Genotype and Lifestyle Influence on Obesity

Body Mass Index

A number used to represent fatness. Calculated using height and weight.

Waist to Hip Ratio

The circumference of the waist over the circumference of the hip.

Environmental

Factors

Factors that include foods available, health care, places to exercise, and other things outside an individual’s control.

Lifestyle Choices

Choices within an individual’s control to eat, exercise, go the doctor, etc. made within the context of the environment.

Genotype Body traits transferred by genetic code.

Comorbidites Diseases highly correlated with other conditions

Lexicon of Obesity

AbstractObesity and its comorbidites have reached epidemic levels in the United States and other parts of the world. Current research indicates that genes play a far more active role than previously thought and hold new promise as treatment options. An assessment of recent scientific peer-reviewed literature shows the heritability of obesity by examining genotypes and pleiotrophy in cases of obesity. The prevalence of genotypic influence in obese children and adults is strong. Current research indicate that if genotypes and the pleiotrophies responsible for obesity could be turned off then obesity could be treated in cases where changes in diet and exercise have failed.

MethodObesity research was reviewed that investigated lifestyle choices and genotypes. From there, I searched peer-reviewed journals for articles that focused on the genetic heritability of obesity and its relative importance compared to lifestyle causes. I then surveyed articles reviewing treatments of obesity that counter the effects of genotypes.

ResultsThe scientific community has long hypothesized that a “thrifty genotype” exists. That would be a holdover from the Homo sapiens past to ward off starvation by gaining weight in times of copious foodstuffs (1). BMI and WHRs ratios are the phenotypes used in finding corresponding genes responsible for the heritability of obesity (2). A French study indicated linkage of childhood obesity with genes on six chromosomes. Children younger than two with high BMIs and poor WHRs exhibited an adiposity rebound, a return of fat, while children without those traits did not. 30% of children who experienced the rebound eventually became obese (3). The Viva la Familia Study found the coefficients of heritability for body composition traits like BMI and WHRs ratios ranged from 0.18 to 0.35. Sex, age, and environmental covariates accounted for none to all of the phenotypic variance in the population (4).

None of the 70 associations brought forth in articles between BMI and common genetic variants have been consistently replicated. Studies’ assertions are hard to accept and require extensive independent testing before acceptance as a generalizable phenomenon or fact. A variety of studies estimate the heritability of obesity to range from 30% to 70%. A typical estimate is 50% of all phenotypic variation (5), (6).

DiscussionI hypothesized that lifestyle choices would have a far greater impact on obesity than genetic forces, but realize that the problem does not exist in such dichotomous terms. The environment interacting with an individual’s genetic code causes obesity. Genotypes affect how the body reacts to the environment and the ease of changing phenotypes. Currently the genes responsible for obese phenotypes are difficult to identify and most associations reported in studies are either very hard to replicate or are just wrong (1). If the genes are discovered, and we understand the root causes of obesity, new therapies may be an option. These will provide new strategies to help people become or keep fit.

1. Hill, James O. 1998. “Genetic and Environment Contribution to Obesity” American Journal of Clinical Nutrition. Vol. 98 991-9922. Comuzzie, Anthony G. Allison David B. 1998 “The Search for Human Obesity Genes.” Science. Vol. 280 1374-1377 3. Dina, Christian; Delplanque, Delplanque, Jérome; Durand, Emmanuelle; Francke, Stephan; Froguel, Philippe; Lecoeur, Cécile; Meyre, David; Vatin, Vicent; Weill, Jacques. “A Genome-Wide Scan for Childhood Obesity-Associated Traints in French Families Shows Significant Linkage on Chromosome 6q22.31q23.2.” 2004 Diabetes Vol. 53 803-811.4. Butte, Nace F; Cai, Guowen; Shelly, Cole A; Comuzzie, Anthony G. “Viva la Familia Study: Genetic and Environmental Contributions to Childhood Obesity and it Comorbidities in the Hispanic Population.” American Journal of Clinical Nutrition. 2006 Vol. 84 646-6545. Allison DB, Kaprio J, Korkeila M, Koskenvuo M, Neale MC, Hayakawa K. “The heritability of body mass index among an international sample of monozygotic twins reared apart.” International Journal of Obesity and Related Metabolism Disorders 1996 Vol. 20 501–66. llison DB, Faith MS, Nathan JS. “Risch's lambda values for human obesity.” International Journal of Obesity and Related Metabolism Disorders 1996 Vol. 20 990–9

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Introduction Obesity has become an epidemic in the United States of America. Quality of life suffers as the disease progresses. Comorbidites like type 2 diabetes and heart disease appear at far higher rates in those who are obese. The Body Mass Index (BMI) and Waist to Hip Ratios (WHRs) are two measures used to determine healthy weights for individuals. Research is investigating the impact of environmental factors and the heritability of BMIs and WHRs. Coefficients of heritability, a number to describe the rate at which some traits are dependent on genotypes, is being sought. Some type of Pleiotrophy, a single gene affecting more than one phenotypic characteristic, is also thought to interact with BMIs and WHRs in a meaningful manner. The degree genotypes and environmental factors cause obesity independent of each other is not clear. I have surveyed phenotypical analysis of people with significant risk for dangerously high BMIs and poor WHRs. I hypothesize that lifestyle choices and environmental factors are more responsible for obesity than genotypes.

Matthew AslesenBiochemistry Program, Beloit College, Beloit, WI