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Are My Genes to Blame?

Are My Genes to Blame?

Recent media attention has been given to scientific discoveries which may suggest that a person is ‘genetically predisposed’ to being fat or lazy. Indeed, our laboratory recently published a scientific paper using rats, suggesting that genetics and gene products can contribute (key word) to laziness1. This report garnered a good bit of media attention, which led to message board posts such as,

“now I can blame my genes for not wanting to get off of the couch”

“leave it to scientists to find another reason for people to be lazy”

Simply stated, geneticists use very intricate calculations to suggest that most traits, body weight or exercise motivation, for example, are about 50% heritable. However, environmental enrichment (i.e., a consistently healthy diet and routine physical activity) can more than make up for poor genetics.

Cases in point are the following scientific findings:

'Lazy' Genes, Physical Activity & Body Composition

In the same study that we published suggesting the lazy genes likely exist, when these ‘lazy’ rats were given access to running wheels over a 6-day period, minimal voluntary running (due to laziness) was still able to completely prevent gains in body fat. When applied to humans, these findings suggest that even a little bit of exercise can cause drastic body composition alterations.

Likewise, muscle samples taken from these ‘lazy’ animals that ran very little daily distances, revealed increases in markers suggestive of positive training adaptations (i.e., mitochondria increased, the aerobic engines of our body). Thus, while one may be more genetically predisposed to be ‘lazy’, a little bit of daily physical activity can go a long way in improving various physiological variables.

The Famous 'FTO' Gene

Humans possessing certain genetic variants of the famous "fat mass and obesity gene", or FTO gene, have an increased risk of being overweight or obese. However, recent data suggests that “obesogenic” variants of the FTO gene are not associated with an obese phenotype in those that maintain routine physical activity levels.2,3 Alternatively stated, this is yet another example whereby exercise can do more than make up for poor genetics.

Our 'Caveman' Genes

Finally, it is very important to point out that humans have generally adapted (and therefore possess genes) to be both overweight and lazy. From an evolutionary standpoint, it makes little sense that our hunter-gatherer ancestors would waste energy performing extraneous exercise when fuel (in the form of food) was hard to come by. Likewise, when these same ancestors feasted on food, their genes (which are now our genes through several generations of inheritance) likely favored fat storage in order to ensure that the body was provided for, in case the next meal didn’t come for weeks. The science supports this, as accelerometer data suggests over 90% of U.S. adults do not engage in the proper amount of physical activity.4

'Inactivity' Genes & Environmental Pressures

While environmental pressures affect this trait (i.e., television, desk jobs, etc.), ‘inactivity’ genes likely exist in all of us at the expense of our ancestors’ survival. Likewise, recent epidemiological data suggests that over 70% of Americans are overweight or obese. Again, environmental pressures have contributed to this obesity epidemic (i.e., overeating and poor food choices which lead to a dysregulation in appetite and calorie-burning mechanisms). However, we all are equipped with ‘thrifty’ genes that favor fat storage over fat burning.

Conclusions

So, are poor genes to blame for most of us being lazy and overweight? Well, geneticists will tell you that genes are one side of the coin, roughly 50%, in this complex paradigm. However, ample evidence suggests that living a consistently healthy lifestyle can override poor genetics. In terms of recommendations for healthy living, stay tuned…


References

1Roberts et al. Am J Physiol Regul Integr Comp Physiol. 2013 Apr 3 [Epub ahead of print]

2Reampersaud et al. Arch Intern Med 168: 1791–1797, 2008

3Kilpelainen et al. PLoS Med 8: e1001116, 2011

4Troiano et al. Med Sci Sports Exerc. 2008 Jan;40(1):181-8

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