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November, 10 2021

What your genes can tell you about your fitness

The real story behind being fit

When it comes to fitness, people are often only concerned with losing fat or building muscles. However, losing fat or building muscles is part of a much bigger picture. Being fit means optimization all your body systems to work well together. Consequently, when discussing fitness, you should consider hormone regulation, joint health, and sleep quality. Genetics also play an essential role.

You need to understand that fitness is oversimplified, and it is not only about fat, muscle, and cardio. Seven main fitness factors actually determine how fit you are.

The Cornerstones of Fitness

Cardiovascular health
Your cardiovascular health grows in importance with age. Boosting it won’t only boost your recovery but will prevent future heart disease.

Testosterone
Optimal testosterone can lead to many benefits like more muscles, more mental clarity, and better mode.

Fat loss
High fat leads to lower testosterone, accelerated aging, and lower self-esteem.

Muscle and exercise performance
Optimal muscle is not only for looks, but it helps keep high testosterone levels and lets you enjoy physical activities.

Sleep
Restful sleep can help your body recover faster and wake you up energized.

Joint health
Healthy joints mean that you will be able to deal with the strains of sports, exercise, and everyday activities. You should not have any joint pain in your normal state.

Genetics
Your genes can affect how your body responds to supplements, food, exercise, and many more factors. Your genes are more important than you think!

 

Now, let’s dig into some of these details. Specifically, your cardiovascular health and exercise endurance and see how our genetics can be related to our fitness.

 

Your exercise performance may change based on your genes

Athletes use caffeine because it can enhance performance, especially in endurance exercises (Del Coso, Muñoz and Muñoz-Guerra, 2011). Studies found that not everyone benefits from this effect, and studies reported fluctuations in individual improvement from 5% to 87% for running and 10% to 156% for cycling! (Graham and Spriet, 1991)

Is it related to DNA? Is it true that some athletes have “good” DNA that makes them more fit than others? Let’s see what the scientific studies say.

 

Endurance, genes, and caffeine

Caffeine is metabolized by cytochrome P450 1A2 (CYP1A2) liver enzyme. Even a single nucleotide difference in the DNA that codes this enzyme can change the enzyme’s effectiveness (Yamazaki et al., 2006). A genotype is a combination of two alleles that affect the characteristics (phenotypes) of an organism. You get one allele from your father and another one from your mother. In the relevant genetic position within CYP1A2, each parent contributes by either an A or C allele, making it possible to have any of these genotypes: AA, AC, or CC. Fast metabolizers of caffeine carry the genotype AA, while slow metabolizers carry the genotype CC.

Studies found that fast metabolizers of caffeine (people who hold the genotype AA of the particular SNP within enzyme CYP1A2) experience better performance benefits when they take caffeine than those with other genotypes. They tend to have increased repetition during resistance exercise and reduced 40-kilometer cycling times (Rahimi, 2019).

Furthermore, in a recently published study, scientists found improved performance by 3% of athletes with the genotype AA. Caffeine did not affect performance in AC genotype carriers and even worsened performance in people with the genotype CC (slow metabolizers) (Guest et al., 2018)!

 

Take-home point

Genetics can provide explanations as to why some people demonstrate better fitness effects while others don’t. People with the genotype AA of the enzyme CYP1A2 benefit the most from caffeine supplementation, while others may get worsened performance.

This means that our genetics could influence our fitness, the effects of supplements (like caffeine), and, ultimately, our exercise performance. But it doesn’t mean that someone has “better” genes than someone else, rather we are all different, and knowing our genetics allows us to tune interventions to be right for each of us individually.

 

Your cardiovascular health and your genetics

We have all heard of the story of good cholesterol (known as HDL-C) and bad cholesterol known as (LDL-C). Most lipid drugs target LDL-C and try to lower its levels. This is because increased LDL-C levels can affect your fitness by increasing your risk of hypertension, diabetes, sexual dysfunction, and heart disease.

On the other hand, drugs that tried to raise HDL-C failed to lower cardiovascular disease risk. At this point, HDL-C’s status as a good guy is being called into question.

 

What do the latest studies say?

A recent paper found that people who have particular variants in the SCARB1 gene had elevated HDL-C levels. Through association studies, scientists found that this specific mutation is related to an increased risk of coronary artery disease and atherosclerosis (Zanoni et al., 2016).

 

NERD: What is the exact function of the SCARB1 gene?

SCARB1 gene codes for the protein receptor SR-BI. This receptor is responsible for the uptake of HDL-C from the periphery to the liver. If this gene is nonfunctional, you will have elevated HDL-C levels because the uptake mechanism is not functioning.

 

What does this study tell us?

  • Again, genetics play an important role in our fitness. A single nucleotide mutation in the DNA was associated with increased HDL-C levels and increased heart disease risk.
  • Higher HDL-C doesn’t mean better. This study found the reverse. Yet, that doesn’t mean that HDL-C is always bad. The results imply that the bigger picture is more complex than just high HDL-C = good.

 

A deeper look at genetic testing

Science fiction has many stories of genetic testing and its potential to revolutionize human performance and medicine. Consumer genetic testing is both accessible and cheap. Will these services result in improvement in fitness or result in better management of health risks? How do genetic tests can change people’s habits based on their genetics?

As the science underpinning genetics continues to advise, so genetic testing will continue to become more relevant. A key challenge will remain, however: how to integrate genetics into the wider wellness and health management plan, rather than leaving consumers on their own to manage ever-increasing amounts of information without help.

 

References

  • Del Coso, J., Muñoz, G. and Muñoz-Guerra, J. (2011) ‘Prevalence of caffeine use in elite athletes following its removal from the world anti-doping agency list of banned substances’, Applied Physiology, Nutrition and Metabolism, 36(4), pp. 555–561. doi: 10.1139/h11-052.
  • Graham, T. E. and Spriet, L. L. (1991) ‘Performance and metabolic responses to a high caffeine dose during prolonged exercise’, Journal of Applied Physiology, 71(6), pp. 2292–2298. doi: 10.1152/jappl.1991.71.6.2292.
  • Guest, N. et al. (2018) ‘Caffeine, CYP1A2 genotype, and endurance performance in athletes’, Medicine and Science in Sports and Exercise, 50(8), pp. 1570–1578. doi: 10.1249/MSS.0000000000001596.
  • Nielsen, D. E. and El-Sohemy, A. (2014) ‘Disclosure of Genetic Information and Change in Dietary Intake: A Randomized Controlled Trial’, PLoS ONE. Edited by M. M. DeAngelis, 9(11), p. e112665. doi: 10.1371/journal.pone.0112665.
  • Rahimi, R. (2019) ‘The effect of CYP1A2 genotype on the ergogenic properties of caffeine during resistance exercise: a randomized, double-blind, placebo-controlled, crossover study’, Irish Journal of Medical Science, 188(1), pp. 337–345. doi: 10.1007/s11845-018-1780-7.
  • Yamazaki, H. et al. (2006) ‘Inter-individual variation of cytochrome P4502J2 expression and catalytic activities in liver microsomes from Japanese and Caucasian populations’, Xenobiotica, 36(12), pp. 1201–1209. doi: 10.1080/00498250600944318.
  • Zanoni, P. et al. (2016) ‘Rare variant in scavenger receptor BI raises HDL cholesterol and increases risk of coronary heart disease’, Science, 351(6278), pp. 1166–1171. doi: 10.1126/science.aad3517.