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.
Obesity And Genetics: Evolution Favored Humans That Could Retain Much Need Nutrients (Fats & Sugars) When Food Was Scarce; Now That Works Against Us
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’s Impact: Disrupts Association Between Obesity And Genetics In 2 Ways-Hormones & Metabolism
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
[ Last editorial review/modification of this page : 10/07/2016]