Eva Emerson, in
Medical News Today (2/11/07) reports on
John Tower's (2006) model for explaining aging and the mortality gap between the sexes. Tower's work with drosophila (fruit flies) suggested that sexula differentiation might come at great cost in terms of aging. Mitochondria seem to be less functional in older fruit flies and mammals, with sex-specific effects.
Yan et al (2004) found mitochondrial aging in monkey cardiac cells was accelerated in males compared to females.
Vina et al (2006) suggest that estrogen may have a protective effect, by "up-regulation of longevity-associated genes."
Ballard and Whitlock (2004 review) point out that much mitochondrial modeling at this point is speculative. Ballard and Whitlock discuss weaknesses in the current data, and in the generalizability of animal models to humans.
I'm still baffled by the mortality gap. Women seem to be more prone to disease, yet outlive men on average. Social theories about fewer violent deaths or lower risk jobs make some degree of sense to me, but considering the other biological costs of accomodating pregnancy, the genetic theories just confuse me. On that note, any comments on my possible misinterpretation of today's results is welcomed.
However, I have to say that the phrase "[estrogen] cannot be administered to males because of its powerful feminizing effects" (Yan et al, 2006) caused me a bit of a chuckle. My male-to-female transsexual friends are constantly complaining about how ineffective estrogen is in comparison to testosterone, because estrogen supplements seem to achieve very little feminization without the complementary testosterone blockers, whereas my testosterone shots shut down my estrogen production on their own.