Despite Predispositions, You Still Can’t Blame Your Genes for Being Obese

By René Eastin, MTI Contributor

The prevalence of obesity has more than tripled over the last five decades.  Growing so rapidly from 13.4% in the 1980’s to 41.9% today that in 1997 it was declared a global epidemic by The World Health Organization.  In 2013 The American Medical Association began recognizing obesity as a chronic disease.

In 1994 Jeffrey Friedman, an American molecular geneticist, identified the hormone Leptin.  Produced by adipose cells, leptin regulates energy and inhibits hunger.  By identifying genetic variations causing disruptions in leptin production Friedman was the first to establish genetic subgroups with a predisposition for obesity.  

Of these subgroups there are two, monogenic obesity and syndromic obesity in which additional genetic studies were able to find common gene trends among different individuals. 

Monogenic obesity is an autosomal form of obesity caused by a mutation or disruption of a single gene.  So far all twenty of the single gene mutations and disruptions found to have direct links to obesity have to do with the leptin/melanocortin pathway in the central nervous system.  This pathway is the central regulator of hunger and food intake.  In a fed state leptin and insulin are released and bind with melanocortin receptors to induce satiety.  Any one of these monogenic mutations or disruptions inhibits the ability for the carrier to feel full causing a potential to overeat.

Syndromic obesity is a chromosomal form of obesity caused by the deletion of X-chromosome 15 from the paternal genes.  The maternal genes reactively form a second, but inactive, X-chromosome 15 to replace the missing paternal chromosome.  Carriers of this syndrome, more commonly known as Prader-Willi’s, exhibit hyperphagia; an extreme drive to eat excessively as the body fails to naturally regulate hunger and fullness.  

The third subgroup; polygenic obesity, otherwise known as common obesity, differs from the previous subgroups in that scientists have been unable to establish repeatable genetic trends among different individuals.   Polygenic obesity is considered inherent based on environmental factors rather than genetics.  Further research is needed but would be invasive and is currently on hold pending funding and the need for larger sample groups.  

Despite research providing a greater understanding of the genetic factors contributing to obesity, each of the variations found to date have been related to satiety and the effect it has on food intake.  Even as the number of genes implicated in obesity continues to grow it is not believed that these genetic mutations alone can account for the drastic trend toward the current epidemic without an accompanying obesogenic environment.  Therefore obesity is thought to be a neurobehavioral issue rather than a metabolic one.  Meaning despite any genetic susceptibility obesity is still considered a manageable condition.  

In the case of monogenic obesity; a genetic predisposition for obesity based on any one of the twenty known gene variances or mutations, carriers don’t know when to stop eating because they never feel full.  Satiety is indeed a useful tool. However, it is not a necessity when it comes to preventing overeating.  We have access to all kinds of methods for measuring food intake other than how we feel.  

In the case of syndromic obesity; a genetic predisposition for obesity based on hyperphagia, carriers exhibit an excessive craving for food similar to that of an addiction.  Unlike other addictions food cannot be expunged but it can be monitored and controlled.  

In the case of polygenic obesity; an inherent predisposition for obesity based on habits learned from those around us.  Bad habits are hard to break but not impossible.  

Obesogenic environments have long been known to include sedentary lifestyles.  With manual labor jobs being taken over by computer based desk jobs throughout the last five decades it becomes an obvious conclusion that this too must be partially to blame for the current obesity epidemic.  Along with time spent watching television, playing video games, and accessing the internet on smartphones people spend far more time inactive than they used to.  While these factors undoubtedly play a role in the rise of obesity; studies have also shown, even collectively, they cannot account for the growth rate of obesity that made it an epidemic any more than genetics can.  

There is no denying certain individuals are more susceptible to becoming obese. However, regardless of any predispositions, inherited genetically or habitually, science still shows it boils down to two factors;  calories in verse calories out and only we control the food that goes into our mouths.

Manufacturers will continue aggressively marketing non healthy chemically enhanced foods.  Fast food restaurants will continue making and selling supersized quantities of less expensive and less nutritious options. Our bodies will continue to try and compensate in order to digest all the synthetic additives.  Scientists will continue to do studies to develop new medications to curb new allergies and ailments.  Doctors will continue to prescribe those medications.  We will continue to find excuses to not have to do the one and only thing that will make the biggest difference for the greatest majority of us; eat a primarily whole food diet that balances our calories in with our calories out.  

If you still want to blame genetics you can blame them for where adipose tissue deposits when it is in excess.  It has been noted that sex hormones play a key part in the manner in which adipose tissue accumulates and multiple studies have shown there is eminent proof that it has a genetic background. 

This was definitely the case for me.  While characteristically I have always been a spitting image of my father I never looked more like my mother than when I was obese.  Neither one of my parents were able to combat their excess body weight and I often blamed them for my similar issues.  It wasn’t until I took ownership of my lifestyle and started paying attention to my food choices that I was able to gain control over my weight and my overall health.  It wasn’t an absence of good genetics that kept me struggling with my weight; it was my lack of commitment, my lack of knowledge, my lack of consistency, and my lack of discipline.  

Looking at it all from a flipped perspective; several years ago my son was in the prime of his career as a college athlete.  Despite being one of the fittest members of his team due to mandatory practices, workouts, and lifting sessions he was often ribbed about not having visible aesthetic abs.  He repeatedly answered, “Because neither of my parents do, it’s genetically impossible for me.”  He recently commented that he has since lost that excuse because both his parents now have abs.  Moral of the story; despite your genetics you still have to do the work.  

René is a personal trainer and nutrition coach in Nevada.

References:

link.springer.com/article/10.1007/s11892-010-0153-z

nichd.nih.gov/health/topics/prader-willi/conditioninfo/causes

royalsocietypublishing.org/doi/abs/10.1098/rstb.2006.1850

onlinelibrary.wiley.com/doi/full/10.1038/oby.2008.514

pnas.org/doi/full/10.1073/pnas.0601752103

https://www.acsh.org>2017/01/20

https://pubmed.ncbi.nlm.nih.gov

 

 


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