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| Yes | 17% | 142 votes | Total: 812 votes | |
| No | 83% | 670 votes |
Yes
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Add to FavoritesGenetics is definitely to blame for the obesity epidemic, in conjunction of course with several environmental factors pertaining to diet and physical activity. The current Western lifestyle is characterized by sedentarism and a typical feeding pattern consisting of high-energy foods, trans-fat, cholesterol, and refined carbohydrates. Red and processed meat, sweets and desserts, potatoes and French fries, and refined grains are favored, while healthier vegetable products, such as fruit, vegetables, and whole-grain cereals are often neglected.
In the light of current knowledge, the influence of genetic factors is undeniable and responsible for an innate susceptibility to developing obesity, as well as obesity-related diabetes, cardiovascular, and kidney disease. In most cases of obesity, a multitude of genes is involved. One of the most important and best studied is leptin. Leptin is a small hormone, the product of the so-called "obesity-gene", which was discovered by Friedman and co-workers in 1994.
Leptin is mainly released by fat cells (or adipocytes), and its blood level is directly linked to body fat mass; therefore, in obese individuals, leptin is found in very high amounts. This hormone has many biological functions, but the most important one is to prevent weight gain, by regulating key processes in the brain and in the fat tissue. In the brain (specifically, in the hypothalamus), leptin induces a decrease in appetite, by suppressing the release of neuropeptide Y, which is a strong promoter of food intake. In the adipocytes, leptin induces thermogenesis, i.e. burning calories to heat instead of turning them into fat. Leptin also works to decrease fat storage by lowering pancreatic insulin release and liver glucose production, and by increasing glucose metabolism.
A few years ago it was suggested that, in obese individuals, the hypothalamus might be abnormally resistant to leptin, therefore releasing high amounts of neuropeptide Y to promote hunger. More recently it has become clear that, as a matter of fact, it is not leptin resistance, but rather low leptin availability to the brain that is responsible for the inadequate activity of the hypothalamus. This concept, labeled "central leptin insufficiency syndrome", could explain the exaggerated appetite, as well as the thermogenesis, insulin secretion, and glucose metabolism abnormalities seen in obese individuals. In other words, low brain leptin levels promote both high-energy food intake and fat deposition to store this excess energy, and, therefore, they may play a key role in the development of obesity. Mutations in the leptin gene have also been described, but these are an uncommon cause of obesity.
Treatment with leptin was studied in experimental mice models, in which substantial weight loss (by 40 percent) was achieved. Leptin therapy also prevented high fat-diet-induced obesity and diabetes, and prolonged survival. Seeing these results in animals, it was suggested that brain leptin gene therapy or leptin-like drugs should further be developed and tested in humans. Such research could provide solutions to control the epidemic of obesity and obesity-associated conditions. Intensive efforts in this direction might lead to inestimable health benefits in the years to come.
Learn more about this author, Stephen Janowsky.
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No
If obesity was genetic people would always have been as obese as they are now, and obviously they were not. Obesity (defined as having a body mass index or BMI of 30 or over) is an increasing problem in almost every Western country, yet our genetic inheritance is still much the same as it has always been.
This does not mean that obesity does not have a genetic component - some people are more prone to obesity than others. Some have a slow metabolism, leading to a tendency to put on weight, and others have a fast metabolism, leading to them being able to burn up more calories. But this applied fifty years ago and a hundred years ago, and yet a much smaller percentage of people were obese than than they are at present.
There are also a few rare conditions in which obesity is directly caused by genes. These include disorders such as Bardet-Biedl syndrome and Prader-Willi syndrome, but very few people who are obese have either of these conditions. Some people also have side effects to drugs such as steroids and some anti-depressants that lead to a gain in weight.
Genetics is therefore a risk factor for obesity, but risk factors are not the cause. For some people genetic factors lead them to be more prone to becoming overweight or obese, and losing weight for them is more difficult, but they cannot become obese without eating too much, or eating the wrong things, such as too much fat.
People in the West are becoming obese at earlier ages, with childhood obesity now a major problem in many countries, and the extent of their obesity is increasing. This is much more to do with the food choices and the amount of exercise that people get than any genetic effect.
An analysis of obesity trends in the US from 1985 to 2006 (see http://www.cdc.gov/n ccdphp/dnpa/obesity/ trend/maps/index.htm
) clearly shows a dramatic increase in obesity in the USA during that period, and obviously this massive change can in no way be explained by genetic changes. The changes were mainly the same people, with the same genes, getting fatter.
Genetics does play a part in making some people more susceptible to obesity than others, and it does mean that some people have more problems losing weight than others do. But obesity is not caused by genetics except in very rare cases. It is most often caused by eating too much food, eating the wrong kinds of food, and/or exercising too little to burn off the calories consumed.
Learn more about this author, Lin Edwards.
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