We think we know, in our more lucid moments, how old we are, but don’t we also know that our age by the calendar is not the whole answer, and not the age that really counts? On a deeper level we know that our body keeps its own calendar, and keeps it hidden. Our body has its biologic age, but we can only guess what it is. So we peer at ourselves and others, guessing at clues of biologic aging in new facial wrinkles, greying hair patterns, a stoop in the neck, or a hint of hesitation in the gait.
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Until recently, we’ve had no better measures of biologic aging, but now we have several, hopefully. And now that we can measure how fast our bodies are aging, we can start asking some new questions. What speeds up the biologic aging process and what slows it down? How does illness or stress or intimacy affect how we age? The development of measures of biologic aging could be a game-changing event for understanding the factors that determine who might live to be a hundred and who is likely to die young.
The first modern effort to measure the biologic aging process was Bruce McEwen’s concept in the 1990’s of “the allostatic load index,” defined as the accumulated burden of the wear and tear of life represented by a set of about 10 measures of physical functioning of a person’s cardiovascular, endocrine, and metabolic systems. McEwen’s hope was that combining multiple measures of physical functioning that worsen with age could capture the state of a person’s body along the path from health to death. Various definitions of the allostatic load index correlated with early chronic illness and early death, but measuring this index has proved too complicated and expensive for clinical practice.
Next came telomeres. In the early 2000’s it became clear that as we age, our telomeres, or the ends of our chromosomes, fray and shorten, just as the ends of shoestrings fray with wear. And the rate at which our telomeres shorten depends in part on our calendar age and in part on the wear and tear of life. In animals as well as humans, telomere length can be a good measure of biologic age. However, like the allostatic load index, there are many ways to measure telomere length in humans, and none has proven reliably better than the others. After twenty years of research on telomere length in humans, the translation of this research into clinical practice is still a thing of the future.
More recently some more accurate measures of biologic aging have been found in the ways that methyl molecules attach to DNA as we age. This process of DNA-methylation can now be read as a kind of epigenetic clock that tells us about how our body is aging. (Epigenetics studies how environmental factors influence the expression of genes.) These measures of DNA-methylation have been associated with heart disease, cancer, Alzheimer’s, and early death.
A study published earlier this year by a group from Emory University found that in a sample of male twins post-traumatic stress disorder (PTSD) was associated with epigenetic age acceleration. That means the persistent stress of PTSD contributed to faster aging. And the more severe the PTSD was in the affected twin, the greater the age acceleration relative to the unaffected twin. This study adds to the growing evidence that some forms of toxic stress can accelerate biologic aging and early death.
For example, we also know from a range of epidemiologic studies that poverty, minority status, chronic physical or mental illness, adverse childhood experiences, loneliness, and discrimination all shorten life by many years. Does that mean that these conditions all exert their toxic effects on aging by somehow speeding up the process of adding methyl molecules to our DNA? It’s possible, but we certainly don’t know yet that these different types and patterns of toxic stress—persistent demands that exceed a person’s resources—all share this common epigenetic mechanism for accelerating biologic aging.
On the brighter side of this story, last year a group from Yale published a study of a healthy community sample in which cumulative life stress was associated with biologic aging measured by DNA-methylation. And they also found that resilience in the form of good emotion regulation protected these healthy people from dying young in spite of high stress. These measures of DNA-methylation are still a research tool, but some version is likely to be developed soon as a clinically useful measure of biologic aging.
It’s still early in the process of developing measures of biologic aging that will be useful to patients and their clinicians, but these studies point to a few lessons worth thinking about. Since genes run the show, the best measures of the speed of aging are likely to be found in our genes, if we can learn to read them. Our environment exerts big effects on the expression of our genes, so we have lots to learn about factors that speed up aging, like PTSD, and factors that slow it down, like emotion regulation. And we don’t yet know which kinds of stress exert big effects on aging and which exert small effects.
The day is coming when “How old are you?” will no longer be a simple question with a simple answer.