Of (Fat) Mice and Men
Public interest was aroused by the 1995 announcement by Rockefeller University geneticist Jeffrey Friedman, M.D., of a genetic mutation in obese mice. The researchers believe this gene influences development of a hormone that tells the organism how fat or full it is. Those with the mutation may not sense when they have achieved satiety or if they have sufficient fatty tissue, and thus can’t tell when to stop eating.
The researchers also reported finding a gene nearly identical to the mouse obesity gene in humans. The operation of this gene in humans has not yet been demonstrated, however. Still, professionals like University of Vermont psychologist Esther Rothblum, Ph.D., reacted enthusiastically: “This research indicates that people really are born with a tendency to have a certain weight, just as they are to have a particular skin color or height.”
Actually, behavioral geneticists believe that less than half of total weight variation is programmed in the genes, while height is almost entirely genetically determined. Whatever role genes play, America is getting fatter. A survey by the Center for Disease Control found that obesity has increased greatly over the last 10 years. Such rapid change underlines the role of environmental factors, like the abundance of rich foods, in America’s overeating. The CDC has also found that teens are far less physically active than they were even a decade ago.
Certainly people metabolize food differently and some gain weight more easily than others. Nonetheless, anyone placed in a food-rich environment that encourages inactivity will gain weight, whatever fat genes the person has. But, in nearly all environments, highly motivated people can maintain lower weight levels. We thus see that social pressure, self-control, specific situations — even seasonal variations — combine with physical make-up to influence diet and determine weight.
Accepting that weight is predetermined can relieve guilt for overweight people. But people’s belief that they cannot control their weight can itself contribute to obesity. No test will ever be performed that can tell you how much you must weigh. Personal choices will always influence the equation. And anything that inspires positive efforts at weight control can help people lose weight, or avoid gaining more.
The case of obesity — along with schizophrenia, depression, and alcoholism — raises a striking paradox. At the same time that we now view these conditions as diseases that should be treated medically, their prevalence is growing precipitously. The very reliance on drugs and other medical treatments has created a cultural milieu that seeks external solutions for these problems. Relying on external solutions may itself be exacerbating matters; it may be teaching us a helplessness that is at the root of many of our problems. Instead of reducing the incidence of these problems, this seems to have fueled their growth.
In 1993, the gene that determines the occurrence of Huntington’s disease, an irreversible degeneration of the nervous system, was discovered. In 1994, a gene was identified that leads to some cases of breast cancer. Utilizing these discoveries, however, is proving more difficult than anticipated. Finding a gene for breast cancer was cause for elation. But of all the women with breast cancer, only a tenth have family histories of the disease. Furthermore, only half of this group has the gene mutation. Scientists also hoped that breast cancer victims without family histories would show irregularities at this same site on the DNA. But only a small minority do. The section of the DNA involved in inherited breast cancers is enormously large and complex. There are probably several hundred forms of the gene. The task of determining which variations in the DNA cause cancer, let alone developing therapies to combat the disease, is tremendous. Right now, women who learn that they have the gene defect know they have a high (85 percent) likelihood of developing the disease. But the only decisive response available to them is to have their breasts removed before the disease appears. And even this does not eliminate the possibility of cancer.
The failure to translate genetic discoveries into treatments has also been true for Huntington’s disease. Scientists have been unable to detect how the flawed gene switches on dementia and palsy. These difficulties with a disease created by an individual gene show the monumental complexity involved in unraveling how genes determine human traits.
When a distinct gene is not involved, linking genes to traits may well be an absurdity. Any possible link between genes and traits is exponentially more complex with elaborate behavior patterns like over-drinking, personality characteristics like shyness or aggressiveness, or social attitudes such as political conservatism and religiousness. Many genes might be involved in all such traits. It is impossible to separate the contributions environment and DNA make to attitudes and behaviors.
Peele, S. (2007). My Genes Made Me Do It. Psych Central. Retrieved on May 23, 2013, from http://psychcentral.com/lib/2007/my-genes-made-me-do-it/
Last reviewed: By John M. Grohol, Psy.D. on 30 Jan 2013
Published on PsychCentral.com. All rights reserved.