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I think one of the most universally embraced ideas when people gather together and pontificate about how their relatives or colleagues turned out they way they did, is that ‘people are a product of their environment’.

I’m not here to make a singular stand against this notion — in fact, it certainly can explain some health outcomes. Consider the following statements:

Parents of higher socioeconomic status may provide healthier food for children.

Being educated about health risks can enable people to make better lifestyle decisions.

These statements emphasize that our social environment can affect our well-being by affecting our choices.

However, this really only scratches the surface. Because social environment not only affects our choices, but also our underlying biology.

In particular, an article in last month’s issue of the Proceedings of the Natural Academy of Science, (PNAS) highlights the specific role of social stressors on genetic structures called telomeres.

Let me explain…

Every time our cells divide, a little bit of DNA gets left out at one end of the chromosome. Yes we lose genetic material! We evolved to have a biological buffer against this – our chromosomes are capped with a DNA sequence called a “telomere”, a series of TTAGGG repeats, which serves as a genetic martyr. Instead of losing critical genes each time our cells replicate, we lose telomere repeats. The telomere, therefore, protects the integrity of our genes, and the consumption of telomere length over our lifetime is associated with cell senescence, physiological aging, and the risk of premature death.

This month’s PNAS article is interesting because it studied how telomere length in African American boys is affected by social environment, taking into consideration economic status, parenting quality, family structure, and maternal level of education. The investigators’ model found that a disadvantaged environment was associated with a 19% shorter telomere length in 9-year old boys. Interestingly, they also show that this difference in telomere length between children from advantaged and disadvantaged environments is affected by the child’s alleles for neurotransmitters important in mood, reward, and behaviour. Having specific alleles (versions of genes) predisposed children to having telomere shortening in the setting of a disadvantaged environment. Basically, our genetics affect how our telomeres respond to social stressors.

Now one category of cells in which the telomere is an absolutely critical structure is the stem cell. If you consider that the most basic features of stem cells are 1) the ability to differentiate into multiple tissue types and 2) the ability to maintain replication, it is this latter characteristic that requires telomeres to be intact. In fact, stem cells are fairly unique in their expression of telomerase, an enzyme that helps to continuously rebuild their telomeres.

Nevertheless, similar to other cells in our body, telomere shortening can and does occur in stem cells, and it can impair their ability to mobilize when needed for tissue repair, as well as disturb their local microenvironment. It’s aging at the level of the tissues!

Taking this information in context with the current study, it would seem that our social environment can affect the functioning of our stem cells, by affecting the length of their telomeres. Furthermore, it could be postulated that people have different genetic susceptibilities to telomere shortening in their stem cells.

It may not be possible to alter our genetic susceptibility or even the degree of social stressors we experience. However, I can’t help but indulge in the idea that whatever healthy lifestyle options I make for myself, they are healthy for me because they are “good for my stem cells”.

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Holly Wobma

MD/PhD student at Columbia University

Holly completed an MD-PhD at Columbia University in New York during which she conducted graduate training in the lab of Gordana Vunjak-Novakovic and helped co-found a cell therapy company called Immplacate. She will soon be starting (June 2019) as a pediatric resident at the Boston Combined Residency Program and is interested in developing and translating cell and gene therapies for pediatric disease.

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