Can a Tendency to Sit Be Inherited ?

by | Sep 15, 2020 | Genetic or Environmental? | 0 comments

Main Takeaways:

  • Sedentary behavior (sitting or lying down for long periods of time) is harmful to your health, increasing your risk for cardiovascular disease, cancer, type 2 diabetes, and other health issues.
  • While the tendency to engage in sedentary behavior appears to be somewhat heritable, it is largely influenced by your environment. This means even if you have a genetic tendency toward sedentary behavior, you aren’t destined to engage in high levels of sedentary behavior; everyone can make small changes to their routine and environment to lessen time spent sitting.
  • More inclusive research in this area is needed, as well as more standardized definitions of sedentary behaviors and measures

How much time do you spend sitting each day? You have probably heard recommendations from health organizations about how much exercise you should get, how many steps you should take, or how much time you should spend looking at digital screens. However, not much is said about your sedentary behavior, or how much time you spend sitting or lying down. Sedentary behavior, which requires very little energy expenditure, is a distinct behavior from physical activity [1] . Physical activity is usually thought of as exercise; for example, you would be meeting physical activity recommendations if you ran for 30 minutes each day. Yet, even if you meet this recommendation, there is still ample opportunity to engage in sedentary behavior. Let’s say you spend an hour total commuting to and from work, sit at your office job for 8 hours, work out at the gym for 30 minutes after work, then come home and watch TV for the rest of the night until bedtime. With that routine, you would be considered physically active while still spending the majority of your waking hours sitting. How does all of this inactivity affect your health?

Sedentary behavior (SB) has repeatedly been linked to negative health impacts. A study by P. T. Katzmarzyk et al. [2] found that greater sitting time is associated with higher all-cause mortality as well as cardiovascular disease. These associations remained even in individuals that were considered physically active. In addition, a meta-analysis found positive associations between SB and cancer, type 2 diabetes, cardiovascular disease, and all-cause mortality [3]. SB has also been linked to shorter telomeres [4], organ damage, neck, shoulder, and back pain, muscle degeneration, poor circulation, and damage to discs in the spine [5].

So who is most likely to be affected by SB, and therefore more likely to suffer from these health impacts? Can you be genetically predisposed to sit more? Over the past 10 years, 8 studies have explored the heritability of SB using heritability estimates. These estimates help us to gauge a trait’s heritability; they suggest the percentage of phenotypic variability that is influenced by genetics within a population. The higher the estimate, the more influence genetics is thought to have on the trait. Heritability estimates for SB range from 7% to 56%, with an average estimate of 26% [8-15]. Twin studies were the most common form of study performed, finding heritability estimates ranging from 26%-56% [8, 13, 14, 15]. Family studies found heritability estimates ranging from 7%-41% [9, 11, 12], and the only genome-wide association study (GWAS) reported estimates of 15% (men) and 18% (women) [10].

This GWAS also discovered four loci associated with SB, near genes MEF2C, EFNA5, LOC105377146, and CALN1 [10]. These genes are related to muscle maintenance, nervous system development, and calcium binding [16-19]. Other possible candidate genes mentioned by these studies but not evaluated directly include DRD1, NHLH2, and MC4R [8]. DRD1 is related to dopamine responses and is thought to be involved with some behavioral responses, which could affect reward systems involved with activity [20]. The effect of NHLH2 on SB is less clear but seems to be related to the process of transcription [21], while MC4R produces a melanocortin hormone and is known to be a cause of monogenic obesity [22]. Each of these genes can be plausibly connected to SB; your muscles, nervous system, reward pathways, and more could all be involved in the regulation of this behavior.

Does this mean you are doomed to a sedentary lifestyle and the resulting negative health consequences if you possess variants in these genes? Luckily, that does not appear to be the case. Each of these studies promoted the idea that environmental factors have a larger influence on SB than genetics alone. This means even if you had a genetic tendency toward sedentary behavior, you wouldn’t be destined to engage in high levels of sedentary behavior; everyone can make small changes to their routine and environment to lessen time spent sitting and diminish SB’s harmful effects of the body [6]. I am currently working with Dori Rosenberg’s research team at the Kaiser Permanente Washington Health Research Institute, supporting an intervention that helps older adults make small changes in their daily lives with the goal of reducing their sitting time. By making participants more aware of how much they sit in addition to providing tools and coaching to help them sit less, this study hopes to see a decrease in SB among participants receiving the intervention. Suggestions for sitting less from the Office of Disease Prevention and Health Promotion include walking or riding a bike to get to work instead of driving, taking regular standing breaks (every 20-30 minutes) from sitting throughout the workday or while watching television, and pacing while talking on the phone instead of sitting[7] . So while studies did identify SB as a heritable trait and there are some candidate genes thought to be associated with SB [8,10], this behavior is largely affected by your environment and daily decisions. You have control over your SB regardless of your genetics.

I would be remiss, however, without describing some of the issues within existing genetic SB research. It is well known that people of non-European ancestries are continually excluded from genetic research, and a large portion of this research focuses on samples drawn from populations of European descent [23]. Six out of the eight studies I reviewed used samples of predominantly European descent [8, 9, 10, 13, 14, 15] , while the two remaining studies focused on Brazilian [11] and Portuguese [12] populations. None of the studies included representative samples of people with African, Asian, or Indigenous descent. It is important to include populations of diverse ancestries in order to increase the chances of discovering variants associated with a trait of interest, better understand the frequencies of a variant of interest in different populations, have more accurate representation of the diversity in humans [11] , and to make research more inclusive.

A second recurring limitation in the literature was the measurement of SB. The studies reviewed provided evidence that different results are seen when data are procured by self-report rather than an objective measure such as a wearable activity monitor. Downfalls of self-report are well documented [24], as this method can result in social desirability bias, recency bias, and a simple inability to accurately remember or estimate their SB. It is possible that studies using objective measurement methods may find higher heritability estimates on average — studies that used objective measurement found an average heritability estimate of 30% compared to 25% in studies that used self-report, though this comparison is based on just a few studies. For these reasons, future research should prioritize objective measurement for more accurate results. In addition, not all studies evaluated SB in the same way even within the categories of self-report and objective measurement. The lack of clear definitions and standard measures complicate comparison between studies, weakening what conclusions can be gleaned from the literature.

Despite these limitations, current evidence suggests that SB is heritable. However, it is also highly modifiable. Even if linkages between increased SB and certain gene variants were identified, knowing your genotype is unlikely to help you reduce your sitting time. This is good news — you can start making changes today to work toward sitting less, improving your overall health, and reducing your risk of chronic diseases. What are you waiting for?

References

  1. Sedentary Behavior Research Network. (2019, September 5). SBRN Terminology Consensus Project. Retrieved from https://www.sedentarybehaviour.org/sbrn-terminology-consensus-project/
  2. Katzmarzyk, P. T., Church, T. S., Craig, C. L., & Bouchard, C. (2009). Sitting Time and Mortality from All Causes, Cardiovascular Disease, and Cancer. Medicine & Science in Sports & Exercise, 41(5), 998–1005. https://doi.org/10.1249/mss.0b013e3181930355
  3. Biswas, A., Oh, P. I., Faulkner, G. E., Bajaj, R. R., Silver, M. A., Mitchell, M. S., & Alter, D. A. (2015). Sedentary Time and Its Association With Risk for Disease Incidence, Mortality, and Hospitalization in Adults. Annals of Internal Medicine, 162(2), 123. https://doi.org/10.7326/m14-1651
  4. Sjögren, P., Fisher, R., Kallings, L., Svenson, U., Roos, G., & Hellénius, M.-L. (2014). Stand up for health—avoiding sedentary behaviour might lengthen your telomeres: secondary outcomes from a physical activity RCT in older people. British Journal of Sports Medicine, 48(19), 1407–1409. https://doi.org/10.1136/bjsports-2013-093342
  5. Berkowitz, B., & Clark, P. (2014, January 20). The Health Hazards of Sitting. Retrieved from https://www.washingtonpost.com/gdpr-consent/?next_url=https%3a%2f%2fwww.washingtonpost.com%2fapps%2fg%2fpage%2fnational%2fthe-health-hazards-of-sitting%2f750%2f%3fitid%3dlk_inline_manual_8&itid=lk_inline_manual_8
  6. Barwais, F. A., Cuddihy, T. F., & Tomson, L. (2013). Physical activity, sedentary behavior and total wellness changes among sedentary adults: a 4-week randomized controlled trial. Health and Quality of Life Outcomes, 11(1), 183. https://doi.org/10.1186/1477-7525-11-183
  7. National Center on Health, Physical Activity and Disability. (2013, January 30). Decreasing Sedentary Behavior and Physical Inactivity by Moving More and Sitting Less. Retrieved from https://health.gov/news-archive/blog/2013/01/decreasing-sedentary-behavior-and-physical-inactivity-by-moving-more-and-sitting-less/
  8. den Hoed, M., Brage, S., Zhao, J. H., Westgate, K., Nessa, A., Ekelund, U., … Loos, R. J. F. (2013). Heritability of objectively assessed daily physical activity and sedentary behavior. The American Journal of Clinical Nutrition, 98(5), 1317–1325. https://doi.org/10.3945/ajcn.113.069849
  9. Diego, V. P., de Chaves, R. N., Blangero, J., de Souza, M. C., Santos, D., Gomes, T. N., … Maia, J. A. R. (2015). Sex-specific genetic effects in physical activity: results from a quantitative genetic analysis. BMC Medical Genetics, 16(1), 1. https://doi.org/10.1186/s12881-015-0207-9
  10. Doherty, A., Smith-Byrne, K., Ferreira, T., Holmes, M. V., Holmes, C., Pulit, S. L., & Lindgren, C. M. (2018). GWAS identifies 14 loci for device-measured physical activity and sleep duration. Nature Communications, 9(1), 1. https://doi.org/10.1038/s41467-018-07743-4
  11. Leite, J. M. R. S., Soler, J. M. P., Horimoto, A. R. V. R., Alvim, R. O., & Pereira, A. C. (2019). Heritability and Sex-Specific Genetic Effects of Self-Reported Physical Activity in a Brazilian Highly Admixed Population. Human Heredity, 84(3), 151–158. https://doi.org/10.1159/000506007
  12. Santos, D. M. V., Katzmarzyk, P. T., Diego, V. P., Blangero, J., Souza, M. C., Freitas, D. L., … Maia, J. A. R. (2014). Genotype by Sex and Genotype by Age Interactions with Sedentary Behavior: The Portuguese Healthy Family Study. PLoS ONE, 9(10), e110025. https://doi.org/10.1371/journal.pone.0110025
  13. Schutte, N. M., Huppertz, C., Doornweerd, S., Bartels, M., Geus, E. J. C., & Ploeg, H. P. (2020). Heritability of objectively assessed and self‐reported sedentary behavior. Scandinavian Journal of Medicine & Science in Sports, 30(7), 1237–1247. https://doi.org/10.1111/sms.13658
  14. van der Aa, N., Bartels, M., te Velde, S. J., Boomsma, D. I., de Geus, E. J. C., & Brug, J. (2012). Genetic and Environmental Influences on Individual Differences in Sedentary Behavior During Adolescence. Archives of Pediatrics & Adolescent Medicine, 166(6), 509. https://doi.org/10.1001/archpediatrics.2011.1658
  15. Waller, K., Vähä-Ypyä, H., Lindgren, N., Kaprio, J., Sievänen, H., & Kujala, U. M. (2018). Self-reported Fitness and Objectively Measured Physical Activity Profile Among Older Adults: A Twin Study. The Journals of Gerontology: Series A, 74(12), 1965–1972. https://doi.org/10.1093/gerona/gly263
  16. (2020a, June 1). LOC105377146 uncharacterized LOC105377146 [Homo sapiens (human)] Retrieved from https://www.ncbi.nlm.nih.gov/gene/?term=loc105377146
  17. NCBI. (2020c, June 7). CALN1 calneuron 1 [Homo sapiens (human)]. Retrieved from https://www.ncbi.nlm.nih.gov/gene/83698
  18. NCBI.(2020d, June 7). EFNA5 ephrin A5 [Homo sapiens (human)]. Retrieved from https://www.ncbi.nlm.nih.gov/gene/1946
  19. NCBI. (2020g, June 28). MEF2C myocyte enhancer factor 2C [Homo sapiens (human)]. Retrieved from https://www.ncbi.nlm.nih.gov/gene/4208
  20. NCBI.(2020b, June 4). DRD1 dopamine receptor D1 [Homo sapiens (human)]. Retrieved from https://www.ncbi.nlm.nih.gov/gene/1812
  21. NCBI. (2020e, June 7). NHLH2 nescient helix-loop-helix 2 [Homo sapiens (human)]. Retrieved from https://www.ncbi.nlm.nih.gov/gene/4808
  22. NCBI. (2020f, June 27). MC4R melanocortin 4 receptor [Homo sapiens (human)]. Retrieved from https://www.ncbi.nlm.nih.gov/gene/4160
  23. Genetics for all. (2019). Nature Genetics, 51(4), 579. https://doi.org/10.1038/s41588-019-0394-y
  24. Rosenman, R., Tennekoon, V., & Hill, L. G. (2011). Measuring bias in self-reported data. International Journal of Behavioural and Healthcare Research, 2(4), 320. https://doi.org/10.1504/ijbhr.2011.043414

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