Dieting does not work, researchers report / Gene deficiency is a protective barrier to obesity

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Dieting does not work, researchers report Will you lose weight and keep it

off if you diet? No, probably not, UCLA researchers report in the April issue of

American Psychologist, the journal of the American Psychological Association.

 

" You can initially lose 5 to 10 percent of your weight on any number of diets,

but then the weight comes back, " said Traci Mann, UCLA associate professor of

psychology and lead author of the study. " We found that the majority of people

regained all the weight, plus more. Sustained weight loss was found only in a

small minority of participants, while complete weight regain was found in the

majority. Diets do not lead to sustained weight loss or health benefits for the

majority of people. "

 

Mann and her co-authors conducted the most comprehensive and rigorous analysis

of diet studies, analyzing 31 long-term studies.

 

" What happens to people on diets in the long run? " Mann asked. " Would they have

been better off to not go on a diet at all? We decided to dig up and analyze

every study that followed people on diets for two to five years. We concluded

most of them would have been better off not going on the diet at all. Their

weight would be pretty much the same, and their bodies would not suffer the wear

and tear from losing weight and gaining it all back. "

 

People on diets typically lose 5 to 10 percent of their starting weight in the

first six months, the researchers found. However, at least one-third to

two-thirds of people on diets regain more weight than they lost within four or

five years, and the true number may well be significantly higher, they said.

 

" Although the findings reported give a bleak picture of the effectiveness of

diets, there are reasons why the actual effectiveness of diets is even worse, "

Mann said.

 

Mann said that certain factors biased the diet studies to make them appear more

effective than they really were. For one, many participants self-reported their

weight by phone or mail rather than having their weight measured on a scale by

an impartial source. Also, the studies have very low follow-up rates — eight of

the studies had follow-up rates lower than 50 percent, and those who responded

may not have been representative of the entire group, since people who gain back

large amounts of weight are generally unlikely to show up for follow-up tests,

Mann said.

 

" Several studies indicate that dieting is actually a consistent predictor of

future weight gain, " said Janet Tomiyama, a UCLA graduate student of psychology

and co-author of the study. One study found that both men and women who

participated in formal weight-loss programs gained significantly more weight

over a two-year period than those who had not participated in a weight-loss

program, she said.

 

Another study, which examined a variety of lifestyle factors and their

relationship to changes in weight in more than 19,000 healthy older men over a

four-year period, found that " one of the best predictors of weight gain over the

four years was having lost weight on a diet at some point during the years

before the study started, " Tomiyama said. In several studies, people in control

groups who did not diet were not that much worse off — and in many cases were

better off — than those who did diet, she said.

 

If dieting doesn't work, what does?

 

" Eating in moderation is a good idea for everybody, and so is regular exercise, "

Mann said. " That is not what we looked at in this study. Exercise may well be

the key factor leading to sustained weight loss. Studies consistently find that

people who reported the most exercise also had the most weight loss. "

 

Diet studies of less than two years are too short to show whether dieters have

regained the weight they lost, Mann said.

 

" Even when you follow dieters four years, they're still regaining weight, " she

said.

 

One study of dieting obese patients followed them for varying lengths of time.

Among those who were followed for fewer than two years, 23 percent gained back

more weight than they had lost, while of those who were followed for at least

two years, 83 percent gained back more weight than they had lost, Mann said. One

study found that 50 percent of dieters weighed more than 11 pounds over their

starting weight five years after the diet, she said.

 

Evidence suggests that repeatedly losing and gaining weight is linked to

cardiovascular disease, stroke, diabetes and altered immune function. Mann and

Tomiyama recommend that more research be conducted on the health effects of

losing and gaining weight, noting that scientists do not fully understand how

such weight cycling leads to adverse health effects.

 

Mann notes that her mother has tried different diets, and has not succeeded in

keeping the weight off. " My mother has been on diets and says what we are saying

is obvious, " she said.

 

While the researchers analyzed 31 dieting studies, they have not evaluated

specific diets.

 

Medicare raised the issue of whether obesity is an illness, deleting the words

" Obesity is not considered an illness " from its coverage regulations in 2004.

The move may open the door for Medicare to consider funding treatments for

obesity, Mann noted.

 

" Diets are not effective in treating obesity, " said Mann. " We are recommending

that Medicare should not fund weight-loss programs as a treatment for obesity.

The benefits of

dieting are too small and the potential harm is too large for dieting to be

recommended as a safe, effective treatment for obesity. "

 

From 1980 to 2000, the percentage of Americans who were obese more than doubled,

from 15 percent to 31 percent of the population, Mann noted.

 

A social psychologist, Mann, taught a UCLA graduate seminar on the psychology of

eating four years ago. She and her students continued the research when the

course ended. Mann's co-authors are Erika Westling, Ann-Marie Lew, Barbra

Samuels and Jason Chatman.

 

" We asked what evidence is there that dieting works in the long term, and found

that the evidence shows the opposite " Tomiyama said.

 

Source: University of California - Los Angeles

http://www.physorg.com/news94906931.html

 

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Gene deficiency is a protective barrier to obesity A search for the

molecular clues of longevity has taken Mayo Clinic researchers down another path

that could explain why some people who consume excessive calories don’t gain

weight. The study, which was done in laboratory mouse models, points to the

absence of a gene called CD38. When absent, the gene prevented mice on high-fat

diets from gaining weight, but when present, the mice became obese.

 

The findings were published this month in the online issue of The FASEB

Journal, the journal of the Federation of American Societies for Experimental

Biology. The study will appear in the November 2007 print issue of the journal.

 

“Obesity is a complex problem compounded by multiple factors, one of which is

our genes. Genes play a role in about 50 percent of cases, and in this study, we

demonstrate that CD38 regulates body weight,” states Eduardo Chini, M.D., Ph.D.,

an anesthesiologist at Mayo Clinic and corresponding author of the study.

 

Identifying the signaling mechanisms that lead to obesity caused by a high-fat,

high-calorie diet is a critical part of understanding and developing new

treatments for obesity, Dr. Chini says.

 

Research in animal models has shown that caloric restriction can lower

cholesterol and blood pressure -- often considered the biomarkers of aging. In

addition, published research in animal models shows that caloric restriction,

defined as consuming 30 percent to 40 percent less than your average daily

intake, can turn on the SIRT1 gene, one of a family of seven genes linked to

longevity.

 

In addition, recent studies have shown that the chemical receptor PGC1

(peroxisome proliferator-activated receptor coactivator) plays a key role in the

development of obesity and control of metabolism. The SIRT genes activate PGC1

and in doing so, can offset the negative effects of obesity -- at least in mice.

But how the SIRT-PGC1 reaction works, hasn’t quite been explained until now.

 

In previous laboratory studies by the Mayo Clinic research team, CD38 was shown

to be involved in regulating a wide variety of signaling pathways, such as those

that regulate energy metabolism. In addition, recent studies in humans also show

a possible connection between CD38 and metabolism, specifically metabolic

syndrome. Metabolic syndrome includes metabolic-related health issues that

usually afflict people who are obese. These health issues include high blood

pressure, elevated insulin levels and high cholesterol levels.

 

In this study, researchers investigated and confirmed that CD38 inhibits SIRT

and the expression of PGC1 in mouse models and, as a result, regulates body

weight. In the absence of CD38, the SIRT-PGC1 pathway was activated and

protected mice models from developing obesity.

 

Researchers studied two groups of mice: one with the gene CD38 and the other

without. Each group was fed a high-calorie diet with 60 percent of calories from

fat. In a second test, each group was fed a standard diet in which 4 percent of

calories came from fat.

 

As a result, the body fat of mice that carried CD38 and were on a high-fat diet

nearly quadrupled and their body weight almost doubled. After eight weeks on a

high-fat diet, mice with CD38 began to show signs of glucose intolerance, one of

the first indicators of diabetes onset. In addition, this group of mice lived

for only four-to-six months compared to the second group of mice that lived for

12 months.

 

For the group of mice that did not carry CD38, their body fat and weight did not

change even though they were on a high fat diet. These mice burned more energy,

were leaner and otherwise healthy.

 

“These changes contributed to the ability of these mice to fend off weight gain

despite a high-fat diet and lack of exercise. Together these results suggest

that a CD38 deficiency has a protective effect against high-fat, diet-induced

obesity,” Dr. Chini says.

 

Dr. Chini and colleagues also examined the effects of resveratrol in mice.

Resveratrol is a naturally occurring substance found in some plants such as

mulberries, peanuts and red grapes used to make wine. It has been marketed as a

drug that mimics the effects of moderate exercise without the physical act of

exercising and also as a longevity drug, despite the lack of evidence that

resveratrol is safe and effective in humans.

 

Mice with CD38 were treated with 30 milligrams (mg) of resveratrol per day. And,

to determine the effects of the SIRT genes on obesity, mice without CD38

received the same dose of sirtinol, a drug that shuts down the SIRT genes.

 

Researchers found that mice with CD38 that were treated with resveratrol for two

weeks were protected from high-fat, diet-induced obesity. By contrast, the

protective effect against high-fat, diet-induced obesity in the absence of CD38

in mice was invalidated by sirtinol. Mice without CD38 that were treated with

sirtinol gained a statistically significant amount of weight when compared with

mice without the gene who were not treated with sirtinol.

 

This data supports the novel notion that CD38 modulates high-fat, diet-induced

obesity by a SIRT- dependent mechanism.

 

“Together these results identify a novel pathway regulating body weight and

clearly show that CD38 is a nearly obligatory component of the cellular cascade

that led to diet-induced obesity,” the authors write.

 

The authors say the study’s results are promising and should be explored in

follow-up studies that will focus on the quality of life and longevity in mice.

 

Source: Mayo Clinic

http://www.physorg.com/news102080220.html

 

 

 

" A trail blazed by an elephant becomes a roadway. " Burmese proverb

 

" The care of the Earth is our most ancient and most worthy, and after

all our most pleasing responsibility. To cherish what remains of it and to

foster its renewal is our only hope. " Wendell Berry

 

 

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