Did you know DNA affects your “good” cholesterol response to exercise?

The PPARD gene and proof that exercise can compensate for your less than perfect metabolism

At the ripe young age of 98, Nanammal from India continues to inspire generations of youth. Ida Keeling from Brooklyn set the world record in the 100m (category of 80 and older), when she finished the race in less than 90 seconds at the age of 100. Finally there’s Charles Eugster, a bodybuilder and sprinter with multiple world records for his age group under his belt. He’s considered to be the world’s fittest 96 year-old. These exceptionally healthy and fit seniors prove to us that staying active is the key to a long and healthy life. But that doesn’t mean all of us will equally benefit from exercise. Undeniably, some of us respond better to exercise than others, with regards to losing weight and keeping it off. Did you know these individual differences in metabolism are sometimes rooted in our DNA? Take the PPARD gene for example. A single defect in PPARD can increase our risk of obesity, type 2 diabetes and cardiovascular disease, all of which can be minimized by choosing to exercise.

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Our talent for losing and keeping off weight depends wholly on how efficient we are at breaking down fat. Burning fat has a number of advantages during exercise. It generates twice as much energy as sugar, and preserves our sugar reserves for organs that can’t burn fat like the brain. However, our bodies prefer sugar as sources of energy rather than fats. This means we need to train them to burn fats. This is exactly what exercise does – especially activities that last at least 30 minutes or endurance activities like mid- or long distance running or biking. Endurance activities encourage our our muscles to adapt, so they switch from burning sugars to burning fats. Not only that, regular exercise also enhances our levels of “good” high-density lipoprotein cholesterol (HDL-C), which protects us against cardiovascular disease. The PPARδ protein (encoded by the PPARD gene) is key to this energy choice between sugars and fats, and what is more, it also governs the exercise-mediated changes in HDL-C.

PPARδ controls the activity of many other genes, particularly the ones involved in fat breakdown. Endurance exercises increase PPARδ levels, enhancing our ability to use fats for energy. Studies in mice show that artificially elevating PPARδ levels makes them resistant to weight gain even in the absence of exercise. This means differences in PPARδ levels can explain at least part to the discrepancy we see between the benefits of exercise in terms of weight loss. Those of us who inherit a version of PPARD, called rs2016520, have lower levels of HDL-C and higher levels of “bad” low-density lipoprotein cholesterol (LDL-C), enhancing the risk of cardiovascular disease. But all is not lost, because according to one study, Caucasian men with rs2016520 experienced significantly higher increases in HDL-C levels following endurance training compared to those with the normal version of PPARD. This means those who are actually at risk tend to benefit more from the “HDL-raising effect” of exercise, and that exercise can mitigate their predisposition to diseases such as type 2 diabetes or cardiovascular disease.

Yet, the story of PPARD is far from simple. The link between PPARD, HDL-C and exercise appears to be ethnicity dependent. Also, this same version (rs2016520), linked to increased predisposition to cardiovascular disease in sedentary individuals, is actually highly prevalent among elite endurance athletes. So there seems to be a disconnect between extreme athletic potential in highly active individuals, versus how an average person with the same variant will reap health benefits from exercise. With so many studies looking at how genetic changes impact our response to exercise, future studies will no doubt settle this intriguing conundrum.

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