By Subhash Reddy

The simple and short answer for this is “probably, but not sure”.  Body weight is the product of genetic effects (DNA), epigenetic effects (heritable traits that do not involve changes in DNA), and the environment.

The majority of the obese population who are intending to lose weight will agree.  One may lose a few pounds by diet modification, exercise, or adding some healthy lifestyle changes. But over a period of time, they regain their lost weight or sometimes even more.  It does not mean that they did not follow healthy rules, it just means their body found a way to slow their metabolism (save energy).  This is the inbuilt mechanism in human beings developed over generations to adapt the body for periods of starvation.

A study done by University of Exeter Medical School in the UK evaluated a bio bank of 120,000 people, and found that many weight-producing aspects of the environment, lifestyle and behavior interact with a person’s genes to influence his or her waistline – and that the strongest influence is from poverty. Poverty and weight gain is related to dietary pattern, activity level, and most importantly, genes.  The conclusion of the article was that policies to fight obesity can’t be done just by focusing on environmental/dietary or activity level in those who are genetically susceptible. A similar study was done by University of San Francisco that was published in JAMA 2016, which looked into 29 obese genetic variants of around 7000 Caucasian and 1300 African American people born between 1900 and 1958 and their influence on weight gain. The number of genetic variants each person had did not increase in the population over time, while their effects on people did, pointing to environmental influences. The analysis found that average BMI (body mass index) increased over time for everyone in the study, even those with quite low genetic risk for obesity. But, people with high genetic risk were affected the most. The study points out that genes that had little or no influence in the past now play a significant role in gaining weight with the changing environment. One possible hypothesis of these obesity genes is that they may increase hunger and make people to look for a high calorie diet, which is readily available in well-developed countries.  The situation is made worse when the population overall is less active. This hypothesis was tested by Uppasala University, where they collected blood samples of the people with the obesity gene variant after overnight fasting, and compared to normal population. People with the obesity variant gene had 8% higher levels of ghrelin (hunger hormone) and 9 % low levels of Leptin (satiety hormone) compared to the normal population, which helped them gain weight easily. Leptin, a naturally occurring hormone, is known for its hunger-blocking effect on a region in the brain called the hypothalamus. Food intake is influenced by signals that travel from the body to the brain. Leptin is one of the molecules that signals the brain to modulate food intake. It is produced in fat cells and informs the brain of the metabolic state. If animals are missing leptin, or the leptin receptor, they eat too much and become severely obese.

People have looked to the concept of starvation to lose weight, which is one of the environmental factors.  Multiple studies have looked into this and found out that it’s not quite helpful in the long run.  In the Minnesota starvation study, the subjects lost 66% of their initial fat mass in response to 24 weeks of semi-starvation (i.e., at 50% reduced energy intake), but re-feeding (normal calories) resulted in a regain of fat mass reaching 145% of the pre-starvation values (i.e., there was an overshooting of fat mass, known as the catch-up fat phenomenon). Further simulation of the Minnesota starvation experimental data suggested that after re-feeding, it may take more than a year for the fat mass to decrease to within 5% of the initial value. These data reflect a transient loss in appetite control (and thus body weight regulation) during the first months of re- and overfeeding. Returning to a pre-starvation (and presumably healthy) lifestyle may take longer time periods as the body reconstitutes or resets its body weight regulatory system. This finding might lead to the more general hypothesis that the biology of body weight regulation is camouflaged by hyperphagia (and presumably a Western lifestyle). The other observation from prior studies was that diet-induced weight loss in overweight subjects does not affect adipose tissue distribution, implying that the different depots (e.g., visceral and subcutaneous) are reduced with weight loss. However, there are preferential losses of visceral adipose tissue and ectopic fat in the liver and these are disproportionately depleted with weight loss.

“A study done by University of Exeter Medical School in the UK evaluated a bio bank of 120,000 people, and found that many weight-producing aspects of the environment, lifestyle and behavior interact with a person’s genes to influence his or her waistline – and that the strongest influence is from poverty.”

The biological control (genes) of weight gain is lost or camouflaged by Western diets, suggesting that the failure of biological control is due mainly to external factors. Biological control, i.e. genes, have a significant role to play in weight gain or control, but are overtly suppressed by the current environmental situation. All the multiple studies looking at the genetic aspect of weight gain have one thing in common: These genes existed hundreds of years ago, but what has changed to trigger weight gain is the biggest mystery. This will be the answer to control the obesity epidemic. Lucky were the older generations who carried these genes, but did not have exposure to the many calorie-dense, processed foods available today.

Texas Bariatric Specialists has locations in San AntonioWestover HillsAustinCorpus ChristiSan AngeloKilleenDel RioLaredo and New Braunfels.

To find out more information, contact (877) 538-6909 or visit Texasbariatricspecialists.com

 

 

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