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Obesity and genetics

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Research
Implications
Future research
Author information
Bibliography
Causes

Research
  • Obesity can result from disorders that have a strictly genetic basis. There is also a significant amount of research from several sources showing a link between an individual's genetic makeup and their environment and how these two factors interact to result in obesity.
  • There are several common types of studies that scientists conduct when studying the effects of genetics on obesity. The first type is called a comparison or resemblance study. Comparison or resemblance studies typically involve siblings, usually twins and adopted individuals, in order to better understand one of the two factors. For example, sets of twins reared in the same family and twins reared in different families allow the researcher to determine whether genetic or environmental factors lead to a particular condition.
  • Association studies have found that some genes serving diverse functions within the human body occur with greater frequency among the obese. These genes may have an impact on many different biological functions, including the regulation of food intake, how the body burns calories, how fat and sugar and metabolized by the body, and how fat is deposited in the body.
  • Other studies examine the outcome when a person from one culture lives in another culture; for example, Japanese people living in Japan are less likely to be obese than those who migrated to Hawaii, where obesity rates are high.
  • Many research tools can aid in understanding the genetics of obesity. These include DNA microarray, a technology that uses a gene chip and DNA probes to detect mutations in thousands of genes in one experiment. Exon arrays target exons, which are the pieces of genes that encode for a particular part of a complete protein. Tiling arrays are similar to microarrays except that they allow for all non-repetitive DNA fragments in a chromosome to be visualized at different resolutions so they can be distinguished from one another. Single nucleotide polymorphism (SNP) arrays are also a type of DNA microarray used to detect two or more different phenotypes within a population. Genotyping refers to determining the genetic makeup of an individual through DNA microarray techniques. High-throughput genotyping technology is based on the same concept as genotyping, but uses more complex and sophisticated technology. Each of these technologies has led to the development of genome-wide association studies (GWA), which identify common genetic factors that influence health and disease among different populations.
  • Current research focuses on what determines how much food people eat and how many calories they burn on a daily basis, and how genetic variability contributes to the tendency for overweight or obesity. Many studies indicate that the effect of genetics on obesity is less about variations in metabolism and more about behavior. Control of food intake may be affected by genetic variability in genes that determine the sensitivity of taste receptors or in genes that determine the level of action of several hormones shown to be involved in producing hunger or stopping hunger, including leptin, ghrelin, cholecystokinin, and related receptors.
  • Some gene targets that have been studied for their effects on obesity include GAD2, leptin, lipoprotein lipase (LPQ), melanocortin 4 receptor (MC4R), and rs110683 and rs4471028, among others.

Implications
  • Findings from research on the genetics of obesity may also help the course of other diseases, such as cardiovascular diseases, cancer, diabetes, and polycystic ovarian syndrome, in which obesity may play a role.
  • Identifying certain genetic mutations that lead to obesity may allow for a more personalized medical approach when it comes to treating this disease.

Future research
  • Future research will likely use the genetic information from various studies to predict obesity in individuals and to provide individuals with personalized medical interventions to help them control their obesity. Knowledge gained from this research may result in the sequencing of genomes, classification of terminology, the creation of publicly accessible databases, and the provision of ethical and scientific guidelines for conducting genetics-based research on obesity.
  • Many organizations and ongoing studies have been created in response to the epidemic of obesity, such as the Obesity Society and Shaping America's Health: Association for Weight Management and Obesity Prevention, both of which are scientifically based societies dedicated to the study of obesity. These organizations aim to improve the understanding of the relationship between nutrition and genetic variations and functions in obesity.
  • Other government-funded programs, particularly within the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), are working to identify genes that influence disease and related anatomical, physiological, and behavioral traits such as body fat composition and distribution, metabolic rate, energy balance, food consumption and preference, and physical activity levels. Programs are also studying patterns of gene expression associated with these traits and the mechanisms of regulating these patterns.
  • Careful attention to the difference between gene mutations, or single nucleotide polymorphisms (SNPs), that are related to obesity and that cause obesity is needed. In addition, research may uncover genes or SNPs that provide some level of protection from obesity, which highlights the need for ongoing research in both lean and obese subjects.

Author information
  • This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (www.naturalstandard.com).

Bibliography
  1. Arkadianos I, Valdes AM, Marinos E, et al. Improved weight management using genetic information to personalize a calorie controlled diet. Nutr J 2007;6:29.
  2. Bouchard C. The biological predisposition to obesity: beyond the thrifty genotype scenario. Int J Obes 2007;31(9):1337-9.
  3. Farooqi IS, O'Rahilly S. Genetic factors in human obesity. Obesity Reviews 2007;8(Suppl 1):37-40.
  4. Fox CS, Heard-Costa N, Cupples LA, et al. Genome-wide association to body mass index and waist circumference: the Framingham Heart Study 100K project. BMC Med Genet 2007;19:8(Suppl 1):S18.
  5. Genetics Home Reference. . Accessed March 11, 2008.
  6. Marshall JD, Beck S, Maffei P, et al. Alstrom syndrome. Eur J Hum Genet 2007;15(12):1193-202.
  7. Martinez-Hernandez A, Enriquez L, Moreno-Moreno MJ, et al. Genetics of obesity. Public Health Nutr 2007;10(10A):1138-44.
  8. Morrison CD, Berthoud HR. Neurobiology of nutrition and obesity. Nutr Rev 2007;65(12 Pt 1):517-34.
  9. Mutch DM, Clement K. Unraveling the genetics of human obesity PLOS Genetics. 2006;2(12):e188.
  10. Natural Standard: The Authority on Integrative Medicine. . Copyright © 2008. Accessed March 11, 2008.
  11. Newell A, Zlot A, Silvery K, et al. Addressing the obesity epidemic: a genomics perspective. Preventing Chronic Disease: Public Health Research, Practice, and Policy. April 2007. Vol 4, No 2. . Accessed March 11, 2008.
  12. Price RA, Li WD, Zhao H. FTO gene SNPs associated with extreme obesity in cases, controls, and extremely discordant sister pairs. BMC Med Genet 2008;9:4.
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Causes
  • Genes may contribute to an individual's risk of becoming obese. The thrifty genotype hypothesis is an explanation for the rise of obesity rates. Furthermore, obesity can be classified according to which genetic and environmental factors may cause obesity.
  • Thrifty genotype hypothesis: One explanation for the rise in obesity rates is the "thrifty genotype" hypothesis. This hypothesis is based on the theory that the current genetic makeup of humans helped past generations to survive periods of food scarcity. However, with the plentiful food supply available in most developed countries, this tendency to conserve energy may result in excess fat storage. Individuals with this theoretical thrifty gene may "overreact" to the current environment by overindulging in food, thereby becoming obese. Certain groups, such as the Pima Indians and Pacific Islanders, have been considered at high risk for having this gene because of the history of famine in these cultures.
  • Monogenic obesity: Monogenic obesity is caused by a mutation in a single gene. There are about 200 cases of obesity in humans associated with a single gene mutation in one of 11 genes. These cases tend to display severe phenotypes, which are the physical characteristics, or traits, that an individual expresses. Symptoms of these disorders are detected during childhood and are often accompanied by additional behavioral, developmental, and endocrine disorders. Studies in animals led researchers to be able to identify which genes were responsible for these disorders. Similar obesity-generating genes were then detected among humans. Because a single gene is responsible for obesity in these disorders, it is easier to understand gene function related to obesity. An example of monogenic obesity is Alstrom syndrome.
  • Alstrom syndrome is characterized by involuntary eye movement (nystagmus), sensitivity to light, an enlarged heart, congestive heart failure, hearing impairment, and obesity. Later in life, individuals with Alstrom syndrome often develop type 2 diabetes and progressive kidney disease. The gene for Alstrom syndrome is on chromosome 2 in band 2p13 and is called Alstrom syndrome 1 (ALMS1).
  • Syndromic obesity: Syndromic obesity is typically associated with mild to severe cognitive deficits, abnormal physical features, and organ-specific deficits. There are about 20-30 disorders in which patients exhibit these features, which have been attributed to mutations in multiple genes within a specific pathway. The most common of these disorders are Prader-Willi syndrome and Bardet-Biedl syndrome.
  • Prader-Willi syndrome is a genetic disorder that occurs when a particular chromosome deletion is passed down from the father. This deletion is known to cause obesity. In the womb, Prader-Willi syndrome is characterized by decreased movement of the fetus and, frequently, abnormal fetal position. In general, patients with Prader-Willi compulsively overeat, have learning disabilities, and have abnormal sexual development. Ghrelin is a stomach hormone that makes a person feel hungry, and has been studied for its potential to mediate the compulsive overeating of Prader-Willi syndrome.
  • At least two gene mutations that result in Bardet-Biedl syndrome have been identified; one is mapped to chromosome 11 and the other to chromosome 16; differences between the two forms have not been identified. Bardet-Biedl syndrome is characterized by early-onset obesity and eye disorders (i.e., rod-cone dystrophy), abnormalities of the fingers, learning disabilities, and kidney disease. This syndrome has been associated with at least 11 different gene mutations at different locations on different human chromosomes.
  • Polygenic obesity: Researchers believe that most types of obesity are polygenic, or the result of numerous genetic and environmental factors. Polygenic obesity is the most common form of obesity, occurring as a result of an interaction between genes and the environment. For example, genetic makeup may "help" an individual become obese if he or she is genetically susceptible to obesity, and if he or she is exposed to an environment that promotes consumption of excess food and a lack of physical activity. This form of obesity is difficult to study because it is subject to so many complex interactions that give way to a number of variable outcomes. Polygenic obesity is largely studied through single nucleotide polymorphisms (SNPs), in which there is a single variation in the sequence of base pairs in the DNA (deoxyribonucleic acid). However, it may be difficult to determine the precise degree to which genes and subtle environmental factors affect complex traits such as obesity.

Copyright © 2011 Natural Standard (www.naturalstandard.com)


The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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