Obesity and Genetics: Is It Possible to Overcome Your Genetic Makeup?
Obesity and genetics are directly related. Combined with environmental influences, your genes are up to 70% responsible for your body’s weight.1,2 Bariatric surgery may be the only effective way to alter these genetically predetermined body processes.
- Why genes cause obesity
- Genetics and hunger
- Genetics, metabolism and weight loss
- Bariatric surgery’s impact on the genetic causes of obesity
If obesity has so many negative mental and physical health consequences, why would our bodies have evolved this way?
To answer this question, let’s consider how the body’s survival requirements have coincided with environmental factors over the course of human history.
Humans have been in their current state (“homo sapiens”) for between 50,000 and 100,000 years. The obesity epidemic has been growing for about 30 years, or between 0.03% and 0.06% of human history.
For the 99.94+% of pre-obesity human history, food was not readily available for most people. Starvation and famine were significant causes of death.
But for people with bodies that stored more fat, or “adipose tissue”, starvation was less likely. Their excess adipose tissue provided the energy needed to survive when food wasn’t available.
Some regions of the world had less food sources (i.e. animals and edible plants), so the bodies of people who survived in those regions had a better ability to store fat. They passed those “fat-storing,” “metabolism-slowing” genes down to their children, who had a better chance of surviving and reproducing as a result.
From a survival standpoint, this passing-down of “fat genes” was a good thing until the last century or so when food started to become abundant. Not only is famine not an issue anymore for people who are obese, but the availability and consumption of high-fat foods combined with a less active lifestyle is like a shock to the genetically obese person’s system. Those fat genes continue to do what they’ve done for thousands of years, despite the fact that their presence is no longer necessary.
One of the most glaring examples of the correlation between obesity and genetics can be found with the Pima Native Americans of southern Arizona, who have lived in that region for over 2,000 years. Before the 1940’s, the average Pima was lean and muscular. Despite the scarcity of energy-rich food (such as animal fat) in a desert region, their bodies evolved to store fat more efficiently in order to survive a highly active lifestyle on a high-fiber, low-fat diet.
After the 1940’s, the Pima slowly began to adopt the more sedentary American lifestyle, including the consumption of foods higher in sugar and animal fat. While the average American slowly gained weight from this lifestyle, the average Pima’s weight grew quickly and significantly. By the 1980’s, the average 44 year old American woman had a body mass index of about 25, while the average 44 year old Pima woman’s BMI was around 35, a full 10 BMI points higher.3
Hunger is the first of two areas demonstrating the correlation between obesity and genetics. Your genetics determine the amount of hunger-causing hormones that are secreted by your body into your blood stream and how your brain interacts with those hormones.
Three types of internal body secretions have been found to regulate hunger:
- Hormones from the digestive system, including ghrelin, peptide YY and GLP-1, let your brain know when more nutrients are “needed” based on your body’s requirements.
- Hormones from fat cells (“adipocytes”) such as leptin keep your brain informed about your body’s level of energy deposits (fat cells).
- Neuropeptides in the brain regulate food intake by responding to signals from hormones secreted by the body.
Ghrelin is the first of three hormones sited most frequently in conjunction with obesity. When your stomach is empty, ghrelin is secreted into your blood stream by your stomach. After you eat, the amount of secreted ghrelin drops, then slowly rises until your next meal.4 Lower ghrelin means less hunger.
Neuropeptide Y neurons in the brain are activated by ghrelin. When your blood carries more ghrelin to the brain, your neuropeptides create “hunger signals” leading you to feel hungry and eat.
Similarly, peptide YY, a protein released by your digestive system after you eat, carries signals that tell your brain you are full. More peptide YY means less hunger.
The third most commonly-referenced hormone associated with obesity is leptin, which is secreted by fat cells. The amount of leptin secreted rises and falls with the amount of fat in your body. When your brain senses less leptin, it creates the feeling of hunger in an attempt to encourage additional energy (fat) storage.5
More fat means more leptin which leads to less hunger for people of normal weight. However, obese people are believed to have built up a resistance to leptin so that despite having more leptin secreted, they do not experience appetite suppression.6
If dieting has not worked for you, ghrelin, peptide YY and leptin are likely to be a few of the main culprits because as you diet…
- The amount of ghrelin your stomach secretes increases, causing your brain to receive more hunger signals.
- The amount of peptide YY your digestive system secretes decreases, causing you to feel hungrier.
- As your leptin-secreting fat deposits dissolve, less leptin is released into your blood causing your brain to want to eat more in order to restore its fat deposits.
In other words, the longer you diet, the more difficult your appetite is to control.
The second area demonstrating the correlation between obesity and genetics is your actual weight.
Under the Set Point Theory, each of our bodies has a set weight that it “wants” to maintain. If your body weight goes above your set point, your metabolism will speed up in an attempt to burn off the excess weight. If your weight falls below your set point, your metabolism will slow down to allow more fat accumulation. See our Metabolic Set Point Theory of Homeostasis page for more information.
In addition, researchers from the Imperial College of London studying obesity and genetics found that missing DNA could be a factor that causes obesity. The study found that about 7 out of every 1,000 morbidly obese people are missing a part of their DNA that contains roughly 30 genes. No people of normal weight were missing the genes.7
Weight loss surgery disrupts the association between obesity and genetics in two ways...
- Hormones and weight loss: surgery impacts the hormones that affect hunger
- Metabolism and weight loss: surgery increases the body’s fat-burning metabolism
Not all bariatric surgery procedures have an impact on the hunger-effecting hormones secreted by your body. Surgeries that bypass or remove part of the stomach, including gastric bypass surgery, gastric sleeve surgery and duodenal switch surgery may reduce feelings of hunger by…
- Reducing the level of ghrelin secreted into the blood stream by the stomach8,9,10
- Increasing the level of peptide YY secreted into the blood stream by the lower digestive system11,12,13
Therefore, it could be suggested that the procedures that remove or bypass part of the stomach (i.e. gastric bypass, gastric sleeve and duodenal switch) could aid in long-term weight loss by causing patients to feel less hungry. At a minimum, sustained weight loss should feel easier to achieve after these procedures due to fewer hunger signals reaching the brain.
However, the evidence from each of the above-referenced studies suggests that ghrelin and peptide YY levels in the blood do not directly correlate with the amount of weight loss in bariatric surgery patients.
As for an obese person’s “set point”, bariatric surgery has been shown to increase glucose metabolism causing the body to burn energy (fat) more quickly. Increased metabolism is the result of and directly proportionate to the amount of fat lost after weight loss surgery.18,19,20
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References for Obesity and Genetics
- A Shuldiner, KM Munir. Genetics of obesity: More complicated than initially thought. Lipids Journal. Vol 38, Issue 2, pgs 97-101. Feb 2003.
- José R. Fernández, David J. Goldstein. The Management of Eating Disorders and Obesity. Pgs 293-306. 2005.
- WC Knowler, DJ Pettitt, MF Saad, MA Charles, RG Nelson, BV Howard, C Bogardus, and PH Bennett. Obesity in the Pima Indians: its magnitude and relationship with diabetes. Am. J. Clinical Nutrition, Jun 1991; 53: 1543S - 1551S.
- Hunger. Citizendium, The Citizens' Compendium. Available at: http://en.citizendium.org/wiki/Hunger. Accessed: Mar 2010.
- Friedman JF. Molecular Studies of Food Intake and Body Weight. Howard Hughes Medical Institute. Dec 2007. Available at: http://www.hhmi.org/research/investigators/friedman.php. Accessed: Mar 2010.
- El-Haschimi K, Lehnert H. Leptin resistance - or why leptin fails to work in obesity. Exp Clin Endocrinol Diabetes. 2003 Feb;111(1):2-7.
- Press Release: Some Morbidly Obese People are Missing Genes, Shows New Research. Imperial College London. Feb 2010. Available at: http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/
- Gema Frühbeck, et al. Fasting Plasma Ghrelin Concentrations 6 Months after Gastric Bypass are not Determined by Weight Loss or Changes in Insulinemia. Obesity Surgery. Vol 14, Issue 9, pgs 1208-1215. Oct 2004.
- Arthur Bohdjalian, et al. Sleeve Gastrectomy as Sole and Definitive Bariatric Procedure: 5-Year Results for Weight Loss and Ghrelin. Obesity Surgery. Jan 2010.
- Efstathios V Kotidis, et al. Serum Ghrelin, Leptin and Adiponectin Levels before and after Weight Loss: Comparison of Three Methods of Treatment – A Prospective Study. Obesity Surgery. Vol 16, Issue 11, pgs 1425-1432. Nov 2006.
- Chan JL, Mun EC, Stoyneva V, Mantzoros CS, Goldfine AB. Peptide YY levels are elevated after gastric bypass surgery. Obesity (Silver Spring). 2006 Feb;14(2):194-8.
- Karamanakos SN, Vagenas K, Kalfarentzos F, Alexandrides TK. Weight loss, appetite suppression, and changes in fasting and postprandial ghrelin and peptide-YY levels after Roux-en-Y gastric bypass and sleeve gastrectomy: a prospective, double blind study. Ann Surg. 2008 Mar;247(3):401-7.
- Ballantyne, Garth. Peptide YY(1-36) and Peptide YY(3-36): Part II. Changes after Gastrointestinal Surgery and Bariatric Surgery: Part I. Distribution, Release and Actions appeared in the last issue (May 2006).
Obesity Surgery, Volume 16, Number 6, June 2006 , pp. 795-803(9)
- Luca Busetto, et al. High Ghrelin Concentration is Not a Predictor of Less Weight Loss in Morbidly Obese Women Treated with Laparoscopic Adjustable Gastric Banding. Obesity Surgery. Vol 16, Issue 8, pgs 1068-1074. Aug 2006.
- le Roux CW, Aylwin SJ, Batterham RL, Borg CM, Coyle F, Prasad V, Shurey S, Ghatei MA, Patel AG, Bloom SR. Gut hormone profiles following bariatric surgery favor an anorectic state, facilitate weight loss, and improve metabolic parameters. Ann Surg. 2006 Jan;243(1):108-14.
- Efstathios V Kotidis, et al. Serum Ghrelin, Leptin and Adiponectin Levels before and after Weight Loss: Comparison of Three Methods of Treatment – A Prospective Study.
Obesity Surgery. Vol 16, Issue 11, pgs 1425-1432. Nov 2006.
- Jean L. Chan, Edward C. Mun, Violeta Stoyneva, Christos S. Mantzoros and Allison B. Goldfine. Peptide YY Levels Are Elevated After Gastric Bypass Surgery.Obesity (2006) 14, 194–198; doi: 10.1038/oby.2006.25
- Peterli R, Wölnerhanssen B, Peters T, Devaux N, Kern B, Christoffel-Courtin C, Drewe J, von Flüe M, Beglinger C. Improvement in glucose metabolism after bariatric surgery: comparison of laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy: a prospective randomized trial. Ann Surg. 2009 Aug;250(2):234-41.
- Garrido-Sanchez L, et al. Improved Carbohydrate Metabolism After Bariatric Surgery Raises Antioxidized LDL Antibody Levels in Morbidly Obese Patients. Diabetes Care. December 2008. vol.31 no.12 pgs 2258-2264
- FRIGE' F., et al. Bariatric surgery in obesity : Changes of glucose and lipid metabolism correlate with changes of fat mass. Nutrition, metabolism and cardiovascular diseases ISSN 0939-4753. 2009, vol. 19, no3, pp. 198-204
[Last editorial review/modification of this page: 2/28/2011]