Posted on 01/04/2010 11:24:33 PM PST by neverdem
Obesity is a disease of excess, but a new study suggests that a few obese patients are actually lacking something--a piece of one of their chromosomes. The loss might remove a gene that helps the body manage blood sugar and appetite.
Obesity runs in families, and researchers have identified several genetic variants that seem to boost the odds of becoming obese. However, these variants only explain a minority of cases. In the last decade, researchers have discovered that genetic differences among people can stem from lost or duplicated sections of chromosomes, called copy number variants (CNVs). Because of CNVs, for example, you and your neighbor might carry different numbers of copies of particular genes. Previous studies have implicated CNVs in disorders such as autism that slow mental development or cause learning disabilities. Autistic patients sometimes have an extra segment on chromosome 15 or are missing a section of chromosome 16. Such patients are often heavy as well, suggesting a connection between CNVs and weight.
To search for that link, endocrinologist Sadaf Farooqi of the University of Cambridge in the U.K. and colleagues analyzed the genomes of 300 extremely obese children for missing or duplicated chromosome segments. As the team reports online this week in Nature, a number of CNVs were more common in the children than in a group of normal-weight people. The most prevalent of these was a deletion from chromosome 16, which occurred in 1.7% of the obese children but only 0.027% of controls. The same deletion also turned up in a separate group of more than 1000 heavyset children. Three subjects with this CNV inherited it from parents who were also obese, the researchers found. "This study shows for the first time that CNVs can cause a metabolic disease like obesity," says Farooqi.
The work also provides a clue about how. The missing segment of chromosome 16 holds nine genes, including one, known as SH2B1, that scientists had already fingered as a possible culprit in obesity. Mice lacking the gene become extremely fat and develop insulin resistance, a feature of obesity and diabetes in which cells become less responsive to insulin. SH2B1 is a key intermediary that enables insulin and leptin, a hormone that helps set appetite, to transmit their messages to cells.
"Given the biological plausibility, it seems to be an exciting finding," says geneticist Alan Herbert of Boston University School of Medicine. However, he cautions, it's too early to rule out the other eight genes on the deleted segment. The CNV on chromosome 16 is rare, and the search is on for other variants that contribute to obesity. "What it tells us," says Farooqi, "is that there is a lot more genetic variation to find."
FReepmail me if you want on or off the diabetes ping list.
It moves me to wonderment how a guy can eat like a pig and still be skinny as a rail, until a few decades have gone by. Then he eats like a bird and becomes as fat as a pig.
As you age your metabolism slows. Also there’s the matter of your own behavior, most athletes gain a bunch of weight right after retirement because they keep eating like they’re spending 6 hours a day at practice and in the weight room but they aren’t spending 6 hours a day at practice and in the weight room.
Lose Jeans, lose weight would seem to be a better alternative.
Alas, there is almost always a downside to everything. Recent studies show that older women who take large doses of vitamin C develop cataracts faster.
The body reacts to everything we do to it. Some of the results are good and some are bad. Nothing is without some kind of side effect.
Because that first diet sets off a chain reaction that screws up your body and your ability to just eat normally forever. People who are naturally thin never give eating a second thought. They don’t obsess over it as we chunky folks do who have been trying to regulate our eating for many years.
(The following is from an article about a device called a Mandometer in the European Eating Disorders Review 12, 333-336 yr. 2004)
“In our framework, reduced food intake and enhanced physical activity are the principle risk factors for eating disorders, rather than an unspecified mental disorder. In support of this notion are data collected by Keys and collaborators, who decreased the food available to mentally and physically healthy men. These men developed most of the symptoms of eating disorder, including the psychiatric symptoms (Keys, Brozek, Henschel, Mickelsen, & Taylor, 1950)
...the behavioral, physiological and psychological changes in eating disorders are the result of eating too little, rather than its cause. To treat the problem we retrain affected individuals to eat normally via continual feedback about their food intake during meals and as they learn to eat normally, the symptoms of their mental disorders disappear.”
Once again, it turns out that correlation is not the same as causation. For years, everyone thought that mental issues caused eating disorders. It turns out that restrictive eating causes mental problems. Well, duh! When you take something that ought to be natural and spontaneous (eating) and micro-manage it, it will make you nutty, just as trying to keep track of every breath you take and ration those would drive you bonkers.
Obsessing about weight is the first step on the road to ruin. The next one is restrictive eating (dieting or what we now call “healthy eating” - it’s still a blasted diet). Too bad it’s the #1 national pastime. I wonder how much we would weigh if we had never started down the diet path in the first place?
Dieting might even prove to be the spark that initiates the metabolic changes that eventually result in the development of type 2 diabetes. Wouldn’t that be a bummer?
Maybe people just shouldn’t obsess on it. I burned off 70 pounds a couple of years ago and have kept it off. But I don’t obsess, I just remind myself that I know better. There was behavior that led to be being over 250 pounds that I knew then was bad but I did it anyway, now I don’t, or if I do I know it’s a “being bad” thing and I’ll have to pay for it on the treadmill later.
Diets are bad because diets are temporary. People diet down to their target weight and then go back to normal forgetting that “normal” was heavier than the wanted to be. If you want to get rid of pounds and keep them off you have to change how you are, in my case that meant stop being the guy that grabs a bag of Doritos and a book and sees which one he can finish first and start being a guy who might have a small snack (yes including possibly Doritos) while reading but only if I’m actually hungry; stopped being the guy who cleans the plate at every meal and started being the guy that stops eating when the food has accomplished the goal; stopped being the guy for whom getting out of bed is the most strenuous activity of the day and started being the guy who swims, bikes, runs, and lifts weights. But no obsession, just the new lifestyle of knowing I prefer to weigh 185 pounds vs 254 and in order to be that there are things that need to be done. Kind of like how in order to be the guy with some money instead of the guy that was always broke I needed to go back to school and get on a career path and now continue to be good at my better paying job.
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