After a big week in Australia and New Zealand talking about fat and cholesterol, things are settling down a bit. As we all draw a collective breath, I have been reflecting on a few things. One thing that struck me was the immediate objection of my position on the study of human food in the context of evolutionary biology. Dr Lisa Te Morenga commented immediately on my blog site after my post laying out some logic and evidence for higher fat lower carb diets. Lisa and I have talked about my approach a bit recently.
Lisa is a Research Fellow in the Department of Human Nutrition at the University of Otago. Her research interests involve the effects of macronutrient composition on physiological endpoints associated with increased risk of preventable diseases. So she is really following this with interest, and skepticism I imagine (we like skepticism, it just goes both ways).
She had some detailed comments about studies which was great. I raced off and found them, so thanks. She also said this “And on the topic of Paleo diets, it is worth remembering that our fabulously healthy paleo ancestors were lucky to make it to the ripe old age of 35, which is hardly a ringing endorsement of the paleo diet.”
Or did they?? Given we are all interested in actual evidence here, I was supplied a very good reference by Jamie Scott and thought I might share some of the conclusions with you here. It was really interesting.
These guys (reference) went and did a massive amount of data collection and modelling looking at life expectancies in Sweden in the 1750s, modern US life expectancies, the life expectancy of several modern hunter gatherer tribes, and that of captive and wild chimpanzees.
First, I won’t pretend I understand all the mathematical modelling. Second, no one actually recorded how long prehistoric hunter gatherers actually did live. So this is speculation, but speculation with serious data and rationale. It’s interesting to think about how long our ancestors lived and what they probably died from.
I think that consideration of the environment(s) our ancestors were exposed to, and how these affected their biology, is what scientists in every area of biology do. Why would nutritional science and the study of chronic disease be any different? Anyway, here is summary of the study’s main findings (their words not mine):
(from the paper)
- Post-reproductive longevity is a robust feature of hunter-gatherers and of the life cycle of Homo sapiens. Survivorship to grandparental age is achieved by over two-thirds of people who reach sexual maturity and can last an average of 20 years.
- Adult mortality appears to be characterized by two stages. Mortality rates remain stable and fairly low at around 1 percent per year from the age of maturity until around age 40. After age 40, the rate of mortality increase is exponential (Gompertz) with a mortality rate doubling time of about 6–9 years. The two decades without detectable senescence in early and mid-adult- hood appear to be an important component of human lifespan extension.
- The average modal age of adult death for hunter-gatherers is 72 with a range of 68–78 years. This range appears to be the closest functional equivalent of an “adaptive” human life span.
- Departures from this general pattern in published estimates of life expectancy in past populations (e.g., low child and high adult mortality) are most likely due to a combination of high levels of contact-related infectious disease, excessive violence or homicide, and methodological problems that lead to poor age estimates of older individuals and inappropriate use of model life tables for deriving demographic estimates.
- Illnesses account for 70 percent, violence and accidents for 20 percent, and degenerative diseases for 9 percent of all deaths in our sample. Illnesses largely include infectious and gastrointestinal disease, although less than half of all deaths in our sample are from contact-related disease.
- Comparisons among hunter-gatherers, acculturated hunter-gatherers, wild chimpanzees, and captive chimpanzees illustrate the interaction of improved conditions and species differences. Within species, improved conditions tend to decrease mortality rates at all ages, with a diminishing effect at older ages. Human and chimpanzee mortality diverge dramatically at older ages, revealing selection for a longer adult period in humans.
Frequency distribution of ages at death f(x) for individuals over age 15 shows strong peaks for hunter- gatherers, forager-horticulturalists, acculturated hunter-gatherers, Sweden 1751–79, and the United States 2002 (both sexes). All curves except for Sweden and the United States are smoothed using Siler estimates.
The seven decades hypotheses – also called the grandmother hypotheses
My second musing this week is the idea that grand parenting and multigenerational survival up to seven decades conferred a reproductive and therefore evolutionary advantage to be selected for in prehistoric humans. It revolves around an extended cultural and skill development related to our big brain and long learning and skill acquisition period.
This is a very cool theory. It proposes that the existence of grand parents of both sexes was a selective pressure on the gene pool.
It proposes that timing of life events is best understood as an “embodied capital” investment process. Embodied capital is organized somatic tissue, which functionally increases lifetime adult income and includes strength, skill, knowledge, and other abilities. Humans are specialists in brain-based capital. High levels of knowledge and skill are required to exploit the suite of high-quality, difficult-to-acquire resources humans consume. Those abilities require a large brain and a long time-commitment to development. This extended learning phase, during which productivity is low, is compensated for by higher productivity during adulthood. Since productivity increases with age, the time investment in skill acquisition and knowledge leads to selection for lowered mortality rates and greater longevity, because the returns on the investments in development occur at older ages. According to this model, the long human life span co-evolved with the lengthening of the juvenile period, increased brain capacities for information processing and storage, and intergenerational resource flows. It is a two-sex model, as it proposes that both men and women engage in learning-intensive food production tasks; these activities result in delayed productivity until older ages, selecting for life span extension in both sexes.
As the number of closely related dependent kin eligible to receive investment decreases after age 65, the fitness benefits of longer life decrease and there is less evolutionary incentive to pay increasing maintenance and repair costs to remain alive and functional beyond this period.
Chronic degenerative diseases rare
Most modern humans will die from a chronic disease or its complications. We all have to die sometime from something, but the problem with chronic disease is the disability and reduced quality of life before death. We now live longer than ever before in human history, but the quality of life may be impaired. What we seek to do in public health is think about how we can maximize both quality and quantity of life (or get the best trade off). There are also economic considerations – if we have people dying slowly form chronic diseases, that costs a lot of money in care and management.
So how do our ancestors compare with us, in terms of cause of death?
Most died from illness or accident; only about 1/10 from degenerative diseases. Remember that the leading cause of death worldwide is now chromic disease and the bulk of people in the developed world can expect to die form a chronic disease. We also know that chronic disease will likely result in more than a decade of health-related disability before death. So people did die young. Many died at birth and in the first few years of life. The overall chance of death at anytime up to the age of 40 was higher and most likely due to illness, accident, or warfare. After that, there is quite an increase in mortality, with the modal age of death around 72 years.
Degenerative deaths were relatively few, confined largely to problems early in infancy and late-age cerebrovascular problems, as well as attributions of “old age” in the absence of obvious symptoms or pathology. Heart attacks and strokes appear rare and do not account for these old-age deaths (see Eaton, Konner, and Shostak 1988), which tend to occur when sleeping. It has often been remarked that few risk factors for cardiovascular disease exist among active members of small-scale societies (Eaton et al. 1994), although compromised lung or kidney functioning can interact with cardiac fibrosis or moderate arterial stenosis to cause cardiac arrest. Obesity was rare, hypertension was low, cholesterol and triglyceride levels were low, and maximal oxygen uptake was high. Overall, degenerative disease accounted for 6–24 percent (average 9 percent) of deaths, with the highest representation among Northern Territory Aborigines. Neoplasms and heart disease each accounted for 9 of the 42 deaths due to degenerative illness. It should be pointed out, however, that chronic illnesses as causes of death are the most difficult to identify, since more proximate causes are likely to be mentioned. To our knowledge there have been no focused studies or mention of Alzheimer’s, Parkinson’s, or other forms of dementia.