New telomerase finding only a small-medium sized deal

The press has been making a big deal of research made public a few days ago that correlates a genetic defect in one of the key telomerase-producing genes TERC with shorter telomeres later in life.  This link leads to 23 news stories on the research.  The abstract of the study itself Common variants near TERC are associated with mean telomere length reads succinctly:  “We conducted genome-wide association analyses of mean leukocyte telomere length in 2,917 individuals, with follow-up replication in 9,492 individuals. We identified an association with telomere length on 3q26 (rs12696304, combined P = 3.72 x 10(-14)) at a locus that includes TERC, which encodes the telomerase RNA component. Each copy of the minor allele of rs12696304 was associated with an approximately 75-base-pair reduction in mean telomere length, equivalent to approximately 3.6 years of age-related telomere-length attrition.“  This site graphically shows key data produced by the study. 

 The study says that people who possessed the gene variation (minor allele of rs12696304) had shorter telomere lengths, equivalent to 3.6 years of aging.  People who had two copies of the variation had telomere lengths expected for people 7.2 years older.  The implication is that people with the gene defect age faster.  I think the study is a good piece of research to add to the aging puzzle but that it is not the big-deal breakthrough suggested in the news headlines because:

–         The result is what would be expected all along; a defect in a telomerase-making gene results in the production of less telomerase resulting in telomere lengths being less than expected.  Some of the headlines make declarations like Scientists find genetic link to ageing  which are rather misleading.  The link of telomerase genes to aging has been known for decades now. “The existence of a compensatory shortening of telomere (telomerase) mechanism was first predicted by Soviet biologist Alexey Olovnikov in 1973^[1], who also suggested the Telomere hypothesis of ageing and the Telomere relations to cancer. Telomerase was discovered by Carol W. Greider and Elizabeth Blackburn in 1985 –(ref).”  We knew back in 1998 that there was Severe growth defect in mouse cells lacking the telomerase RNA component.

–         Several other gene variations also lead to telomere dysfunction or shortening and/or accelerated aging.  See, for example, the blog posts Werner Syndrome – another model for aging, Progerin, HGPS and a possible new theory of aging and Hoyeraal-Hreidarsson Syndrome and telomere dysfunction.Gene variations that lengthen telomeres or extend lifespans tend to grab me more.  For example, a report on how adding extra copies of a telomerase gene and a P53 gene can extend the life of mice by 26% to 40%(ref).

The idea raised by this study of people aging at variable rates depending on their genes is an interesting and probably valid one though definitely not new. Children born with a mutation in the LMNA gene look old and wizened and are experiencing the ravaging diseases of old age when they are only 14 or 15.  See the blog entry Progerin, HGPS and a possible new theory of aging.  Personally, I believe lifestyle and behavioral factors affect the rate of aging along with the genetic ones.  That is the point of the lifestyle and dietary supplements regimens suggested in my treatise ANTI-AGING FIREWALLS THE SCIENCE AND TECHNOLOGY OF LONGEVITY.