A recent study of 9-YO African-American boys showed that increased stress led to increased shortening of telomeres that was presumed to be related to dopamine and seroatonergic genotypes.
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Stress causes accelerated “aging” in children

A recent study of 9-YO African-American boys showed that increased stress led to increased shortening of telomeres that was presumed to be related to dopamine and seroatonergic genotypes.


African-American boys age faster when socially stressed


This correlation had previously been shown in Romanian orphans in 2011:

Foster care helps protect DNA


But reexamine the headline and we must admit that the language is failing us.  The symbols we use to encode the headline reflect the flawed assumptions of the signified relationships.  When we say stress causes “aging” in children we are really implying the following inferences subtextually:

We assume that white blood cell telomere length as we measured it is an indication of the biological age of these children because broadly speaking, it appears that shortening of telomeres is associated with aging and is therefore an accurate and direct reflection of it.  Furthermore, we assume that aging is a real thing and not just a subjective and amorphous concept which emerges from our human-scale perceptions.

Furthermore, we assume that social stress somehow impacts telomere regeneration via decreased telomerase activity or increased erosion although we arbitrarily presuppose that the mechanism is dopaminergic and seratonergic in etiology because that is the core premise of previous research in this area of social science. We ignore that their poor telomere maintenance could also be considered to be mitigated through disturbed sleep, cortisol excess, anxiety, and other covariables in poor holistic wellness.

Finally, we are so driven to be interesting and evocative in our take-home conclusion, that we gloss over the the fact that all humans, from embryo to supercentenarian, are subject to the very same detriments to telomere maintenance and repair and that the primary mediator of this poor telomere health appears to be insufficient telomerase activity, which is not measured or considered in our explanatory model.”


What I find the most interesting is that if we’re using telomere length as a proxy for aging, the most rapid “aging” occurs in utero, not when we are older.  In other words, the loss of 1/3 of our life expectancy from (15,000 base pairs at conception to 10,000 at birth) represents the hyperaging at the opposite end of the life spectrum where we would normally even use such a term.  This is unlikely to be seratonin and dopamine-mediated as even the most blissful of maternal-fetal dyads share the same erosion. Therefore,  the likely culprit is the incredibly rapid cell divisions causes replicative senescence that simply cannot be compensated for by standard telomerase activity levels between subsequent cell divisions. In fact, all of childhood appears to be a time of much more rapid telomere “aging” than adulthood!

After I get “probonotrials.org” off the ground, one of the most interesting studies will be to see whether in utero exposure to telomerase activation can safely maintain the birth endowment of telomere length in an animal model. If that holds true, then consider that a developing human embryo/fetus that is exposed to steady-state telomerase maintenance could have a median life expetctancy of 120 with a maximum of 160 if the birthday length remained at the 15,000 that was present at conception.

So perhaps an improved headline would have been: “insufficient telomere relengthening is associated with social stressors although the mechanism is unclear.”  But I suppose that would be a pretty unappealing headline despite its relatively clean and valid text and subtext.

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