Science, Aging, and Yoga

by Brad

Paris in the Rain by Brad Gibson 

So I promised I would get back to the question of how one would use science to study the effects of yoga on aging. As a starting point, let’s look at one highly publicized study that appeared a few years ago in Lancet Oncology (see here).

This work was collaboration between Elizabeth Blackburn, a prominent and highly respected biochemist at UCSF and recent Nobel Prize winner in Medicine, and Dean Ornish, a clinician at UCSF and well-known author of books and articles linking better nutrition to health and disease prevention, especially for coronary heart disease. The basic premise of their 2009 Lancet study was to examine whether relatively short-term lifestyle changes consisting of a low-fat diet, moderate exercise and yoga-based stress management could effect telomerase activity in circulating blood peripheral blood mononuclear cells (PBMCs) that are largely cells involved in immunity. 

The authors enrolled 30 men with a pre-diagnosed low-risk for prostate cancer for a three-month regimen. They measured telomerase activity, an enzyme present in certain class of replicating cells that maintains the length of telomeres. Telomeres are repetitive stretches of DNA at the ends of chromosomes that protect the integrity of chromosomes, and with each cell division gets shorter. Telomere shortening has been shown to negatively affect a cells capacity to replicate and general maintenance. Telomere shortening has been suggested as a biomarker of aging, acting as a type of clock for cellular aging. This so-called “telomere theory of aging” has gone out a favor among some scientists in recent few years, and its role in aging is controversial. Nonetheless, the basic premise underlying this study is that higher telomerase activity will lead to longer telomere lengths, which will set back the aging clock a bit in some way, or at least lead to healthier immune cells.

The author’s conclusions were as follows: “Comprehensive lifestyle changes significantly increase telomerase activity and consequently telomere maintenance capacity in human immune-system cells. Given this finding and the pilot nature of this study, we report these increases in telomerase activity as a significant association rather than inferring causation. Larger randomized controlled trials are warranted to confirm the findings of this study.”

What they mean here is that the number of patients in the study was low (N=30 is very small for a study of this type, and only 24 of these could actually be followed up the multiple times needed over this three-month period for technical reasons), the patients were pre-selected as having a clinical diagnosis of possible “low-risk prostate cancer” (that is, not a random group and probably motivated for a positive outcome), and that the results can at best be interpreted as an association and not necessarily a cause of the three-month lifestyle change (that is, just because thus group showed an increase in their telomerase activity, it doesn’t mean it resulted from the lifestyle intervention, but it could be the result of any one of a number of variables that were unaccounted for during this period, sometimes referred to as “confounders”).

But larger randomized properly controlled trials are expensive to run, and without a serious backer—the government or a drug company—don’t expect to see a follow-up any time soon. Just think about the large-scale trails of vitamin E that after many years and millions of dollars not only failed to establish a link but also showed a possible negative association. This is part in parcel of the tough love and art of large-scale clinical trials that are required if you want to prove something using rigorous scientific methods. 

So what did this study actually show? At minimum they showed what was needed for carrying out a larger study (power calculation) to actually determine a causal relationship. No mechanism was defined for why telomerase activity increased, although several were suggested (reduction in oxidative stress and inflammation, for example). Otherwise one shouldn’t draw too many conclusions from this study, especially since three independent variables were introduced (diet, exercise and yoga) and the study group was so small and biased. And one has to also keep in mind that the telomere length was not directly measured, as the authors themselves pointed out that telomere length changes would likely to be too small to measure in such a short time (three months). So I guess there’s another message to take home: some things take time.

Reports like these remind me of one of the reasons I have sympathy for the “N of 1” studies, that is, experimenting on yourself. Not real science, but you’ve got to try something. Take up yoga, improve your diet, have a walk everyday, and see what happens. 

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