In fact, people with FTO tend to weigh 6. Our bodies were made to be flexible and change based on environment and how we treat them. These types of results take time and effort on your part, but it means that you have the power to sculpt your very own genetic makeup.
Save my name, email, and website in this browser for the next time I comment. All Rights Reserved. Privacy Policy. Home - Salk News - Are genes our destiny? Salk Scientists discover "hidden" code in DNA evolves more rapidly than genetic code.
While the study was limited to a single plant species called Arabidopsis thaliana, the equivalent of the laboratory rat of the plant world, the findings hint that the traits of other organisms, including humans, might also be dramatically influenced by biological mechanisms that scientists are just beginning to understand. The more biologists map the genomes of various organisms their entire genetic code , the more they are discovering discrepancies between what the genetic code dictates and how organisms actually look and function.
In fact, many of the major discoveries that led to these conclusions were based upon studies in plants. There are traits such as flower shape and fruit pigmentation in some plants that are under the control of this epigenetic code.
Such traits, which defy the predictions of classical Mendelian genetics, are also found in mammals. In some strains of mice, for instance, a tendency for obesity can pass from generation to generation, but no difference between the genetic code of fat mice and thin mice explains this weight difference. Scientists have even found that identical human twins exhibit different biological traits, despite their matching DNA sequences.
They have theorized that such unexplained disparities could be the work of epigenetic variation. Ecker and other scientists have traced these mysterious patterns to chemical markers that serve as a layer of genetic control on top of the DNA sequence.
This article briefly outlines the contributions of genes and gene-environment interactions to the development of obesity. Several rare forms of obesity result from spontaneous mutations in single genes, so-called monogenic mutations.
Such mutations have been discovered in genes that play essential roles in appetite control, food intake, and energy homeostasis-primarily, in genes that code for the hormone leptin, the leptin receptor, pro-opiomelanocortin, and the melanocortin-4 receptor, among others.
Obesity is also a hallmark of several genetic syndromes caused by mutation or chromosomal abnormalities, such as Prader—Willi and Bardet-Biedl syndromes. In these syndromes, obesity is often accompanied by mental retardation, reproductive anomalies, or other problems. In the 21st century, obesity is a health problem affecting rich and poor, educated and uneducated, Westernized and non-Westernized societies.
Body fat level varies from person to person, however, and some people have always tended to carry a bit more body fat than others. Evidence from animal models, human linkage studies, twin studies, and association studies of large populations suggests that this variation in our susceptibility to obesity has a genetic component.
But rather than being controlled by a single gene, susceptibility to common obesity is thought to be affected by many genes polygenic. Twin studies offer some insight into the genetics of common obesity. Based on data from more than 25, twin pairs and 50, biological and adoptive family members, the estimates for mean correlations for body mass index BMI are 0. These studies can be used to find gene variations that play a role in common, complex diseases such as obesity.
The second obesity-associated gene variant that researchers identified lies on chromosome 18, close to the melanocortin-4 receptor gene the same gene responsible for a rare form of monogenic obesity. To date, genome-wide association studies have identified more than 30 candidate genes on 12 chromosomes that are associated with body mass index. Genetic changes are unlikely to explain the rapid spread of obesity around the globe.
It takes a long time for new mutations or polymorphisms to spread. So if our genes have stayed largely the same, what has changed over the past 40 years of rising obesity rates? Our environment: the physical, social, political, and economic surroundings that influence how much we eat and how active we are.
Environmental changes that make it easier for people to overeat, and harder for people to get enough physical activity, have played a key role in triggering the recent surge of overweight and obesity. Work on obesity-related gene-environment interactions is still in its infancy. Rather, it seems that eating a healthy diet and getting enough exercise may counteract some of the gene-related obesity risk.
In , for example, Andreasen and colleagues demonstrated that physical activity offsets the effects of one obesity-promoting gene, a common variant of FTO. The study, conducted in 17, Danes, found that people who carried the obesity-promoting gene, and who were inactive, had higher BMIs than people without the gene variant who were inactive.
Having a genetic predisposition to obesity did not seem to matter, however, for people who were active: Their BMIs were no higher or lower than those of people who did not have the obesity gene. Subsequent work on the relationship between the FTO gene, physical activity, and obesity yielded contradictory results.
But once again, being physically active lowered the risk: Active adults who carried the obesity-promoting gene had a 30 percent lower risk of obesity than inactive adults who carried the gene.
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