Anyone want to explain this result?
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.
Eat tart cherries to help keep off excess weight?
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 tehy 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?
Beware a hypofunctioning reward circuit.
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.
Over half of olive oil is a fatty acid called oleic acid, which at least in rats boosts production of a hormone that decreases hunger.
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?
Need a vagal nerve blocking device to help you lose weight?
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.
The hormone ghrelin increases hunger while also reducing stress.
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.
Cutting back on TV and video games cut weight of heavier weight kids.
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.
But the reduction in TV and computer use did not work by increasing exercise.
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.
Skipping breakfast probably causes rebound eating later in the day and weight gain.
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.
Skipping breakfast leads to a life of vice.
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.
Its not nice to fool mother nature.
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).
But a causal link between diet soda consumption and obesity is not proven.
“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?”
Maybe video games and TV are keeping the kids up and that is causing the childhood obesity epidemic?
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 lack of sleep is stressful and increases disease risks.
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.
Some research backs up the idea of letting babies cry themselves to sleep.
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.
Another method is called core night. See some other techniques for getting babies to sleep/.
Expect the "Chocolate Talk Diet" book coming to a store near you.
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.
Chocolate lovers have a metabolic signature that differentiates them from non-chocolate lovers.
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 thinks anorexia should be treated like an addiction.
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).
Genetic engineering as the solution to weight control problems?
“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.
Flies and mice react the same ways to higher and lower levels of adipose gene expression.
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.
If you want to stay skinny avoid getting too stressed out.
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.
Why let your spouse blame your diet for your unwanted fat when you can blame your genes instead?
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.
Evidence for the idea that exercise is the key to controlling weight:
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.
A genetic variation seems to prevent higher fat consumption from contributing to obesity.
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