Humphrey's grandmother/redundancy hypothesis could be strengthened; it has problems which indicate that the expertise capacity hypothesis offers a better explanation for the expansion of human brain size. Only research upon microcephalics and others with Homo erectus sized brains and normal IQ can enable us to determine what factor in human evolution led to our enlarged brains.
2. This theory was a conjecture. Without candidate mechanisms, papers arguing for anomalies do not get the attention given to those that argue for anomalies in the context of offering explanatory mechanisms. (One need only think of the reception given to the scientific anomaly normally associated with Wegnener: until the early 1960s, geologists were aware that the continents of South and North America and Africa appeared to have originally formed one land mass which had fragmented, but rejected the importance of this until a physically plausible mechanism, that of plate tectonics, was provided for this fragmentation). I judged that the anomalous existence of individuals with normal IQ and brains no larger than Homo erectus would only be taken seriously if an explanation could be offered as to why humans evolved larger brains if not to increase IQ.
3. Obviously increased expertise is not the only possible theory. Humphrey (1999) has proposed that large brains provide cognitive resilience to the effects of ageing. As he notes, this might have been critical to the reproductive success of early humans, owing to the 'grand mother' hypothesis. Elderly kin, while no longer able to further the propagation of their genes in their own children, can do so through their grandchildren, who will contain a quarter of their grandparents genes. This quarter share of their genes can only be propagated if they are not demented from brain injury or degeneracy. Dementia arises from lack of intact brain; if grandparents have larger brains, they will be less likely to develop dementia, and therefore more able to aid the survival of their genes through their grandchildren. Any gene that prevents dementia, for example by expanding brain size, will enhance its own propagation.
4. Humphrey fails to provide much of the substantive evidence that supports this argument. He discusses the vulnerability of the brain to 'structural damage' from 'external knocks, and internal haemorrhages and tumours, but also to intrinsic processes of cell death and decay'. Mild intellectual impairment has been found in those with head traumas in a study of early-onset dementia of the Alzheimer type (Molgaard, Stanford, Morton, et al, 1990). Neurofibrillary tangles occur in the neurons of those who suffer head injuries, leading to damage to blood vessels or perivascular elements of the kind found in Alzheimer's disease (Geddes, Vowles, Nicoll, & Revesz, 1999). More importantly for his theory, Alzheimer's disease is reported by several groups to be specifically increased in those with small brains (Graves et al., 1996; Mori et al., 1997; Schofield, Mosesson, Stern, & Mayeux, 1995; Schofield et al., 1997).
5. The protective effect of the near doubling of brain size could be significant. Women whose head circumference was within the lowest quintile were found to be at 2.9 (95% CI 1.4-6.1) increased risk of Alzheimer's disease (men, 2.3 times; 95% CI 0.6-9.8) (Schofield et al., 1997). An important factor here is that the lowest quintile contains mostly brains that are fairly large compared to those of Homo erectus size; thus if the effect is proportional to brain size, such individuals must be at far greater risk than 2.3-2.9.
6. Humphrey's theory has been presented here more forcefully than in his commentary. There are, however, several problems with his view.
7. Humphrey does not mention the age of grandmothers and the age of their grandchildren. This matters because the risk of Alzheimer's disease is strongly linked to age. Between the ages of 60 and 69, it is only about seven in a thousand. Even for those between 70 to 79, it is still only just over seven in every hundred (Hagnell, Frank, Grsbeck, et al, 1991). The numbers are only large for those between 80 to 89, where it is one in four (Hagnell, Frank, Grsbeck, et al, 1991); and those that pass 95, of whom 43% have Alzheimer's disease and 15% have some of other kind of dementia (Ebly, Parhad, Hogan & Fung, 1994). Given that early hominids, unlike modern humans, did not delay child rearing, a female would start having children in her teens and continue until menopause in her forties. She would thus start becoming a grandmother in her late thirties and continue until her daughter's menopause. Her grandchildren would require her aid mostly in their preteen years. As a result, most of the help she would give to her grandchildren would occur before she reached 70 when the risk of Alzheimer's disease is still less than 1%. As noted above, people with small brains are at increased risk of Alzheimer's disease. Even so, it would have needed a very large increase in this effect before it prevented grandmothers from aiding most of their grandchildren.
8. This theory assumes that Alzheimer's disease significantly impairs the help grandparents can offer their grandchildren. The numbers above do not distinguish between mild and severe Alzheimer's disease: most people with the disease have the mild form, and the life time risk is about one in four, compared to a one in seven risk for severe Alzheimer's disease (Hagnell, Frank, Grsbeck, hmann, jesj, Otterbeck, et al, 1991). Moreover, much of the impairment of modern people with Alzheimer's disease is a consequence of old people living alone, rather in supportive extended families. In hunter-gatherer bands, old people lived in extended kinship groups which could provide the organisational support necessary to enable those with mild Alzheimers disease to remain productive. For example, manually gathering foods (as opposed to locating them) does not require much mental ability. Likewise, baby sitting requires few mental faculties and can thus free parents for productive activities away from base camp.
9. This theory assumes that increasing brain size does not put the brain at greater risk of brain injury. Physically, however our brains are not well supported in the cranium, and this is made worse when brain mass is increased. Like a large jelly, the human brain twists, moves and wobbles when hit. Such contusions tear blood vessels, axons, and rip the lower side of the brain against the bone protrusions of the lower cranium cavity. Counter-coup injuries occur where the brain is damaged on the side opposite to that upon which it is hit. Such injuries are increased in large brains since while the external membranes that hold the brain in place increase to the square with increased size, mass increases to the cube. Therefore the doubling of brain size results in only a 60 percent increase in its structural support. In addition, body height shows how increasing one bodily dimension creates a disproportionate risk: increasing the height of humans 20% increases the kinetic energy with which they fail by 210% (Samaras, Elrick, H., & Storms, 1999). Any calculation of the benefits of large brains in providing redundancy must subtract the effect of the increased vulnerability to damage.
10. Increased brain size is not the only means by which 'cognitive reserve' can be expanded. Those in education, jobs involving interpersonal skills, or work which involves strenuous activity will have some protection against Alzheimer's disease (Stend, Alexander, Prohovbik, Stricks, Link, Lennon & Mayeux, 1995). While the equivalent of modern job classification used in this study is unknown, it is reasonable to suspect that our earlier ancestors would have scored higher than most modern individuals with regard to social skills (their lives depended upon the alliances and networks they formed) and physical activity. This would mean that the above figures for AD could overestimate their risk for ancient AD.
11. Humphrey's hypothesis shows the critical importance of funding focused research which targets those with normal IQ but Homo erectus sized brains. Such research will provide insight into why our evolution selected large brain size. Do such individuals show severe dementia with age? Do they show defects in the ability to acquire expertise? Indeed, if Humphrey is correct, there are strong clinical grounds for investigating how brain size links to cognitive reserve, since this is directly relevant to understanding the development of dementia, a practical problem in our increasingly ageing population.
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