October 31, 2005
Paternal Inheritance Found For Telomeres Which Influence Longevity

A research team at UmeŚ University in Sweden have found that the telomere length influence on aging appears to be inherited from fathers, not mothers.

Telomeres are genetic material with repetitive content at the ends of DNA, and their main function is believed to be to protect the rest of the genetic material from degradation. Telomeres are shortened each time a cell divides, which in broad terms means that the longer a cellís telomeres are, the longer the individual can live, in theory. A personís telomeres are shortened with age, which the findings of the study indeed show: telomeres were shortened by an average of 21 nitrogen base pairs per year in the subjects studied.

The study, soon to appear in the U.S. scientific journal PNAS, Proceedings of the National Academy of Sciences, was carried out on 132 healthy subjects in 49 different families with no close kinship to each other in northern Sweden. The subjects consisted of fathers and mothers (mean age 66 years) and their daughters and sons (mean age 37 years). Blood samples were taken, and mononuclear immune cells were culled.

Half of these were simply frozen, while the other half were infected with Epstein-Barr virus (EBV) and cultured for 18-55 days, whereupon the surviving cells were frozen. DNA was then extracted from both cell types using standardized techniques, and the length of the telomeres was ascertained.

The findings show that changes in the length of the telomeres in the cultured cells are determined by the original length of the telomeres, and the length of the telomeres in the second generation, both sons and daughters, proved to be inherited from the father.

Telomeres are caps on the ends of chromosomes. They get shorter each time cells divide. As the telomere caps become really short they start to interfere with cell division. This is one of the causes of aging. Telomere cap shortening is probably an evolved mechanism to reduce the risk of death from cancer. Cancers need to undergo a mutation to activate telomerase to grow longer telomere caps so that the cancer cells can divide many more times than normal cells can.

Given that shorter telomere lengths probably reduce cancer risk it is by no means guaranteed that people who inherit longer telomeres from their father will live longer on average.

I would be curious to know what the mechanism might be to cause telomere length to track with paternal inheritance. Do sperm genes for telomerase expression have a methylation pattern or other circumstance that makes them become active as soon as the sperm and egg meet? Does paternal telomerase regulatory genes get turned on while maternal telomerase regulatory genes are suppressed?

Suppose this finding holds up upon further investigation. The female line of descent still has at least one big unique influence upon longevity: mitochondrial DNA. That comes solely from the female line of descent the vast bulk of the time (though perhaps not always).

The abstract and full paper can be found here.

Also see my previous posts "Telomere Length Indicates Mortality Risk" and "Chronic Stress Accelerates Aging As Measured By Telomere Length".

Share |      Randall Parker, 2005 October 31 09:15 PM  Aging Studies


Comments
James Bowery said at November 1, 2005 10:54 AM:

Another interesting question is whether this mechanism, whatever it is, is really selectively neutral or whether the evolutionary pressures which tend to create more robust telomeres fall primarily on the males.

It may be the case that this selective pressure has to do with the capacity for technology transfer between generations.

A way to test the hypothesis is to see if this mechanism also exists in species where R-strategies predominate.

Kelly Parks said at November 1, 2005 12:01 PM:

So do commercially available telomere-length blood tests exist yet?

Patrick said at November 1, 2005 2:17 PM:

My long lived ancestors are on my mother's side. Doh!

Radford Neal said at November 2, 2005 11:04 AM:

Perhaps this is an anti-cancer mechanism. If only one copy
of the gene that preserves telomeres is activated, there's
only half the chance of a mutation that would allow cancer
cells to preserve their telomeres for longer. (I suspect
that the true situation would be more complicated than this,
but maybe there's something to the idea.)

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