Of the many methods of slowing aging discovered to date most have only a small effect in short-lived species such as mice, around a 10% increase in healthy or maximum life span. Based on what we know of methods where we do have data for comparison, such as calorie restriction, these methodologies are expected to have even smaller effects in longer-lived species such as ourselves. Worth spending time on? Probably not. We need to chase after new and better biotechnology that can provide comprehensive repair of the damage that causes aging, not slight optimizations to our internal engines so that they wear out just a little bit more slowly.
Interestingly, many methods of modestly slowing aging in mammals such as mice have strongly gender-specific effects. This comes as part and parcel of the overall effect being small. Presently envisaged repair biotechnologies to treat aging and bring it under medical control will probably also have gender-specific differences in outcome or implementation to some degree, but these will be very small in comparison to the benefits provided:
A robust, often underappreciated, feature of human biology is that women live longer than men not just in technologically advanced, low-mortality countries such as those in Europe or North America, but across low- and high-mortality countries of the modern world as well as through history. Women's survival advantage is not due to protection from one or a few diseases. Women die at lower rates than men from virtually all the top causes of death with the notable exception of Alzheimer's disease, to which women are particularly prone. Yet, despite this robust survival advantage, women across countries of the world suffer worse health throughout life.
The biological mechanisms underlying either longer female survival or poorer female health remain elusive and understudied. Mechanisms of mammalian biology, particularly with respect to aging and disease, are most easily studied in laboratory mice. Although there are no consistent differences in longevity between mouse sexes even within single genotypes, there are often substantial differences in individual studies, sometimes favoring females, other times males. Investigating the environmental causes of this puzzling variation in longevity differences could prove illuminating.
Sex differences in response to life-extending genetic or pharmacological interventions appear surprisingly often in mice. Longevity enhancement due to reduced signaling through IGF-1 or mTOR signaling typically favors females, whereas enhancement via a range of pharmacological treatments favors males. These patterns could be due to interactions of the interventions with sex steroids, with adiponectin or leptin levels, or with the sex differences in immune function or the regional distribution of body fat. Clearly, generalizations from one sex cannot be extended to the other, and inclusion of both sexes in biomedical studies of human or other animals is worth the effort and expense.