisted of 31,406 individuals born between 1935 and 1958. None of the previous studies had samples nearly as large, Bulik said.
Twin studies continue to produce a wealth of scientific information about the human heredity.
An estimated 0.5 to 3.7 percent of females suffer from anorexia nervosa in their lifetime.
The mortality rate among people with anorexia has been estimated at 0.56 percent per year, or approximately 5.6 percent per decade, which is about 12 times higher than the annual death rate due to all causes of death among females ages 15-24 in the general population.
ROCHESTER, Minn. — A long-term study of patients in Rochester, Minn., with the eating disorder anorexia nervosa found that their survival rates did not differ from the expected survival rates of others of the same age and sex.
The results, published in the March issue of Mayo Clinic Proceedings, add to the knowledge of anorexia nervosa and point to other areas that need greater study from researchers.
“Although our data suggest that overall mortality is not increased among community patients with anorexia nervosa in general, these findings should not lead to complacency in clinical practice because deaths do occur,” says L. Joseph Melton, III, M.D., Mayo Clinic epidemiologist and an author of the report.
One argument for the cause of the discrepancy is that other studies used anorexia nervosa sufferers who were sick enough to require hospitalization. Whereas a larger set of all anorexia nervosa sufferers as the Mayo Clinic used brings in people who have less severe cases.
Anorexia typically has numerous complications. At its most severe, it can be fatal. Anorexia has one of the higher deaths rates among all mental illnesses, hovering around 5 percent but perhaps even higher than that.
Perhaps some anorexia patients have such severe symptoms that they damage their bodies through malnutrition while other anorexia patients end up eating more like calorie restriction dieters and perhaps even gain some life expectancy as a result. Though that seems unlikely since the calorie restrictionists try hard to make sure they get enough vitamins, minerals and other essential nutrients aside from calories. Whereas I doubt the bulk of anorexia sufferers manage to do that.
SAN FRANCISCO – In the face of the growing obesity health challenge, "appetite suppressants are increasingly interesting because they work on the very simple premise of 'What you don't eat now, you won't need to lose later,'" Alexandra Einerhand, director, nutrition and toxicology-Europe at Lipid Nutrition notes.
Einerhand says that in a study, polyunsaturated fatty acids (PUFAs) derived from "Korean pine nuts, which have been part of our diet since before ancient Greek and Roman times, stimulated two well-known appetite suppressing peptide hormones at the same time that overweight women reported significantly less desire to eat only 30 minutes after ingestion," compared with an olive oil placebo.
In a paper being presented in an American Physiological Society session at Experimental Biology 2006, Einerhand reports that "in this randomized, double-blind cross-over trial, the greatest effect was observed after just 30 minutes, with the 18 women reporting a 29% reduction in "desire to eat" and a 36% drop in "prospective food intake" scores. Their subjective feelings of appetite were evaluated by visual analog scales, a validated scoring system.
The experiment found a parallel and significant increase in cholecystokinin (CCK) of 60% and glucagon-like peptide 1 (GLP1) of 25% that remained as long as four hours after ingestion. CCK and GLP1 are appetite suppressors, which "send signals of satiation to the brain diminishing the desire to eat and food intake usually significantly," she adds.
In my own sample of one eating a few Brazil nuts seems like it causes a reduction in my appetite lasting for hours. I've long suspected that some nuts have this effect. But until now I haven't come across any research that provided a mechanism to support my intuition about nuts and appetite. Anyone else find that some type of nuts reduces your appetite?
(Phoenix, AR) - Women who lift weights twice a week can prevent or at least slow down "middle-age spread" and weight gain, a University of Pennsylvania School of Medicine researcher reported today at the American Heart Association's 46th Annual Conference on Cardiovascular Disease Epidemiology and Prevention.
A study of 164 overweight and obese (body mass index of 25-35) women between 24 and 44 years of age, found that strength training with weights dramatically reduced the increase in abdominal fat in pre-menopausal participants compared to similar women who merely received advice about exercise.
"On average, women in the middle years of their lives gain one to two pounds a year and most of this is assumed to be fat," said lead author Kathryn H. Schmitz, PhD., Assistant Professor, Center for Clinical Epidemiology and Biostatistics. "This study shows that strength training can prevent increases in body fat percentage and attenuate increases in the fat depot - or 'belly fat' - most closely associated with heart disease. While an annual weight gain of one to two points doesn't sound like much, over 10 to 20 years, the gain is significant."
Women in the two-year weight-training program decreased their body fat percentage by 3.7 percent, while body fact percentage remained stable in the controls. The strength-training reduced intra-abdominal fat, which is more closely associated with heart disease and metabolic disturbances. More specifically, the women who did strength-training experienced only a 7 percent increase in intra-abdominal fat compared to a 21 percent increase in intra-abdominal fat among controls.
The study - dubbed The SHE study, for The Strong, Healthy, and Empowered - examined whether twice-weekly strength-training would prevent increases in intra-abdominal and totally body fat in women who were overweight or obese. The women initially were separated by baseline percentage body had booster session four times yearly with certified fitness professionals over two years. The control fat and age. The strength-training group participated in supervised strengthening classes for 16 weeks, and group received a brochure recommending 30 minutes to an hour of exercise most. days of the week. All of the women were asked not to change their diets in ways that might lead to weight changes while they were participating in the study.
The weight-training sessions took about an hour, and the women were encouraged to steadily increase the amount of weight they lifted. The weight training included exercises for all major muscle groups, including the chest, upper back, lower back, shoulders, arms, buttocks and thighs. The maximal amount of weight women could lift once - called a one-repetition maximum test - increased by an average of 7 percent in bench pressing and 13 percent in leg press exercises.
Researchers measured the participants' body composition with a dual energy X-ray absorptiometry (DEXA) scan and measurements of abdominal and total body fat by single slice CT scan at baseline, and again at one and two years.
Why does weight training have this effect? Does it act only by the increase in calories burned during the exercise? Or does the resulting increase in body muscle mass cause an on-going higher rate of calorie burn that is not offset by higher appetite? Or does the exercise release endorphins or other compounds that decrease appetite? Or some combination of the above?
To put it another way: Why doesn't appetite regulation by the brain prevent weight gain as people age? Was the weight gain selected for to prevent starvation in our ancestors? Or is it a side effect of reduced ability to regulate bodily functions due to brain aging or signalling systems aging elsewhere in the body?
Here is some news you can use to keep off excess pounds. Opaque rather than clear containers make a big difference in the amount of candy consumed from nearby containers.
When it comes to candy, it is out of sight, out of the mouth, a Cornell University researcher finds.
The study finds that women eat more than twice as many Hershey Kisses when they are in clear containers on their desks than when they are in opaque containers on their desks -- but fewer when they are six feet away.
"Interestingly, however, we found that participants consistently underestimated their intake of the candies on their desks yet overestimated how much they ate when the candies were farther away," said Brian Wansink, the John S. Dyson Professor of Marketing and of Applied Economics at Cornell.
The study -- one of the few experiments to quantify the "temptation factor" -- was presented at the Obesity Society meeting of the North American Association for the Study of Obesity in September in Vancouver, Canada. It is published online and will be published in an upcoming February issue of the International Journal of Obesity.
Wansink and his co-authors, James E. Painter and Yeon-Kyung Lee, assistant professor and visiting scholar, respectively, in food science at the University of Illinois-Champaign, gave 40 university female staff and faculty members 30 chocolate Kisses in either clear or opaque candy jars on their desks or six feet away. Each night, the researchers counted how many candies were eaten and refilled the jars.
"Not surprisingly, the participants ate fewer candies when the Kisses were in opaque rather than clear candy jars on their desks and even fewer when the opaque jars were six feet away from their desks," Wansink said. "The less visible and less convenient the candy, the less people thought about it and were tempted."
Specifically, participants ate an average of 7.7 Kisses each day when the chocolates were in clear containers on their desks; 4.6 when in opaque containers on the desk; 5.6 when in clear jars six feet away; and 3.1 when in opaque jars six feet away.
This cogs with my everyday experience at my work desk. If I put food in a cabinet and close the cabinet door I'm less likely to munch during the day.
I've also noticed I eat more dried cranberries than dried Montmorency cherries at similar sweetness levels. I like the Montmorency cherries better. But they are so rich in flavor compared to the cranberries that I eat them more slowly since each one provides more flavor experience than a similar quantity of cranberries. So maybe foods with more intense flavors (and by flavors I'm not referring to either sweetness or fattiness) could reduce food consumption.
University of Florida researchers have identified one possible reason for rising obesity rates, and it all starts with fructose, found in fruit, honey, table sugar and other sweeteners, and in many processed foods.
Fructose may trick you into thinking you are hungrier than you should be, say the scientists, whose studies in animals have revealed its role in a biochemical chain reaction that triggers weight gain and other features of metabolic syndrome - the main precursor to type 2 diabetes. In related research, they also prevented rats from packing on the pounds by interrupting the way their bodies processed this simple sugar, even when the animals continued to consume it.
The findings, reported in the December issue of Nature Clinical Practice Nephrology and in this month's online edition of the American Journal of Physiology-Renal Physiology, add to growing evidence implicating fructose in the obesity epidemic and could influence future dietary guidelines. UF researchers are now studying whether the same mechanism is involved in people.
"There may be more than just the common concept that the reason a person gets fat is because they eat too many calories and they don't do enough exercise," said Richard J. Johnson, M.D., the J. Robert Cade professor of nephrology and chief of nephrology, hypertension and transplantation at UF's College of Medicine. "And although genetic predispositions are obviously important, there's some major environmental force driving this process. Our data suggest certain foods and, in particular, fructose, may actually speed the process for a person to become obese."
Physical inactivity, increased caloric intake and consumption of high-fat foods undoubtedly account for part of the problem, Johnson said. But Americans are feasting on more fructose than ever. It's in soft drinks, jellies, pastries, ketchup and table sugar, among other foods, and is the key component in high fructose corn syrup, a sugar substitute introduced in the early 1970s.
Since then, fructose intake has soared more than 30 percent, and the number of people with metabolic syndrome has more than doubled worldwide, to more than 55 million in the United States alone, Johnson said. The condition, characterized by insulin resistance, obesity and elevated triglyceride levels in the blood, is linked to the development of type 2 diabetes and hypertension.
"If you feed fructose to animals they rapidly become obese, with all features of the metabolic syndrome, so there is this strong causal link," Johnson said, "And a high-fructose intake has been shown to induce certain features of the metabolic syndrome pretty rapidly in people."
An increase in uric acid is involved in creating the negative consequences from fructose consumption.
Now UF research implicates a rise in uric acid in the bloodstream that occurs after fructose is consumed, Johnson said. That temporary spike blocks the action of insulin, which typically regulates how body cells use and store sugar and other food nutrients for energy. If uric acid levels are frequently elevated, over time features of metabolic syndrome may develop, including high blood pressure, obesity and elevated blood cholesterol levels.
Researchers from UF and the Baylor College of Medicine studied rats fed a high-fructose diet for 10 weeks. Compared with rats fed a control diet, those on the high-fructose diet experienced a rise in uric acid in the bloodstream and developed insulin resistance.
Blocking of uric acid prevented the weight and blood sugar problems.
"When we blocked or lowered uric acid, we were able to largely prevent or reverse features of the metabolic syndrome," Johnson said. "We were able to significantly reduce weight gain, we were able to significantly reduce the rise in the triglycerides in the blood, the insulin resistance was less and the blood pressure fell."
UF researchers are now studying the uric acid pathway in cell cultures in the laboratory, in animals and in people, and are also eyeing it as a possible factor in the development of cardiovascular and kidney diseases because of its effects on blood vessel responses. They are conducting a National Institutes of Health-funded trial to determine if lowering uric acid in blacks with hypertension improves blood pressure control and are collaborating with scientists at Baylor to determine if lowering uric acid will reduce blood pressure in adolescents with hypertension.
"We cannot definitively state that fructose is driving the obesity epidemic," said Johnson. "But we can say that there is evidence supporting the possibility that it could have a contributory role - if not a major role. I think in the next few years we'll have a better feel for whether or not these pathways that can be shown in animals may be relevant to the human condition."
Findings to date suggest certain sugar carbohydrates are actually better than others, he added, because some do not activate the uric acid pathway.
I love it when a scientific discovery suggests obvious practical ways to make use of the new information.
"It may well be we don't need to cut out carbohydrates but just certain types of carbohydrates," Johnson said. "So this may be an alternative to the Atkins type of approach, which cuts out carbohydrates indiscriminately."
As scientists learn more about the pathway, Johnson said, and as studies are completed in people, the findings may influence how to make wise choices about the foods we eat.
"With the caveat that people are different from rodents in many ways, the link between urate levels, blood pressure elevation and insulin resistance demonstrated in rats fed fructose is extremely provocative," said Brian F. Mandell, M.D., Ph.D., vice chairman of medicine for education and a professor of medicine at the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University. "Whether the fructose supplementation to the diet in the United States is partially responsible for the 'epidemic' of obesity remains to be proven - but this is an association which can be tested, and the work of Dr. Johnson and his collaborators makes the evaluation of the fructose-metabolic link in people an academic and public health imperative."
So how can one keep uric acid levels down? Anyone know?
Also see my previous post "Fructose Consumption May Lead To Obesity".
A team at New York's Columbia University has shown the key is falling levels of the hormone leptin, which controls appetite.
They found that giving people who had recently lost weight injections of the hormone helped them to avoid putting the pounds straight back on.The study features in the Journal of Clinical Investigation.
Leptin is a peptide (i.e. it is a sequence of amino acids and peptides are what make up protein). Peptides taken orally get digested. So to use it you'd have to inject it with a syringe.
To test their theory, the researchers gave doses of leptin to lean and obese volunteers who had recently lost weight.
They found that most of the metabolic and hormonal changes which mean people cannot keep the weight from creeping back on were reversed once leptin levels were restored to pre-weight loss levels.
Leptin is known to play a role in controlling appetite, but as yet the exact way that it works is unclear.
Injections of leptin have been used to help morbidly obese people with a deficiency of the hormone to lose weight, but a similar approach has no effect on obese people with normal leptin levels.
So go on a diet. Lose weight. Then start taking leptin injections to keep the weight off.
A new study by researchers at UT Southwestern Medical Center suggests that when fat cells increase in size – as they do during the development of obesity – the cells progressively lose receptors for the hormone leptin, a powerful stimulus for fat burning.
Leptin, a hormone produced by the body’s fat cells and involved in the regulation of body weight, was first discovered in 1994. It was thought leptin itself would be a key to curing obesity in humans, but the hypothesis did not readily translate into weight loss in obese people. Using mouse models, UT Southwestern researchers have now shown that if enough receptors are present on the fat cells, it is impossible for the cells to store fat and obesity would be blocked.
The new findings, appearing in an upcoming issue of the Proceedings of the National Academy of Sciences and currently available online, bring researchers a step closer to understanding obesity in humans, said Dr. Roger Unger, director of the Touchstone Diabetes Research Center at UT Southwestern and senior author of the study.
“We now think that people with naturally high levels of leptin receptors may not gain weight as rapidly over time as people who have low levels of leptin receptors,” said Dr. Unger. “It could explain why some people can eat more and do not gain weight.”
To test this hypothesis, the UT Southwestern researchers used genetically modified rats in which the leptin receptor remained present in large quantities even during marked overfeeding. In normal mice, the high-fat diet caused massive obesity with enlargement of fat cells to almost three times their normal size. In mice with the forced overexpression of the leptin receptor on their fat cells no obesity occurred, even though they too were fed high-fat, highly caloric diets.
“The fat-storing function of the fat cells requires the disappearance of the leptin receptor,” Dr. Unger said. “This is done in order to block the action of the leptin fat cells produce.”
Examination of the ghrelin gene showed Hsueh, Zhang and their colleagues that it in fact codes for a second peptide hormone — the hormone they named obestatin.
“Obestatin appears to act as an anorexic hormone,” said the Nov. 11 ‘Science’ article, “by decreasing food intake, gastric emptying activities, jejunal motility and body-weight gain.”
These observations led to the christening of the newly discovered hormone.
“On the basis of the bioinformatics prediction that another peptide also derived from proghrelin exists, we isolated a hormone from rath stomach and named it obestatin — a contraction of obese, from the Latin ‘obedere,’ meaning to devour, and ‘statin,’ denoting suppression,” Hsueh said.
Also see my previous post Obestatin Hormone Suppresses Appetite.
We might be perhaps 10 or 15 years away from effective weight control treatments. Keep in mind that drugs normally take as long as 10 years to make it through the drug approval process. Some drug already it the pipeline might cure obesity. Or perhaps leptin could be sold for injections without a lengthy approval process. So it is hard to guess when obesity will become easily curable. But the knowledge about the mechanisms which cause obesity has advanced so much in the last few years that we now have sufficient scientific understanding on which to base development of obesity control therapies and appetite control therapies.
The scientific understanding of the mechanisms of appetite control in the last few years has been making some pretty big leaps. This trend continues. Stanford researchers have discovered an appetite suppressing hormone which they have named obestatin,
STANFORD, Calif. — When the appetite-enhancing hormone ghrelin was discovered a few years ago, researchers thought they had found the last of the major genes that regulate weight.
They were wrong.
Introducing: obestatin, a newly discovered hormone that suppresses appetite.
The finding, published in the Nov. 11 issue of Science, offers a key to researchers developing treatments for obesity. In a nation that desperately needs to slim down—the U.S. Centers for Disease Control and Prevention estimates 65 percent of Americans over the age of 20 are either overweight or obese—obestatin is likely to generate interest from scientists and drugmakers alike.
The financial incentives for appetite suppressant drug development are huge because so many people are, er, huge.
The research was sponsored by Johnson & Johnson Pharmaceutical Research & Development, LLC, which has certain license rights to the discovery.
Researchers at the Stanford University School of Medicine uncovered obestatin by using the principles of evolution to pick clues from data held in the Human Genome Project, as well as the genome sequencing projects for many other organisms, among them, yeast, fruit flies and mice.
Charles Darwin is everywhere. He's like Elvis.
"Darwin led us to this new hormone," said senior author Aaron Hsueh, PhD, an endocrinologist and professor of obstetrics and gynecology. Jian V. Zhang, PhD, a postdoctoral scholar in Hsueh's laboratory, is the lead author.
Drugmakers could use new insights into weight regulation. The discovery of the appetite-suppressing hormone leptin in 1994 and the appetite-boosting hormone ghrelin in 1999 offered high hopes of more effective drugs. And in the past few years, the influence of melanocortin hormones on regulating leptin has become clearer. But these insights have yet to yield a treatment for obesity.
"There are several known pathways that regulate body weight: ghrelin, leptin and melanocortin," explained Greg Barsh, MD, PhD, a Stanford professor of genetics who studies melanocortin, and was not involved in the obestatin project. "This work is notable because it represents a completely new pathway."
The new finding could clear up some confusion over how appetite-regulation hormones work. Since the ghrelin protein increases appetite, scientists had expected that animal experiments deleting the protein's gene would turn appetite off.
But when they tested this theory, they found that deleting the gene linked to ghrelin had almost no effect on growth or appetite. The likely reason? Hsueh's finding shows that deleting the gene for ghrelin also takes out obestatin.
It's rare for more than one protein to come from a single gene sequence. What makes this case even more unusual is that two proteins from the same sequence have such opposite effects: Obestatin behaves in some ways as the "anti-ghrelin."
"That was a big surprise," said Hsueh.
The identification of obestatin occurred as part of the researchers' study of a specific category of hormones-relatively small protein molecules called peptide hormones. These are of particular interest to drug developers because they bind to a type of receptor molecule known as a G-protein-coupled receptor, or GPCR. "These receptors represent targets for almost 50 percent of the drugs in the market," said Hsueh.
GPCRs activated by small-peptide hormones are especially promising. That's because small peptides, unlike larger ones, tend to be easier to synthesize and deliver to patients.
So why does Darwin's theory deserve some credit? Hsueh explained that before he and his colleagues started the project, they used the genome projects' information to create a database of GPCRs that grouped them according to their evolutionary relatedness.
From the 300 GPCRs found in the human genome, the researchers selected about 100 that had no known hormone partner. They then chose those 30 that seemed most likely to interact with a peptide hormone, basing this choice on evolutionary analyses.
"These sequences stood out because they each have evolutionarily close 'sister genes' known to bind peptide hormones," said Hsueh.
Next, they focused on identifying the unknown hormone partners. Darwin again lent a hand. Hsueh and colleagues narrowed the search by focusing on sequences that have been conserved during hundreds of millions of years of evolution-in organisms as diverse as fish and humans-because these are likely to be of greatest biological importance. They zeroed in on several sequences, including the one known to make ghrelin, the appetite-enhancing hormone. That sequence appears in humans and at least 10 other mammals.
Analysis of the ghrelin pre-hormone sequence revealed an additional protein tacked on at the end. The researchers promptly set out to synthesize and learn more about this protein, which they later named obestatin.
"There are no set rules for identifying bioactivity but most of the known peptide hormones are brain/gut hormones," said Hsueh. So the researchers set out to discover whether obestatin is present in rat stomach tissues and brain. It is.
After identifying a peptide candidate hormone they injected the peptide into rat brains and found it cut appetite in half.
Encouraged, they investigated obestatin's effects on laboratory animals. They found that injecting it into rats' abdomens and brains decreased food intake and suppressed weight gain. Rats given obestatin injections ate about half as much as those given no obestatin. Obestatin treatment also slowed the movement of digested food from the stomach into the intestines.
All that remained for the researchers to do was to match this newly discovered hormone to the right receptor.
Once again, evolutionary conservation made their work a little easier. Instead of testing each of the 30 previously identified GPCRs, they started with what the evolutionary record told them was the most likely candidate. Their hunch was that the receptor for obestatin would be closely related to the receptor for ghrelin. A whirl through their database showed them that GPR39 was closely related to the receptor for ghrelin.
Sure enough, later experiments showed them that GPR39 was in fact a receptor for ghrelin's antithesis, obestatin.
Evolutionary theory has become a lot more useful for medical research because of the declining cost of DNA sequencing technologies. Cheap DNA sequencing leads to large quantities of genetic data and that data gets analyzed with computer software written with insights gleaned from theoriizing about natural selection. Evolutionary theorizing therefore increasingly get used by clinical researchers. This is all taking place against the backdrop of political fights over whether kids should even be taught to take the theory of evolution by natural selection. seriously Well, the theory of evolution by natural selection is incredibly useful and medical science would be advancing more slowly without it.
A hormone found in the small intestine has provided a crucial breakthrough in developing new drugs to tackle the growing obesity epidemic, claim scientists. Obesity now affects more than half of all UK adults, costing the UK up to £3.7 billion a year in sickness absence and treatments.
In an article published today in Diabetes, the world's top diabetes research journal, a team from Imperial College London and Hammersmith Hospitals NHS Trust has used injections of oxyntomodulin, a naturally occurring digestive hormone found in the small intestine, to reduce body weight and calorific intake in overweight volunteers.
The injections boost existing levels of oxyntomodulin, normally released from the small intestine as food is consumed, signalling to the brain that the body is full and has had enough to eat.
Professor Steve Bloom, senior researcher at Imperial College London and Hammersmith Hospital, says: "The discovery that oxyntomodulin can be effective in reducing weight could be an important step in tackling the rising levels of obesity in society. Not only is it naturally occurring, so has virtually no side effects, it could be ideal for general use as it can be self administered. Despite this, we still need to conduct larger clinical trials to test its effectiveness over longer periods."
The researchers found that over four weeks, injections of oxyntomodulin three times a day in 14 volunteers reduced their body weight by an average of 2.3kg. They also found that daily energy intake by the test group was reduced by an average of 170kcal after the first injection, to 250kcal at the end of four weeks. The average recommended intake is 2500 kcal per day for men, and 1940 for women.
The researchers also found that volunteers in the study group had lesser appetites without a reduction in food palatability.
Note the unfortunate need to inject the hormone. In the longer run I can imagine a way to avoid the need for injection. Cells genetically engineered to make oxyntomodulin could be implanted in the body With sufficiently sophisticated genetic engineering the cells could be designed to only secrete the oxyntomodulin when some activating drug is taken. That would provde a way to avoid the risk of excessive skinniness and even starvation.
The subjects receiving oxyntomodulin had less leptin and adipose hormones in their blood.
The study found that leptin, a protein responsible for regulating the body's energy expenditure was reduced in the study group. They also found reduced levels of adipose hormones, a hormone which encourages the build up of adipose tissues, a type of tissue where fat cells are stored.
The lead researcher has unsurprisingly wasted no time in creating a company to commercialize this discovery.
Professor Bloom has set up a spin-out company, Thiakis, to commercialise this discovery, and run further trials.
Expect obesity to be rare 20 years from now. It is a lot easier to solve than a lot of other behavior disorders because the bloodstream carries messages to the brain that change whether we feel full or sated or hungry. Behavioral problems that occur entirely within the brain are much less tractable.
UC Irvine psychologist Elizabeth Loftus has found that students can be fooled into believing that some foods caused them to get sick as children.
After 204 students completed questionnaires about their food preferences, they received computer-generated analyses – some of which included false feedback indicating they had gotten sick from eating strawberry ice cream as a child. Researchers used two techniques to encourage the participants to process the false information, which resulted in 22 percent and 41 percent of the participants believing they had such a childhood experience.
Participants even provided details of the experience such as “May have gotten sick after eating seven cups of ice cream.” However, both groups showed similar tendency to want to avoid that food now that they “remembered” getting sick from it as a child.
“People do develop aversions to foods; for example, something novel like béarnaise sauce may make someone sick once, and they can develop a real aversion to that food,” said Loftus. “And with alcohol, there’s a medication that actually makes alcoholics sick if they drink, and the idea is to develop an aversion so that the person avoids drinking. It may be possible to do something similar with food, but without the physical experience.”
Loftus points out that further research must be done to show whether the effects are lasting and whether people who believe the false memory actually avoid the food when it is in front of them, as they indicated in the surveys.
People are awfully gullible.
In experimenting with false memories about fattening foods, Loftus’ team looked at both chocolate chip cookies and strawberry ice cream. Because participants were more likely to believe strawberry ice cream had made them ill, the researchers speculate that only novel food items are effective with the false feedback technique – a finding consistent with research showing real taste aversions are more likely to develop with novel foods. How recently participants had eaten the food appeared to have no effect.
Their next challenge is to try to fool people into liking vegetables.
In next study, Loftus and her team will look at whether people can be led to falsely believe that as a child they really liked certain healthful vegetables, like asparagus, and whether that will make them more inclined to eat such foods as adults.
The techniques these researchers employed to implant false memories are too weak. But surely false memory implantation technologies will improve. But also memory erasure technology might work just as well or better. If you had no memory of a particular food's taste you couldn't crave that taste. If you had a bad memory you'd even be averse to eating that food.
Parents are in the best position to use false memories. Start telling a 7 year old that ice cream made his tummy hurt each time he ate it. Probably 5 or 10 years of telling him that lie and encouraging him to repeat it back would leave a lasting effect. But I suspect that obese kids would respond by finding other foods to pork out on. Unless one can create a more general aversion to calorie consumption or at least an aversion to junk food consumption this sort of deception seems pointless.
I can see memory erasure and false memory implantation technologies as useful to treat for the effects of traumatic events and to get over addictions and compulsions. But we really need better technologies for reducing cravings and compulsions. Such technologies will come in the form of neural stem cell therapies targetted to specific regions of the brain.
Using today's technology a constant stream of PDA messages could tell dieters that high fat foods are disgusting and nauseating or tell them how great they are going to look if they avoid snacks would provide some benefit. PDA message streams could be automated to send out an assortment of encouraging messages with all sorts of justifications and praise for sticking to a diet. The messages could include suggestions for low calorie foods to eat or activities to engage in instead of eating. The same could be done with cell phone voice mail.
University of Florida at Gainsville researchers have found that exerise in cold water boosts appetite as compared to resting or exercise in warm water.
For her study, published in February in the International Journal of Sport Nutrition and Exercise Metabolism, White tracked the energy used by 11 UF students as they rode a stationary bicycle submerged in water for 45 minutes. The students exercised in cold water of 68 degrees Fahrenheit and warm water of 91.4 degrees Fahrenheit. The same students, ages 21 to 31, also spent 45 minutes resting.
The study found the students used a similar amount of energy during the exercises, 517 calories in the cold water and 505 in the warm water. Students expended 123 calories while resting.
After each exercise session and the rest period, the students were allowed into a room to measure their blood pressure and heart rates. They were left to rest for one hour in the same room and had free access to a standard assortment of food of known caloric values. However, the students didn't know their caloric intake was going to be measured.
"We found that during the recovery period when the subjects had access to an assortment of foods that significantly more calories were eaten after exercise in cold water compared to exercise in warm water or at rest," White said.
Caloric intake after exercise in cold water was 44 percent higher than exercise in warm water and 41 percent higher than in the resting periods. The students consumed a mean 877 calories after exercise in cold water, 608 calories after exercise in warm water and 618 after resting periods.
Water exercise appeals to obese people people because water reduces the strain on joints. But exercise in cold water may make weight problems even worse.
Staying up past bedtime, skipping meals, and snacking constantly all add up to weight gain, fatty livers, and high cholesterol levels for an unlucky group of mice whose internal biological clocks are genetically disrupted.
Researchers at Northwestern University and the Howard Hughes Medical Institute have identified wide-ranging molecular and behavioral changes in mice that have a faulty circadian system. In people, similar changes in body fat and metabolic activity are known as metabolic syndrome, which can lead to cardiovascular disease and type 2 diabetes.
Lots of things go wrong metabolically when mice don't sleep regularly.
The Clock mutant mice lost both their alarm clocks and their internal dinner bells. Mice typically sleep during the day and then eat a meal at the beginning and at the end of their active nocturnal day, akin to breakfast and dinner. Instead, the Clock mutant mice skipped their meals, stayed awake far into the usual rest time, and snacked often.
The insomniac mice also were a little more sluggish, as measured by infrared sensors in their cages. The researchers removed the exercise wheels normally used to gauge mouse activity, because regular spins can help the mice reset their biological clocks, just as a daily walk might help a person sleep better at night.
In repeated round-the-clock measurements, the researchers found signs of further trouble emerging in the mice's early adult months. The circadian-challenged mice developed high cholesterol, high triglycerides, high blood sugar, low insulin, bloated fat cells, and lipid-engorged liver cells. Some of these changes appeared to be independent of the weight gain, Bass said.
So then does artificial light contribute to human obesity? Probably. Note that exercise helps mice reset their biological clocks. Could be that lack of exercise causes people to stay up too late and also to eat too much, and have lousy blood lipid and sugar profiles.
Also see my previous post "Sleep A Lot To Avoid Burn-Out From Stress And To Stay Skinny".
The first year results of the two-year trial Rimonabant In Obesity -- Europe (RIO-Europe), a Phase III clinical study comparing rimonabant, the first agent in a new therapeutic class known as selective cannabinoid type 1 (CB1) blockers, to placebo, were published today in The Lancet. The reported findings in overweight or obese patients taking rimonabant 20 mg once daily show a significant reduction in body weight, waist circumference -- a marker of intra-abdominal adiposity -- as well as improvements in insulin resistance and lipid and glucose profiles. The improvement in lipids (HDL-cholesterol and triglycerides) was shown to be partially independent from weight loss, suggesting a direct effect of rimonabant on these important metabolic cardiovascular risk parameters. The trial findings also revealed a decrease in the number of patients with metabolic syndrome(i) in the rimonabant 20 mg/day group.
Patients on rimonabant lost an extra 10 lbs over placebo, had higher HDL cholesterol, lower triglycerides, lower blood glucose, and lower insulin. All these are changes in healthy directions.
At one year, patients treated with rimonabant 20 mg/day lost an average of 14.55 lbs (p < 0.001 vs placebo) compared to 7.5 lbs for patients on rimonabant 5 mg/day (p = 0.002 vs placebo) and 3.97 lbs for those on placebo. Patients on rimonabant 20 mg/day also had an average decrease in their waist circumference of 2.56 inches (p < 0.001) versus 1.54 inches for those on rimonabant 5 mg (p = 0.002 vs placebo) and 0.94 inches for those on placebo.
Among patients completing the study, 67.4% of patients treated with rimonabant 20 mg/day lost more than 5% of their initial body weight (p < 0.001 vs placebo), compared to 44.2% of patients in the rimonabant 5 mg/day group (p = 0.001 vs placebo) and 30.5% in the placebo group. Moreover, 39% (p < 0.001 vs placebo) of patients on rimonabant 20 mg/day lost more than 10% of their initial body weight compared to 15.3% of those on rimonabant 5 mg/day and 12.4% of those on placebo.
The percentage of patients fulfilling the criteria for the metabolic syndrome was reduced by 54% after treatment with rimonabant 20 mg compared to 21% treated with placebo (p < 0.001). In addition to the reduction in weight and waist circumference, a statistically significant improvement in metabolic risk factors with rimonabant 20 mg vs. placebo was also observed. In patients treated for one year with rimonabant 20 mg/day, HDL-cholesterol (good cholesterol) increased by 22.3% (p < 0.001 vs placebo), compared to 16.2% (p = 0.005) in the rimonabant 5 mg/day group and 13.4% in the placebo group. Triglycerides were reduced by 6.8% in patients treated with rimonabant 20 mg (p < 0.001 vs placebo), compared to an increase of 5.7% and 8.3% in rimonabant 5 mg and placebo groups, respectively. Almost 50% of the rimonabant-induced changes in HDL-cholesterol and triglycerides were independent of the weight loss observed, suggesting a direct effect of the drug on lipid metabolism.
A significant reduction in fasting plasma glucose of 0.09 mmol/L was seen in patients treated with rimonabant 20 mg (p = 0.026 vs placebo) compared with an increase of 0.03 mmol/L in the placebo-treated group. A similar pattern was observed for insulin levels which decreased by 1.0 micron IU/mL in the rimonabant 20 mg group (p < 0.001 vs placebo) versus an increase of 1.8 micron IU/mL in the placebo-treated group. Finally, a decrease of 0.3% in HOMA-IR (a measure of insulin resistance) was seen in the rimonabant 20 mg group (p = 0.002 vs placebo) compared with an increase of 0.4% in the placebo-treated group.
Accomplia is made by the French pharmaceutical firm Sanofi-Aventis which is applying for licences to market it early in 2006 in Europe and the U.S. It is also known by its generic name Rimonabant.
Obesity contributes to heart disease, stroke, cancer, type II diabetes, and likely dozens of other diseases. A drug that reduces the incidence of obesity could substantially improve the long term health outlook for hundreds of millions of people. If no problems turn on Sanofi-Aventis stands to earn huge profits. But patients will receive the lion's share of the benefits from an effective and safe anti-obesity drug.
Rimonabant acts by blocking receptors in the endocannabinoid system, one of the body's pleasure centers -- the same class of centers affected by marijuana.
The drug, which has progressed to phase III development, works by blocking endogenous cannabinoid binding to neuronal CB1 receptors. Activation of these receptors by endoegenous cannabinoids, such as anadamide, increases appetite. It is the only endocannabinoid receptor antagonist in clinical development and thus offers a unique therapeutic approach to appetite control and weight reduction. The drug also has potential as a treatment for smoking cessation because the endocannabinoid system is also involved in the body's response to tobacco dependence.
As things stand now many people who give up smoking gain weight. With this drug smokers may be able to lose weight and stop smoking at the same time. Imagine if this drug works out as advertised. Millions of people will be skinnier and healthier and gain longer life expectancies.
Here is some news you can use. First off, Torbjörn Åkerstedt, a sleep researcher at the Karolinska Institute in Sweden, has found that stress without a disruption of sleep patterns is not enough to cause work burn-out.
While stress is clearly involved, the precise causes of the symptoms have been unclear. A high level of the stress hormone cortisol has been blamed, for instance. But based on his team’s recent work, Åkerstedt says: “We think that people can function quite well on high levels of stress - it’s only when their sleep is disrupted that you get burnout.”
The team took regular sleep EEG readings of 35 patients who had been off work for a minimum of three months. The tests consistently showed extreme sleep fragmentation and disruption. These patients were living on as little as four or five hours of sleep each night, with a 40% reduction in slow-wave sleep compared with healthy people.
One weakness of this study is that a person who doesn't have to get up and go to work every day lacks that motivation to get up in the morning and go to sleep at night. It might be that the lack of participation in work activities causing the disruption in sleep cycle.
If you are going to work heavily it can be counterproductive to let the work interfere too much with your sleep cycle. It would be interesting to know whether people who burn out and who are not sleeping regularly would benefit from melatonin supplements or some other treatment or therapy to get the sleep cycle restored to a healthy pattern.
Burn-out is not the only risk that comes from poor sleep habits while under stress. James Gangwisch and colleagues at Columbia University found that getting fewer hours of sleep per night puts one at substantial risk for obesity.
(Las Vegas, NV) - November 16, 2004 - The less you sleep, the more likely you are to become obese, according to a study being presented at the North American Association for the Study of Obesity (NAASO)'s Annual Scientific Meeting held November 14-18.
The study, by researchers at Columbia University's Mailman School of Public Health and the Obesity Research Center, demonstrated a clear link between the risk of being obese and the number of hours of sleep each night, even after controlling for depression, physical activity, alcohol consumption, ethnicity, level of education, age, and gender. The study was an analysis of data taken from the National Health and Nutrition Examination Survey I (NHANES I).
Specifically, the study found that subjects between the ages of 32 and 59 who slept four hours or less per night were 73 percent more likely to be obese than those who slept between seven and nine hours each night. People who got only five hours of sleep had a 50 percent higher risk than those who were getting a full night's rest. Those who got six hours of sleep were just 23 percent more likely to be substantially overweight.
"The results are somewhat counterintuitive, since people who sleep less are naturally burning more calories," said lead researcher James Gangwisch, a post-doctoral fellow in psychiatric epidemiology at Columbia University. "But we think it has more to do with what happens to your body when you deprive it of sleep as opposed to the amount of physical activity that you get. Other studies have shown that leptin levels decrease and grehlin levels increase in people who are sleep-deprived, leading to increased appetite and consumption."
Why would that happen? According to Gangwisch, one possible answer can be found in looking back at our early forebears. "The metabolic regulatory system may have evolved to motivate humans to store fat during summer months when the nights are shorter and food is plentiful, which was a survival mechanism for the body to prepare for the dark winter months when food would not be as plentiful," said Gangwisch. "As a result, sleeping less could serve as a trigger to the body to increase food intake and store fat."
"Sleep deprivation activates a small part of the hypothalamus (region of the brain) that is also involved in appetite regulation," says Eve Van Cauter of the University of Chicago, one of the nation's leading sleep researchers.
If the rise in obesity is caused, at least in part, by poorer sleep habits why is this the case? One explanation is that electric light allows us to more easily continue do things when it gets dark rather than go to sleep. Another possibility is that electric light causes a stimulation of cells in the eye that are involved in telling the brain whether it is day or night. Biological clocks may be getting thrown off by artificial light sources. Increased viewing of TV and computer web surfing may each be contributing to the obesity epidemic.
It might be easier to prevent undesired weight gain if we turned down the brightness levels of our TV sets and computer monitors and if we turned down internal lighting to the bare minimum. Or the use of melatonin to make one tired might help keep or take the weight off.
A number of web sites claim that it would take 40 bananas to get 1 mg of melatonin. But in my experience a few bananas can help to make one drowsy. A number of foods contain melatonin.
Pineapples, apples, oranges, bananas, strawberries, kiwi fruits, peppers, spinach, nuts and tomatoes contain melatonin. The highest melatonin concentration has been found in oats, rice and sweet corn.
Of all the plant-based foods, oats, sweet corn and rice are richest in melatonin, containing between 1,000 and 1,800 picograms (1,000,000 picograms = 1 milligram) of melatonin per gram. Ginger, tomatoes, bananas and barley have about 500 picograms per gram. However, very large amounts of food would be necessary to equal the amount of melatonin available in a supplement pill. For example, 20 bowls of oats would yield just one milligram of melatonin
One web site claims that Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) depress melatonin levels and evening exercise depresses melatonin for up to 3 hours afterward. So are people who exercise at gyms in the evening interfering with their ability to get to sleep at night? If they treat their aches and pains from a work-out by taking aspirin or ibuprofen are they increasing their likelihood of insomnia and weight gain? Could be.
Also, if you are trying to fall asleep at night it might make more sense to listen to a book-tape in the dark than to read a book using a light.
Update: There are a couple of additional reasons why getting more sleep may make weight control easier. First of all, the more hours you are awake the more hours you have to eat. Go to bed a couple of hours earlier and you might avoid one last snack before bedtime. Also, a well rested mind is more capable of judging the consequences of decisions to eat and has a stronger will to resist.
It also hurts ''executive function'' -- the ability to make clear decisions, said Dr. Philip Eichling, sleep and weight-loss specialist at Arizona. ''One of my treatments is to tell them they should move from six hours to seven hours of sleep -- less sleepy, less hungry,'' he said.
“One reason the genes for disruptive sleep may have persisted is that poor sleep patterns make people gain weight and retain fat,” said Professor Tim Spector, director of the Twin Research Unit at London’s St Thomas’ Hospital, which carried out the research.
He added: “These genes may have helped our ancestors through periods of famine and the Ice Age.”
One problem with this argument is that there are genes that can be mutated to cause people to put on more weight that would not have had the effect of disrupting sleep. Wouldn't mutations in those other genes been more heavily selected for since the sleep disrupting mutations would tend to decrease efficiency while awake? On the other hand, some people do have sleep-disrupting genetic variations. So perhaps there is something to Spector's theory.
During the study, the researchers examined the sleep patterns of 1,024 volunteers from the Wisconsin Sleep Cohort Study, a population-based longitudinal study of sleep disorders that began in 1989. Participants between the ages of 30 and 60 underwent nocturnal polysomnography (a test during which a number of physiologic variables are measured and recorded during sleep) and blood sampling once every four years. They also reported on their sleep habits every five years through questionnaires and six-day sleep diaries.
The researchers' data showed a 14.9 percent increase in ghrelin and a 15.5 percent decrease in leptin in people who consistently slept for five hours compared with those who slept for eight. Mignot said the results were consistent regardless of participants' gender, BMI or eating and exercise habits. "The effect must be very strong to appear in [this entire] population," he said.
"It was quite amazing that a hormone can track a person's self-reported amount of sleep so well," he added. "To my knowledge, this is the first time that a peripheral marker in the blood is shown to correlate with habitual sleep amounts in a general, normally behaving population."
The researchers also found that in people sleeping less than eight hours (74.4 percent of the sample), increased BMI was proportional to decreased sleep. They reported that a 3.6 percent increase in BMI corresponded to an average nightly sleep duration decrease from eight hours to five hours.
Patricia Prinz reviews the latest results in PLoS Medicine. (PDF format) Also in PDF format is the full text of the paper in PLoS Medicine.
In another study Eve Van Cauter, Esra Tasalim, Plamen Penev at the University of Chicago and colleagues found that reducing sleep in health male volunteers upped the ratio of ghrelin to leptin.
Van Cauter and colleagues studied 12 healthy male volunteers in their early 20s to see how sleep loss affected the hormones that control appetite. Theses hormones -- ghrelin and leptin, both discovered in the last ten years -- represent the 'yin-yang' of appetite regulation. Ghrelin, made by the stomach, connotes hunger. Leptin, produced by fat cells, connotes satiety, telling the brain when we have eaten enough.
Van Cauter's team measured circulating levels of leptin and ghrelin before the study, after two nights of only four hours in bed (average sleep time 3 hours and 53 minutes) and after two nights of ten hours in bed (sleep time 9 hours and 8 minutes). They used questionnaires to assess hunger and the desire for different food types.
"We were particularly interested in the ratio of the two hormones," said Van Cauter, "the balance between ghrelin and leptin."
After a night with four hours of sleep, the ration of ghrelin to leptin increased by 71 percent compared to a night with ten hours in bed.
Get lots of sleep!
University of Chicago researcher Martha McClintock and colleagues have found that
Breastfeeding women and their infants produce a substance that increases sexual desire among other women, according to research at the University of Chicago.
"This is the first report in humans of a natural social chemosignal that increases sexual motivation," said Martha McClintock, the David Lee Shillinglaw Distinguished Service Professor in Psychology at the University, and the lead researcher in a team at the University's Institute for Mind and Biology. Chemosignals are substances that while not necessarily perceived as odors, nonetheless have an impact on mood and menstrual cycles when absorbed through the nose.
The researchers found that after being exposed to the breastfeeding compounds for two months, women with regular partners experienced a 24 percent increase in sexual desire as reported on a standard psychological survey. Women without partners experienced a 17 percent increase in sexual fantasies after exposure for the period.
Women in the control group with partners who were exposed to a neutral substance reported an insignificant decrease in sexual desire, while women without partners in the control group experienced a 28 percent decrease in fantasies.
The work on sexual desire is reported in the paper "Social Chemosignals from Breastfeeding Women Increase Sexual Motivation," being published in the latest issue of Hormones and Behavior.
Joining McClintock in writing the paper were Natasha Spencer, Sarah Sellergren, Susan Bullivant and Suma Jacob, researchers at the University of Chicago, and Julie Mennella, a scientist with the Monell Chemical Senses Center, in Philadelphia. The study was conducted both in Chicago and Philadelphia.
In Philadelphia, Mennella recruited 26 breastfeeding women, who were asked to eat a bland diet to avoid transmitting odors such as curry through the breast milk. The breastfeeding women wore pads in their nursing bras, where the saliva from their infants in addition to their own perspiration and milk was collected. They also wore pads secured by underarm shields to collect perspiration.
The pads were collected, cut in pieces and frozen. Other studies in the McClintock lab have shown that the procedure is effective in collecting chemosignals.
In Chicago, the researchers recruited about 90 women between the ages of 18 and 35 who had not born a child. The women were divided into two groups, one group exposed to the pads with breast feeding substances, and the other group exposed to pads with potassium phosphate, a substance that mimics the concentration of the sweat and breast milk.
"Because preconceived ideas about pheromones could potentially influence their responses, study participants were blind to the hypotheses and the source of the compounds," Spencer said. "The study was presented to the subjects as an examination of odor perception during the menstrual cycle."
Participants were given a set of pads on a regular basis and asked to swipe them under their noses in the morning and at night and any other time of the day in which they may have wiped their upper lips, showered or exercised.
The women with partners were asked about their moods and were asked to complete daily a survey with a scale indicating "the degree you felt desire today for sexual intimacy." They also recorded their sexual activity. Women without partners were also asked about their moods and reported whether they experienced "any fantasies/daydreams today of a sexual or romantic nature." Among women exposed to the breastfeeding substance, "The effect became striking during the last half of the menstrual cycle after ovulation when sexual motivation normally declines," McClintock said.
Here, we demonstrate that natural compounds collected from lactating women and their breastfeeding infants increased the sexual motivation of other women, measured as sexual desire and fantasies. Moreover, the manifestation of increased sexual motivation was different in women with a regular sexual partner. Those with a partner experienced enhanced sexual desire, whereas those without one had more sexual fantasies.
Suppose this compound is identified. How it gets used will depend on how rapidly it works. If it works rapidly then expect guys to wear it as a perfume. If it takes a few hours to work then guys will want to go on longer dates to allow more time for it to take effect. If it takes days then it will be a lot harder for a single guy to use it for his own benefit. However men in longer term relationships or even men travelling with women on extended business trips would have obvious incentives to use it.
Will women want to use such a compound on themselves? That depends in part on whether it just enhances desire to have sex or does it also enhance the pleasurability of the sexual experience?
Also, some women will want to defend themselves against having their sex drive manipulated by someone else without their knowledge. One way to do that defense would be to develop compounds that block the effect of whatever compound(s) that will be isolated and found to be involved in this effect. However, another line of defense is detection. Imagine a chemical strip that is designed to react only to the aphrodisiac. A woman could wear such a strip as, perhaps, a ribbon tying up her hair or somewhere else inconspicuous and then she could check whether the strip changed color while she was sitting in a bar or restaurant.
A growing knowledge about what increases and decreases sexual drives is inevitably going to be used in the war between the sexes. Whether the net increase in knowledge will end up being used more by the offensive or the defensive or perhaps only under negotiated peace treaties remains to be seen. My guess is all of the above.
Professor Terry Davidson and associate professor Susan Swithers, both in the Department of Psychological Sciences, found that artificial sweeteners may disrupt the body's natural ability to "count" calories based on foods' sweetness. This finding may explain why increasing numbers of people in the United States lack the natural ability to regulate food intake and body weight. The researchers also found that thick liquids aren't as satisfying - calorie for calorie - as are more solid foods.
Our attempts to fool ourselves are defeated because the parts of our brain that regulate appetite can monitor signals that provide an indication of how much calories were consumed.
"The body's natural ability to regulate food intake and body weight may be weakened when this natural relationship is impaired by artificial sweeteners," said Davidson, an expert in behavioral neuroscience. "Without thinking about it, the body learns that it can use food characteristics such as sweetness and viscosity to gauge its caloric intake. The body may use this information to determine how much food is required to meet its caloric needs."
Over the past 25 years, there has been a dramatic increase in the consumption of artificially sweetened foods and low viscosity, high-calorie beverages, said Swithers, a developmental psychobiologist.
"Incidence of overweight and obesity has also increased markedly during this period," she said. "Our hypothesis is that experience with these foods interferes with the natural ability of the body to use sweet taste and viscosity to gauge caloric content of foods and beverages. When you substitute artificial sweetener for real sugar, however, the body learns it can no longer use its sense of taste to gauge calories. So, the body may be fooled into thinking a product sweetened with sugar has no calories and, therefore, people overeat."
Swithers said that the loss of the body's ability to gauge caloric intake contributes to increased food intake and weight gain, especially when people do not count calories on their own. A similar dynamic is at work with foods' texture and thickness.
"Historically, we knew that our body learns that if the food is thick, such as whole milk, it tends to have more calories than compared to a thinner liquid such as skim milk," Swithers said. "Now, our research reinforces this and takes it one step further, showing that our bodies translate this information about perceived calories into a gauge to tell us when to stop eating."
Two studies on rats yielded results that led to this theory.
Davidson and Swithers' findings are based on two studies.
In the first study, two groups of rats were given two different sweet-flavored liquids. In the first group, both liquids were sweetened with natural high-calorie sweeteners so there was a consistent relationship between sweet taste and calories. For the second group, one of the flavored liquids was artificially sweetened with non-caloric saccharin so that the relationship between sweet taste and calories was inconsistent.
After 10 days of exposure to the flavors, the rats were allowed to eat a small amount of a sweet, high-calorie chocolate flavored snack. The researchers compared the two groups' ability to compensate for the calories contained in the chocolate snack. The rats that had experienced the inconsistent relationship between sweet taste and calories were less able to compensate for the calories contained in the snack and ate more than the rats that had experienced the consistent relationship between sweetness and caloric intake.
"This suggests that experience with the inconsistent relationship reduced the natural ability of the rats to use sweet taste to judge the caloric content of the snack," Swithers said.
In the second study, two groups of rats were given a high-calorie dietary supplement along with their regular food every day for 30 days. Although the supplements were identical in calories and nutritive content, they differed in viscosity. For one group the supplement had the consistency of thick chocolate pudding, whereas for the other group, the supplement was similar to chocolate milk. Davidson and Swithers found that over the course of the study, the rats given the milk-like supplement gained significantly more weight than the rats given the more viscous, pudding-like supplement.
"This finding indicates that rats are less able to estimate and compensate for the calories contained in liquids than in semi-solid foods," Davidson said. "If the body is less able to detect and compensate for calories contained in liquids, then intake of high-calorie beverages compared to semi-solid or solid foods could increase the tendency to gain weight."
There are a couple of obvious lessons here. First of all, do not use artificial sweeteners. Second, drink water and get all your calories for semi-solid and solid foods. This is wise advice for other reasons anyway. You are better off eating an apple than drinking apple juice because the solid apple has more vitamins, minerals, antioxidant compounds, and fiber. The same holds true for other fruits and vegetables versus their juices in the vast majority of cases.
One of the great challenges of adapting human bodies to the modern era is to get control of appetite. Humans tend to eat too much when food is cheap, easily available, and prepared to appeal to their cravings. As a result, the incidence of obesity is rising rapidly in the industrialized countries and this is causing a higher incidence of a large range of obesity-related diseases including joint problems, heart disease, and even an increased risk of cancer. Therefore research into factors that affect appetite and the tendency to gain weight is very important for finding ways to make humans more adaptive to environments that are much different from our ancestors' environments which selected for our food cravings.
In America trade restrictions on sugar imports under a tariff rate quota system have increased the cost of the common table sugar sucrose (which is a dimer of glucose and fructose covalently bonded to each other). The result has been such high costs for table sugar that liquid beverage makers responded by switching to using high fructose corn syrup as a sweetener. Your FuturePundit been annoyed about this for a long time and have been aware of theories of potential harm from excess fructose consumption for years. Well, science has begun to confirm at least one of those theories with a new report which shows that fructose consumption in place of glucose consumption causes blood changes which are unfavorable and which may lead to obesity.
Philadelphia, PA -- Researchers at the Monell Chemical Senses Center, the University of California, Davis and other collaborating colleagues report that drinking beverages containing fructose, a naturally-occurring sugar commonly used to sweeten soft drinks and other beverages, induces a pattern of hormonal responses that may favor the development of obesity.
It is estimated that consumption of fructose has increased by 20-30% over the past three decades, a rate of increase similar to that of obesity, which has risen dramatically over the same time span. Data from the present study suggest a mechanism by which fructose consumption could be one factor contributing to the increased incidence of obesity.
In the study, reported in the June 4 issue of the Journal of Clinical Endocrinology and Metabolism, 12 normal-weight women ate standardized meals on two days. The meals contained the same number of calories and the same distribution of total carbohydrate, fat and protein. On one day the meals included a beverage sweetened with fructose. On the other day, the same beverage was sweetened with an equal amount of glucose, another naturally-occurring sugar that is used by the body for energy.
Following meals accompanied by the fructose-sweetened beverage, circulating levels of insulin and leptin were decreased compared to when the women ate the same meals accompanied by the glucose-sweetened beverage. Lower levels of insulin and leptin, hormones that convey information to the brain about the body's energy status and fat stores, have been linked in other studies to increased appetite and obesity.
In addition, levels of ghrelin, a hormone thought to trigger appetite that normally declines following a meal, decreased less after meals on the day the women drank the fructose-sweetened beverage. And, the fructose also resulted in a long-lasting increase of triglycerides, fatty molecules in the blood that are indicators of risk for cardiovascular disease.
Together, the hormonal responses observed after drinking beverages sweetened with fructose suggest that prolonged consumption of diets high in energy from fructose could lead to increased caloric intake and contribute to weight gain and obesity. Lead author Karen Teff, Ph.D., a physiologist at Monell, comments, "Fructose consumption results in a metabolic profile of hormones which would be predicted to increase food intake, thereby contributing to obesity in susceptible populations."
Teff notes that this pattern of hormonal responses is similar to that observed after consuming a high-fat meal, and continues, "Based on our previously published work, this metabolic profile resembles that of fat consumption. Thus, despite the fact that fructose is a sugar, metabolically the responses are similar to those seen following fat ingestion." The elevated levels of plasma triglycerides observed after fructose consumption further suggest that frequent fructose consumption could also contribute to the development of atherosclerosis and cardiovascular disease.
According to co-author Dr. Peter Havel, a research endocrinologist at the University of California, Davis, "Although this short-term experiment provides important new data, additional research is needed to investigate the long-term impact of consuming fructose in humans, particularly its effects on lipid metabolism and on endocrine signals involved in body weight regulation. New studies should also be conducted in subjects who are at increased risk for metabolic diseases such as type-2 diabetes and cardiovascular disease and who may be more susceptible to the adverse effects of overconsuming fructose".
Who do we have to blame for all the fructose in Coca Cola and Pepsi? Well, leaving aside an apathetic public that shouldn't allow its politicians to be bought off or the politicians themselves how about the Fanjul sugar family formerly of Cuba and now of Florida?
The Fanjuls are formidable adversaries. They control about 40 percent of Florida’s sugar crop, and last year they made contributions to 31 political candidates, giving more than any other sugar power. They deeply resent their nickname: the first family of corporate welfare. Little known to the American public, Pepe and Alfy Fanjul operate within the hidden world of implicit linkage, the grand club of the country’s power brokers, who routinely trade favors like baseball cards. "There is a rule to understanding life in South Florida," author and Miami Herald columnist Carl Hiaasen tells me. "Alligators don’t give to political campaigns, and the Fanjuls do." Last year the Fanjuls and Florida Crystals gave $486,000 to Democratic candidates and $279,000 to Republicans. (Alfy, who co-chaired Clinton’s Florida campaign in 1992, is the family’s Democrat; Pepe, who was on Bob Dole’s finance committee in 1996, is the family’s Republican.) "The most telling thing about Alfy Fanjul is that he can get the president of the United States on the telephone in the middle of a blow job. That tells you all you need to know about their influence," Hiaasen says.
Read Marie Brenner's full article from that last link if you are in the mood for some moral outrage.
There is some obvious personal take-home advice here: avoid refined fructose. Consider avoiding the sweetest fruits and If you are having a problem with obesity avoiding fructose is probably even more important.
Obesity is a serious problem. The Scientist has an excellent survey of the costs and the scientific advances being made in appetite and obesity research. (requires free registration and it is an excellent site to register for access)
Obesity is also about money. Last year, the United States spent $75 billion on medical expenditures attributable to obesity; about one-half of this money came from public coffers.3 The US Federal Trade Commission estimates that North Americans spend $35 billion per year on weight-loss products and programs. "Industry has recognized that this is the largest possible market worldwide ever," says Tschöp. "This is a large amount of people that will have to take a drug until the end of their life, and those people have money." Seckl, whose team identified 11beta-hydroxysteroid dehydrogenase, an enzyme linked to obesity, says that one drug company recently sold an inhibitor for $86 million.
My guess is those numbers underestimate the real costs of obesity because it increases so many disease risks. A major reason why obesity is harmful to you is that fat cells secrete hormones and when a person is obese the doses of those secreted hormones become so great that they cause toxic effects on the body.
The problem is the volume of chemicals these oversize cells churn out, says Dr. George Bray of Louisiana State University. "The big cell secretes more of everything that it secreted when it was small. When you get more of these things, they are not good for you."
The future achievement of control over human appetite will therefore be an enormous health benefit.