Human lifespan

Our hunter-gatherer forebears would have had a high infant and juvenile mortality, which biases the calculation of population life expectancy and probably led to the famous ‘nasty, brutish and short’ (Thomas Hobbes) concept of our ancestors’ lives. But, those that did survive into adulthood could actually live a long time. The current estimate for average (more correctly, modal) age at death in Homo erectus hunter-gatherers is 60 years. By comparison, the figure is 15 years for our closest living relative, the chimpanzee.

It is intriguing to consider why, and also how, humans evolved to live so long, and in particular, to live so long after their reproductive period had ceased.

The best bet for ‘why’ seems to be the Grandmother Hypothesis. Post-reproductive parents (grandparents) can help their own offspring with child-rearing and foraging for food, thereby improving the reproductive rate of their children and thus their own genetic success. But it would require high levels of physical and cognitive health in the elderly.

The ‘how’ is more uncertain. What limits our lifespan? Lots of things really, but a conundrum has been a brain protein abbreviated as APOE. APOE is implicated in Alzheimer’s disease, other age-related dementias and cardiovascular disease (stroke and heart attack). APOE regulates cholesterol and lipid levels, and in modern humans it comes in three variants (alleles): e2, e3 and e4. Think of e2 and e3 as helpful, and e4 as a potential trouble-maker. Carrying e4 is associated with increased cholesterol (LDL) levels and increased susceptibility for dementias (including Alzheimer’s) and cardiovascular disease. APOE-e4 is also considered a frailty gene, reducing the likelihood of ‘successful’ ageing. The e2 and e3 forms do the job of e4 without these risks.

Hunter-gatherers had only the e4 variant. Modern humans can retain some e4, but the newer e2/3 have evolved to do its job.

The conundrum is, if hunter-gatherers only had e4 with its associated physical (heart), cognitive (dementia) and frailty risks, how is it they enjoyed a long lifespan?

There’s more than one hypothesis, but one recently put forward is that it had something to do with increased exercise. Great apes and chimps are sedentary by comparison to Homo erectus. The hunter-gatherer lifestyle, which emerged ~2 million years ago, involves trekking over large distances, endurance running and remembering what is good to eat and where it might be found. It was a lifestyle of physical and cognitive exercise. And even the grandparents had to keep up with the tribe and its nomadic pursuits. Our ancestors were endurance athletes, and were able to live into old age despite carrying e4.

There is mounting evidence that in present day humans, physical exercise, such as cardio-vascular exercise, is good for the ageing brain. Notably for carriers of e4.  The mechanisms whereby this occurs are still not well understood, and neither is the form of exercise, the intensity, the frequency or the stages of life at which it should be undertaken. But there is an emerging view that physical, mental and social aspects of health are more interrelated than once thought, and together make for an updated definition of ‘fitness’.

The later evolution of e2/3 variants in H. erectus/sapiens may have arisen to further extend lifespan (so that grandparents could live to help with their great-grandchildren). It has also been suggested that it was secondary to an increased dietary fat intake – as hunters became more successful and meat/fat intake rose, exercise alone may not have been enough to counter the negative aspects of e4.


Reference:
D.A. Raichlen and G.E. Alexander “Exercise, APOE genotype, and the evolution of the human lifespan”. Trends in Neurosciences (2014) 1047: In Press.