That was TIME’s lazy headline yesterday about a study on the effects of physical activity on telomeres.
Telomeres are the caps at the ends of DNA strands that protect our genetic information.
Every time our cells replicate, the caps get a little bit shorter and a little less capable of protecting our DNA. Eventually they become so short that they fail to work at all and our cells stop dividing.
So the shorter our telomeres, the thinking goes, the older our cells are biologically and the more susceptible we become to diseases that may kill us.
That’s the thinking, anyway — and this narrative was pushed hard not just by TIME but by a variety of other outlets that all bore a striking resemblance to a UC San Diego news release headlined, “Too Much Sitting, Too Little Exercise May Accelerate Biological Aging.”
HealthDay: Too Much Sitting Ages You Faster
Agence France Press: How too much sitting and too little exercise could be aging you
What about the larger body of evidence?
Had they done more than scratch the surface of this topic, journalists would have quickly realized that the science here is a lot more complicated — and questionable — than the narrative on offer from UCSD.
For one thing, the relationship between telomere length and aging is not nearly as straightforward as these stories suggest. Take the findings of a 2013 review of epidemiological studies on the topic:
Although shorter leukocyte telomere length seems to be associated with older age, male gender, and Caucasian race, leukocyte telomere length has been inconsistently associated or not associated with other characteristics of aging or age-related chronic disease, including death. Inconsistency might be due partly to differences among study populations, measurement methods, and statistical modeling, although it also could imply that an association does not exist.
The association might not exist?
That’s not something I saw in any of these sitting stories, which were all oddly precise in claiming that too much couch time would age your body by exactly 8 years.
James C. Coyne, PhD has written extensively on the problems of using telomere length as a biomarker of aging and compares it to premature acceptance of prostate specific antigen (PSA) levels to guide prostate cancer treatment. The adoption of PSA led to “So much needless worry, treatment, and so many men left with impaired functioning, with negligible effects on prostate cancer mortality,” he says.
Coyne’s own look at the literature raises some fundamental concerns with telomere science.
- Widely-accepted claims about telomeres predicting mortality are contradicted by some quality meta-analyses and large-scale population-based studies.
- Predictions of future onset of chronic illnesses from telomere length have not been reproducible in meta-analyses and large-scale population-based studies.
- Even when found, the associations in large scale, quality studies between telomere length and outcomes like disease onset and mortality are quite modest.
- Associations claimed between exposure to stress and telomere length have not been reproducible in large scale studies.
- Cross-sectional associations of telomere length are often not borne out in prospective longitudinal studies.
None of the stories I looked at consulted an independent source like Coyne, nor did any of them apparently do a cursory search about the evidence on telomeres. Had they done so, they would have quickly run into Daniel Engber’s excellent Slate piece that shreds one of the seminal studies in this field and raises questions about the fundamental science behind telomeres.
Incomplete stories help to market dubious products
These stories aren’t harmless. They feed into a narrative that’s the foundation for tests, supplements, and “programs” that promise to lengthen your telomeres but which aren’t backed up by evidence. We’ve seen it all before a number of times.
Michael Joyner, MD, a Mayo Clinic researcher, told me the current frenzy around telomeres reminds him of similar claims made about sirtuins, a class of proteins that are thought to regulate aging. GlaxoSmithKline in 2008 paid $720 million for Sirtris pharmaceuticals — a company that sought to make drugs that act on these proteins. Despite claims that these proteins act as a “molecular fountain of youth,” the promised anti-aging drugs have yet to materialize. GSK shuttered Sirtris’s Cambridge offices in March 2013, spinning the move as an opportunity to take sirtuins “to the next level of development.”
“Let’s just say given the [poor] track record of even the most bio-plausible ideas by the most prominent people (going back to Linus Pauling and before), great care needs to be taken with any such claims” about anti-aging interventions, says Joyner. “The bar needs to be set very high.”
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