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CHICAGO (AFP) – The bugs that help digest food may also cause the body to pack on the pounds if they are not properly regulated, a new study has found.

That is because if the wrong kinds of bacteria take over they can cause a low-level inflammation that leads to a pre-diabetic condition and an elevated appetite, the study published Thursday in the journal Science found.

"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost, high-calorie foods," said senior author Andrew Gewirtz of Emory University School of Medicine.

"However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism."

Gewirtz and his colleagues studied mice that were genetically engineered to be deficient in a key immune system protein - TLR5 - which helps cells sense the presence of bacteria.

"This protein serves as the neighborhood cop of the intestinal community," Gewirtz told AFP.

"It knows which bacteria it has to keep in check and it knows not to apply too much force and doesn't harm the good bacteria."

The immune system can continue to regulate bacteria without TLR5, but it does a poorer job. The bacterial composition changes, a low level inflammation sets in and insulin receptors are desensitized.

The protein-deficient mice ate about 10 percent more food and ended up about 20 percent heavier than normal mice.

They also developed metabolic syndrome, a cluster of disorders that in humans increases the risk of developing heart disease and diabetes.

While it was possible to get the mice to keep the weight off by restricting their food intake, they continued to show a decreased sensitivity to insulin.

That suggests that "at least some portion of obesity may result from insulin resistance rather than the commonly held view that type 2 diabetes and insulin resistance is a consequence of obesity," Gewirtz said.

Another key discovery was that if these bacteria were transferred to the intestines of mice which were not deficient in the protein, they would also develop metabolic syndrome.

This only worked, however, in mice whose intestines had been cleared of all other bacteria.

Humans have relatively stable intestinal bacterial populations which are acquired at birth but can be influenced by diet and antibiotics.

However, other studies have found that this baseline bacterial population is changing as a result of improvements in sanitation and the widespread use of antibiotics.

"It suggests that a portion of the epidemic of obesity and metabolic symptoms may be resulting from early environmental conditions that affect one's gut microbiota," Gewirtz said in a telephone interview.

While the study suggests a possible genetic predisposition to obesity, a deficiency in the TLR5 only affects a small percentage of the population, he said.

Changes in intestinal bacterial compositions could be significantly more widespread and could potentially one day be resolved by giving babies the right kind of bacteria before the wrong kind settles in, he added.

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If you're fighting the battle of the bulge, most of your attention - and frustration - is probably aimed at your midsection. It makes sense, since that's where the extra pounds tend to gravitate, especially with the creep of middle age, piling on to form that dreaded spare tire. (See 10 myths about dieting.)

But a growing body of research suggests there's another, less visible reason to focus on your gut if you want to lose weight. Scientists led by Andrew Gewirtz at Emory University reveal that your intestines harbor a universe of bacteria - the so-called gut microbiota - that may play an important role in whether your body will store the food you eat as extra pounds. (See pictures of what the world eats.)

Gewirtz's team, including researchers at Emory, Cornell University and the University of Colorado at Boulder, became intrigued by the relationship between gut bugs and weight when they noticed that lab mice lacking a certain protein had more of the bugs than other animals and were about 15% heavier. These mice also had a higher level of inflammation, which the authors explain in their paper published online Thursday in Science Express is what may account for the extra weight. Inflammatory signaling can promote a condition called metabolic syndrome, which causes weight gain, high blood pressure and high cholesterol levels and a higher risk for developing diabetes and heart disease.

The fatter mice in Gewirtz's study had been bred to lack a protein known as toll-like receptor 5 (TLR5), which most intestinal cells sprout on their surface. Its job is to recognize and bind to the whiplike flagella that bacteria use to move around. TLR5 acts as a traffic cop for controlling the mass of pathogens living in the intestine; without it, the normally harmless gut bacteria tend to overflourish and expand in number. (See and listen to an audio slideshow about obesity rehab.)

When that happens, the study found, it triggers an inflammatory state, as the body attempts to respond to the increasing population of bugs, and at the same time makes cells less sensitive to insulin. In a way, inflammatory factors and insulin compete for the attention of the same intestinal cells; if the cells are busy responding to inflammatory factors, then they are less likely to take up glucose and process it effectively. Such a desensitization to insulin and glucose then leads to the symptoms of metabolic syndrome, such as weight gain, high cholesterol and triglyceride levels and elevated blood pressure - which were all present in the TLR5-deficient mice. (See the top 10 medical breakthroughs of 2009.)

"We don't think the bacteria are directly making the mice eat more, but the bacteria are causing low-grade inflammation, which causes insulin resistance and then makes the mice eat more," says Gewirtz.

To test that theory, the researchers conducted a series of experiments, the most illuminating of which revealed that when the TLR5-deficient mice were given unrestricted diets, they ate 10% more than normal mice, and that even when their food was limited, they were still less sensitive to insulin than their normal counterparts.

The finding was confirmed when the team transferred the bacterial gut population from TLR5-deficient mice into animals that were specially bred to have no immune system, making them incapable of rejecting foreign cells and bacteria. When these animals received the teeming gut world of the TLR5-deficient mice, they too began eating more and developed the same metabolic-syndrome symptoms that their donors had. In other words, the obesity profile of the heavier mice had been transferred to normal mice. "So, applying the logic to humans," says Gewirtz, "we know that to gain weight and become obese, [it] requires you to eat more. The question is, Why do people eat more? Our results suggest that one reason people might be eating more is because of changes in their intestinal bacteria." (Comment on this story.)

A more fundamental question, then, is, What causes changes in gut microbiota? Many things, says Gewirtz, including the use of antibiotics, cleaner water and improved sanitation and hygiene in general, which influences the type and amount of microbes that reside in the intestines. In the current study, scientists found that in TLR5-deficient animals, the total percentage of 150 species of bacteria in the gut was three to four times higher than in normal mice, while 125 other types of bacteria were less common. "We don't have a sense of which is more important yet - that some of those species are missing, or that some are in greater abundance," he says. The net effect, however, is that in the absence of TLR5, the community of microbes changes and, as Gewirtz says, "when the intestinal bacteria is changed, the host response changes with them, and that may predispose you to a variety of diseases of which obesity and metabolic syndrome are perhaps the most mild." (See the 10 worst fast food meals.)

Studying those changes is the next step for scientists like Gewirtz who want to understand the precise link between intestinal microbiota and obesity. An important part of that investigation will involve having an accurate map of the genetic makeup of those gut bugs. And in a separate paper published Wednesday in Nature, an international group of scientists generated the most comprehensive genetic map to date of human gut microbes, using 124 human fecal samples, which gives scientists just the critical window they need to figure out which species of bugs tend to reside in our intestines and which may contribute to weight gain. (See how to prevent illness at any age.)

While Gewirtz's latest findings are limited to mice, experts believe they may be just as applicable to humans; previous work on gut microbiota has found that obese individuals tend to have a makeup of pathogens in their intestines different from that of people who are of normal weight. "Our results suggest that the tendency to eat more may not only be driven by the fact that food is cheaper and more available, but by a change in the bacteria in the intestines," he says. "People may be eating too much because their appetite is stronger due to a low-grade inflammation they have, which could be due to changes in their gut bacteria relative to what their grandparents or someone else might have had 50 years ago."

If that's true, then studies like this one could open new doors into understanding the myriad ways that pathogens like bacteria can cause disease - including methods that have nothing to do with infection.

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THURSDAY, March 4 (HealthDay News) -- Intestinal bacteria may contribute to obesity and metabolic syndrome, a new study in mice suggests.

"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost, high-calorie foods. However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism," senior study author Andrew Gewirtz, an associate professor of pathology and laboratory medicine at Emory University School of Medicine, said in a university news release.

He and his colleagues found that increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria. The findings are published online March 4 in the journal Science.

It's believed that intestinal bacteria populations in people are acquired at birth from family members and are relatively stable. However, they can be affected by diet and antibiotics.

"Previous research has suggested that bacteria can influence how well energy is absorbed from food, but these [new] findings demonstrate that intestinal bacteria can actually influence appetite," Gewirtz explained.

He said the findings from mice suggest "that it's possible to 'inherit' metabolic syndrome through the environment, rather than genetically. Do obese children get that way because of bad parenting? Maybe bacteria that increase appetite are playing a part."

A gene called toll-like receptor 5 (TLR5) plays an important role in controlling intestinal bacteria. Gewirtz and colleagues plan to investigate TLR5 variations in humans and how bacteria in TLR5-deficient mice influence appetite and metabolism.

More information

The American Academy of Family Physicians has more about metabolic syndrome.

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Diet not working? Blame your genes. That's the pitch behind a new test that claims to show whether people will do better on a low-fat or a low-carb weight loss plan.

We're all hard-wired with DNA that controls how we burn and store calories from various foods, and the test claims to sort out this machinery. A study this week found that women on diets well-matched to their genes, as defined by the test, lost roughly five times more weight than those on mismatched diets.

"We were able to explain why some people were successful" and others were not, even though they ate the same way, said Mindy Dopler Nelson, a nutritional biologist at Stanford University who led the study but has no financial ties to the maker of the test.

Some scientists find this hard to swallow. It's another test being peddled without enough research to show it really works, they say.

"I'm afraid this may be another attempt to lure the public into purchasing genetic tests that provide little value for those struggling with their weight," said Raymond Rodriguez, director of the National Center of Excellence for Nutritional Genomics at the University of California, Davis.

The research shows "nothing that should move the American public out to get their genome tested," said Dr. Robert Eckel, a former American Heart Association president and cardiologist at the University of Colorado-Denver.

But it sure has appeal.

Gene testing originally was aimed at finding risk for things like cancer, diabetes and Alzheimer's disease. Lately, genes have been linked to things you might not suspect, such as stuttering or compulsive leg-jiggling.

The latest trend is to connect genes to lifestyle counseling, determining what type of diet or exercise is best. That's what the maker of the new diet test hopes to do.

The company, Waltham, Mass.-based Interleukin Genetics Inc., looked at studies on hundreds of genes and chose three genes that show a pattern for metabolizing fats and carbohydrates, said its chief scientific officer, Ken Korman.

The company then hired Stanford researchers to do a validation study of its $149 test, using people who took part in diet research that was published in 2007. That study tested four diets — Atkins (ultra-low-carb), the Zone (low-carb), Ornish (very low-fat) or a low-fat diet following the federal Food Pyramid.

About one-third of the original participants, 138 women, sent cheek swabs with their DNA to Interleukin, which tagged them as "low-carb appropriate" or "low-fat appropriate."

Looking back at the original study's results, researchers saw that women whose diets matched their genetic makeup lost more than 13 pounds over a year compared to less than 3 pounds for women on mismatched diets, Nelson reported at a heart association conference this week.

Some scientists were unpersuaded. Sticking with a diet is more important than what diet you choose, as is not regaining weight, Eckel said.

"I have serious reservations with this study and studies like it," Rodriguez agreed. "The idea that genetic variants in these genes can predict the likelihood for weight loss in such a small population, particularly since the tendency for weight loss is probably more behavioral than genetic, is simply hard to believe."

However, one of the study participants, Jacqueline Gardner, 55, of Evergreen, Calif., does believe. She went from 200 pounds at the start of the study to 185, but was back to 200 pounds two years later.

"I now know why I gained it back," she said — the gene test showed she does not metabolize carbohydrates well. More recently, she has been on a high-protein diet and weighs 180.

"I wish I had had a DNA test 10 years ago," she said.

The researchers also tested themselves.

"It confirmed my suspicion," Nelson said of her result. "When I eat a lot of carbohydrates, I tend to put on weight."

Do we really need a gene test to tell us that?

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On the Net:

UC Davis nutrigenomics center: http://nutrigenomics.ucdavis.edu

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NEW YORK (Reuters Health) – People who are obese are at increased risk of becoming depressed, and people who are depressed are at increased risk of becoming obese, Dutch researchers have found.

"There is a reciprocal association over time between depression and obesity," Dr. Floriana S. Luppino, of Leiden University Medical Center, the Netherlands, told Reuters Health by email.

Obesity, Luppino and colleagues found, increases the risk of depression in initially non-depressed individuals by 55 percent and depression increases the risk of obesity in initially normal-weight individuals by 58 percent.

Luppino said the analysis was not designed to determine a given person's risk of depression, only to figure out how much obesity increased that risk. However, for comparison, a recent study funded by the National Institute of Mental Health found that nearly one out of four cases of obesity is associated with a mood or anxiety disorder.

These findings, the NIMH notes on its website, appear to support what other studies have found - that obesity, which is on the increase in the US - is associated with increasing rates of depression and other mental health problems.

The new findings stem from pooled data from 15 published studies that looked at whether being overweight or obese is associated with depression, and vice versa.

The studies, which collectively involved more than 58,000 people, used body mass index, or BMI, to gauge how fat or thin a person is. For reference, a US adult with a BMI of 25 or more is considered overweight, while one with a BMI of 30 and above is considered obese.

Being obese, Luppino told Reuters Health, not only increases the risk of depression, but is more likely to fuel the onset of clinical depression, rather than merely depressive symptoms.

In contrast to obesity, the association between depression and being overweight (but not obese) did not run the other way, Luppino noted. Being overweight increased the risk of depression in initially non-depressed individuals somewhat, but depression did not increase the risk of being overweight over time.

The findings, reported in the latest issue of the Archives of General Psychiatry, also suggest that the link between obesity and later depression is more pronounced among Americans than among Europeans.

Why? "A dose-response association -- meaning the higher the BMI, the more people get depressed -- might explain the association," Luppino said. And the average American weighs more than the average European.

However, the effect of the psychological distress should not be neglected, the researcher said. "Overweight and obesity, can induce low self-esteem and body dissatisfaction," Luppino explained, "especially in Western countries where thinness is often considered a beauty ideal. Both low self-esteem and body dissatisfaction are known to increase the risk of depression."

Because both depression and obesity carry "major health implications, it is very important to try to prevent and treat both," Luppino said.

The Dutch team encourages doctors and other health professionals, working in different fields, to collaborate and exchange their expertise. Doctors treating patients who are overweight or obese could screen their patients for depression and vice versa -- psychiatrists or general doctors encountering depressed patients could suggest their overweight patients see a dietitian, Luppino suggests.

SOURCE: Archives of General Psychiatry, March 2010.

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THURSDAY, March 4 (HealthDay News) -- Intestinal bacteria may contribute to obesity and metabolic syndrome, a new study in mice suggests.

"It has been assumed that the obesity epidemic in the developed world is driven by an increasingly sedentary lifestyle and the abundance of low-cost, high-calorie foods. However, our results suggest that excess caloric consumption is not only a result of undisciplined eating but that intestinal bacteria contribute to changes in appetite and metabolism," senior study author Andrew Gewirtz, an associate professor of pathology and laboratory medicine at Emory University School of Medicine, said in a university news release.

He and his colleagues found that increased appetite and insulin resistance can be transferred from one mouse to another via intestinal bacteria. The findings are published online March 4 in the journal Science.

It's believed that intestinal bacteria populations in people are acquired at birth from family members and are relatively stable. However, they can be affected by diet and antibiotics.

"Previous research has suggested that bacteria can influence how well energy is absorbed from food, but these [new] findings demonstrate that intestinal bacteria can actually influence appetite," Gewirtz explained.

He said the findings from mice suggest "that it's possible to 'inherit' metabolic syndrome through the environment, rather than genetically. Do obese children get that way because of bad parenting? Maybe bacteria that increase appetite are playing a part."

A gene called toll-like receptor 5 (TLR5) plays an important role in controlling intestinal bacteria. Gewirtz and colleagues plan to investigate TLR5 variations in humans and how bacteria in TLR5-deficient mice influence appetite and metabolism.

More information

The American Academy of Family Physicians has more about metabolic syndrome.

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WASHINGTON (Reuters) – Germs that make their home in the gut may help cause obesity and a range of health-threatening symptoms that go along with it, researchers reported on Thursday.

It could be that certain bacteria cause inflammation that can affect appetite as well as inflammatory bowel conditions like Crohn's disease and colitis, the researchers reported in the journal Science.

In other words, the germs make you overeat, Andrew Gewirtz of Emory University in Atlanta and colleagues reported.

"Previous research has suggested that bacteria can influence how well energy is absorbed from food, but these findings demonstrate that intestinal bacteria can actually influence appetite," Gewirtz said.

"The obesity epidemic is driven by people eating too much, but why are people eating more?"

Gewirtz said the research suggests that bacteria may play a role -- perhaps a population of bacteria that thrive because other, competing organisms have been wiped out by antibiotics, access to clean water and other factors of modern life.

His team stumbled on the findings by accident.

"We were studying mice that had colitis," Gewirtz said in a telephone interview.

The team suspected some kind of germ was responsible, so they transferred mouse embryos into surrogate mothers to prevent them from being infected by their own mothers.

Babies are colonized by bacteria and other micro-organisms soon after birth and the makeup of these colonies -- which persist for life in the skin and bowels -- are very similar to those of the mother.

The colitis was better but the baby mice became obese and developed metabolic syndrome -- a cluster of symptoms that include unhealthy cholesterol levels, too much fat around the midsection, high blood pressure and insulin resistance.

Insulin resistance means the body does not use insulin effectively to break down food and Gewirtz believes this may be the key.

PREVIOUS RESEARCH

The researchers remembered a recent study in which normal, slender mice became obese when fed gut bacteria from fat mice.

They worked with that team, including Ruth Ley of Cornell University in New York, to see what role the gut bacteria may be playing.

"What we think is that the mice are prone to intestinal inflammation," Gewirtz said. "If you have a lot of inflammatory signals about, insulin won't work properly."

Weeks of antibiotic therapy helped, and so did diets.

"If we limit their food intake they are mostly OK; they certainly are no longer obese," he said. "They are, however, insulin-resistant."

Gewirtz's team is now working to see if they can identify the micro-organisms involved. They are also working to see if obese people have unique patterns of gut bacteria.

Scientists know that hundreds of species of bacteria live in the gut and an average person carries about 5 pounds (2 kg) worth. On Wednesday, Chinese scientists reported in the journal Nature that they found 1,000 different species in human intestines.

So could you treat obesity by taking an antibiotic to wipe out the offending germs that are making people overeat?

"It is very hard to replace the bacteria that you have," Gewirtz said. Studies already show it is difficult to treat conditions like Crohn's disease, even with months of antibiotics.

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WASHINGTON (Reuters) – Can't lose weight on a low-fat diet? Maybe you need to cut carbs instead, and a new genetic test may point the way, maker Interleukin Genetics Inc reported on Wednesday.

The small study of about 140 overweight or obese women showed that those on diets "appropriate" for their genetic makeup lost more weight than those on less appropriate diets, researchers told an American Heart Association meeting.

"The potential of using genetic information to achieve this magnitude of weight loss without pharmaceutical intervention would be important in helping to solve the pervasive problem of excessive weight in our society," Christopher Gardner at Stanford University in California, who worked on the study, said in a statement.

Massachusetts-based Interleukin's $149 test looks for mutations in three genes, known as FABP2, PPARG and ADRB2.

The company says 39 percent of white Americans have the low-fat genotype, 45 percent have the type that responds best to a diet low in processed carbohydrates and an unlucky 16 percent have gene mutations that mean they have to watch both fat and processed carbohydrates.

The researchers randomly assigned around 140 women to one of four diets -- the low-carb Atkins diet, the ultra low-fat Ornish diet, the very low-fat LEARN diet or the more balanced Zone diet.

Interleukin went back and tested about 100 of the women for their DNA by using a cheek swab and then looked to see if the women on the "right" diets lost more weight.

MOST EFFECTIVE MATCHES

Over a year, people on diets appropriate to their genetic makeup, as determined by the test, lost 5.3 percent of body weight. People on mismatched diets lost 2.3 percent, the Stanford researchers told the meeting.

Cholesterol levels improved in line with weight loss, they said.

The company said the test looks for genes that affect metabolism.

"One of the gene variations affects absorption of fats from the intestine," Ken Kornman, chief scientific officer at Interleukin, said in a telephone interview. He said people with that particular mutation absorb more fat from their food and thus should avoid fat if they want to lose weight.

Another of the variations affects insulin response -- the body's production of insulin to metabolize sugar, he said. Simple carbohydrates such as sugar and processed flour stimulate people with that particular gene type to store more of the energy as fat.

Ten percent to 16 percent of people have both mutations, and must watch both carbs and fat, Kornman said.

"What we don't know is if they are on the right diet for their genotype whether it affects satiety or feeling full," he said. He said the company planned broader studies to ask these questions.

Interleukin markets the test under the brand name Inherent Health. It also can test who might best lose weight in response to exercise.

(Editing by Xavier Briand and Todd Eastham)

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WASHINGTON (Reuters) – Can't lose weight on a low-fat diet? Maybe you need to cut carbs instead, and a new genetic test may point the way, maker Interleukin Genetics Inc reported on Wednesday.

The small study of about 140 overweight or obese women showed that those on diets "appropriate" for their genetic makeup lost more weight than those on less appropriate diets, researchers told an American Heart Association meeting.

"The potential of using genetic information to achieve this magnitude of weight loss without pharmaceutical intervention would be important in helping to solve the pervasive problem of excessive weight in our society," Christopher Gardner at Stanford University in California, who worked on the study, said in a statement.

Massachusetts-based Interleukin's $149 test looks for mutations in three genes, known as FABP2, PPARG and ADRB2.

The company says 39 percent of white Americans have the low-fat genotype, 45 percent have the type that responds best to a diet low in processed carbohydrates and an unlucky 16 percent have gene mutations that mean they have to watch both fat and processed carbohydrates.

The researchers randomly assigned around 140 women to one of four diets -- the low-carb Atkins diet, the ultra low-fat Ornish diet, the very low-fat LEARN diet or the more balanced Zone diet.

Interleukin went back and tested about 100 of the women for their DNA by using a cheek swab and then looked to see if the women on the "right" diets lost more weight.

MOST EFFECTIVE MATCHES

Over a year, people on diets appropriate to their genetic makeup, as determined by the test, lost 5.3 percent of body weight. People on mismatched diets lost 2.3 percent, the Stanford researchers told the meeting.

Cholesterol levels improved in line with weight loss, they said.

The company said the test looks for genes that affect metabolism.

"One of the gene variations affects absorption of fats from the intestine," Ken Kornman, chief scientific officer at Interleukin, said in a telephone interview. He said people with that particular mutation absorb more fat from their food and thus should avoid fat if they want to lose weight.

Another of the variations affects insulin response -- the body's production of insulin to metabolize sugar, he said. Simple carbohydrates such as sugar and processed flour stimulate people with that particular gene type to store more of the energy as fat.

Ten percent to 16 percent of people have both mutations, and must watch both carbs and fat, Kornman said.

"What we don't know is if they are on the right diet for their genotype whether it affects satiety or feeling full," he said. He said the company planned broader studies to ask these questions.

Interleukin markets the test under the brand name Inherent Health. It also can test who might best lose weight in response to exercise.

(Editing by Xavier Briand and Todd Eastham)

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WEDNESDAY, March 3 (HealthDay News) -- Wondering if you'd do better to cut carbs or fats to lose weight? A DNA test using a cheek swab may reveal which approach would work best for you, new research suggests.

Researchers from Stanford University used data on a study from 2007 in which 138 overweight or obese women were assigned to one of four popular diets for a year. The diets included: the Atkins diet (very low carbohydrate), the Zone diet (low carbohydrate), the Ornish diet (very low fat) or a health professional's diet (a low-fat diet that generally follows the U.S Agriculture Department's Food Pyramid). The women also had the inside of their cheeks swabbed to collect a DNA sample.

Researchers used the genetic information to assign women to a "genotype-appropriate" diet, an eating plan that would seem to be the most effective for them given their particular genetic makeup.

Women assigned to the correct diet based on their genotype lost two to three times more weight at 12 months than those who were assigned to a diet that was inappropriate. When the researchers looked at only the most extreme diets (Atkins versus Ornish), the results were even more stark. Women assigned to their correct diet for their genotype lost five times as much weight as those on the incorrect diet, the study found.

The women on the correct diets also showed improvements in their "good" (HDL) cholesterol and decreases in harmful triglycerides.

"The weight loss differences between the various diets were not that dramatic, but the weight loss difference within a particular diet was," said lead study author Mindy Dopler Nelson, a Stanford postdoctoral research fellow. "On each diet, there were a lot who lost weight, there were a lot who didn't lose weight and there were even some that gained weight. By looking at the genetics we were able to see it was less the particular diet than the individual's response to the diet."

The study was to be presented Wednesday at the American Heart Association's Nutrition, Physical Activity and Metabolism Conference 2010, in San Francisco.

The DNA test, made by Interleukin Genetics in Waltham, Mass., sells for $149. It works by honing in on certain genes that play a role in the way people metabolize food, said Lew Bender, CEO of Interleukin Genetics.

From among hundreds of genes believed to be involved with obesity, researchers from Interleukin Genetics identified three genes that had been implicated in multiple clinical studies to play a role in weight management. The genes include fatty acid binding protein 2, peroxisome proliferator- activated receptor gamma, and beta 2 adrenergic receptor, Bender said.

"We went through a rigorous scientific process to find those that were the most validated and the most functional, and these were the three," he said.

In those genes, a so-called single nucleotide polymorphism -- or a variation of a DNA sequence within a gene fragment -- causes the gene to produce a form of protein that changes the way it functions. In the case of fatty acid binding protein 2, for example, the polymorphism leads to the production of a protein that can cause a greater absorption of fat, Bender said.

"If you look at someone who has a polymorphism that causes them to absorb more fat, combined with another polymorphism that causes them to not burn fat well, they would be more prone to obesity from diets that are high in fat," he said. "In those cases, we would recommend they go on a low-fat diet."

Dr. Robert Eckel, past president of the American Heart Association and a professor of medicine at University of Colorado School of Medicine, said the study results were very preliminary and had to be confirmed by larger studies before he would recommend that anyone have their diet genotyped.

"The three genes they have identified are all genes that could affect energy balance, and the idea that polymorphisms in these genes could affect energy balance is of interest scientifically," Eckel said. "This could explain small differences in the way people respond to diet. But right now the most important predictor of successful dieting is compliance."

Stanford's Nelson, a nutritional scientist, said she was encouraged by the findings but not surprised. During her career, she's seen wide variations in weight loss among people assigned to identical diets. Some results could be explained by how well people adhered to the diet, but not all, she said.

"You do need to be on a reduced-calorie diet. You still need to eat healthy. But there is a difference in how people process calories," Nelson said. "Knowing your genotype is just one more tool to help the weight-loss process."

Interleukin Genetics has applied for a patent on the DNA test, Bender said.

More information

For tips on losing weight, visit the U.S. National Library of Medicine.

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