However, in the short term there are more telling pressures. A key consideration throughout our story has been genetic diversity; it is, after all, the slowly evolving diversification of mitochondrial DNA and Y-chromosome lines that has been helping us to trace our past. What has not been emphasized so far is the fact that, while we are still recovering from the last ice-age cycle and previous bottlenecks, our total genetic diversity remains relatively low. Our lack of diversity as a species lays us open to new pandemics of infection in crowded, interacting communities.
Diversity, diversity, diversity
Here’s an anecdote. When I was working in Hong Kong, one of my senior lecturers was a charming and sincere Taiwanese paediatric cardiologist. She asked me once what the difference was between killing a tiger for its body parts and slaughtering cattle. This was not an insensitive question. She did not personally take any tiger-bone medicine and felt sorry for tigers and their loss, because they were such beautiful animals. In short, she disagreed with the trade; but she was not convinced by the Western-imposed philosophical argument that the act of killing was immoral for one large animal and not for another. Nor could she see from a logical, detached point of view why it is necessarily more important to preserve a large, and to us beautiful, mammalian species than, say, a rodent.
I scratched my head for an appropriate philosophical answer to the question as posed, an answer which would avoid the issue of whether we had the right to take animal life at all, and would also avoid invoking the aesthetic appeal of big cats. Eventually, I think, I persuaded her that the objective difference between killing members of the two large species, one wild and one domestic, from the perspective of conservation was in preserving biological diversity or variety.
Domestic cattle, as a whole, have very little of their ancestral (aurochs) genetic diversity left, but they have millions of copies of that remaining diversity. Domesticating a species always reduces its overall diversity, though it may introduce variation in specific qualities such as size. By contrast, each of the few thousand remaining wild tigers still holds a significant proportion of the original diversity of their various races, so any one tiger is a unique genetic treasure house for the species and therefore much more valuable than one cow. So, apart from the fact that tigers are at greater immediate risk of extinction than cows, killing one tiger also affects a much greater proportion of species diversity than killing one cow.
Another big cat, the cheetah, is at even more at risk of extinction than the tiger. This is not just because of low numbers, but because there is virtually no diversity left in wild cheetahs – they are nearly all related to possibly a single pair that survived the last ice age. Surprisingly, non-Africans are closer to cheetahs and cattle than they are to tigers in respect of their genetic diversity, since they can all trace their lines back to a few mothers and fathers who left Africa only 85,000 years ago.
So what is so important about diversity, apart from the aesthetic aspect of variety? The answer is survival. Random diversity is nature’s and evolution’s fuel depot. Without randomly generated genetic diversity, species lack the flexibility to survive and adapt to the various stresses imposed upon them. Random diversity takes many generations to develop from a single breeding pair, so species which have gone through a tight genetic bottleneck have a lot of catching up to do.
Killer disease
It may come as a surprise to hear that we are still under constant evolutionary stress. The best and most important example of an ever-present and ever-changing evolutionary stress is infectious disease. Bacteria and viruses evolve much faster than we do. To combat new varieties of disease which bugs evolve to ‘invade’ us with, we each have built-in diversity in our immune system to enable us to identify new varieties of bugs and set up a specific defence. The capacity of the body to recognize and combat a variety of different infectious diseases is genetically determined. The diversity of immune response held in each of us has limits, however, and depends partly on the particular bugs that our own community has met in the past.
Most of such genetic variation in resistance to disease operates through the adaptive immune system. Some populations appear to have a sounder immune response to certain diseases which may have afflicted their ancestors in the past. I came across an example when I was working in Hong Kong, where ethnic Chinese children almost never fall sick with meningococcal disease (meningitis and/or septicaemia). They usually develop detectable specific immunity to meningococci in the blood but, unlike Europeans and other non-Chinese groups, they completely avoid the disease and also do not act as carriers for the bug. In contrast, the commonest organism to find in Hong Kong Chinese with meningitis is the tuberculosis bacillus, which is extremely rare as a cause of meningitis in other developed populations. This implies that there are differences in the quality of aquired immunity to specific diseases between different modern populations.
Against other infections such as malaria, our innate defences are not solely immunological. Certain genetic disorders common in the tropics, as a result of evolutionary selection, directly impair the successful multiplication of the malarial parasite. This mechanism of genetic protection against disease in the case of malaria, one of the greatest killers, lies in inherited disorders of red blood cells, where the parasite seeks to make its home. These genetic disorders, a large proportion of which go under the general name the ‘thalassaemias’, are common in regions that suffer or have suffered malaria in the recent past. The name derives from Greek ‘θαλασσα’ for the sea, since some Mediterranean islands such as Cyprus have high rates of these diseases. These disorders however occur throughout tropical and sub-tropical regions.
As the host evolves more appropriate defences for the bugs, however, the bugs are themselves busy evolving to get round the new defences. The trouble is their evolution is faster than ours. The smartest are those that do not kill their host. Unfortunately not all bugs realize this. The evolutionary leapfrog race between infectious disease and animal hosts often takes a bad turn for the host when the bugs jump from one species to the next. Some of our most virulent viral and bacterial diseases, including bubonic plague, emerge from animals living in the wildernesses we invade. Another such hitchhiker is the human immunodeficiency virus (HIV), which is now overtaking tuberculosis and malaria as the modern captain of death.
There is a self-comforting myth that Aids is a one-off ‘bad luck’ plague, uniquely super-lethal because it attacks the immune system, and its like will not appear again. Not so: it is a warning of the complex opportunism of infectious disease, which we will meet more and more as we expand into the corners of our shrinking world. In any case, the two varieties of the virus, HIV1 and HIV2, may derive independently from two different African primate species. In turn, our increasing fondness for intercontinental travel and fraternization helps spread diseases which, in the past, might have remained localized. As I write, a new infectious disease going by the acronym SARS has arisen in South China and simply adds to the list of exotic and serious infections that may have arisen in animals; it has then subsequently spread internationally from human to human aided by the jet plane.
Genetic intervention
One answer to the increasing threat of pandemic disease may seem to be genetic intervention. Every few weeks, documentaries and newspaper stories tell us of advances in genetic prediction and intervention which are going to change our lives and those of future generations. Genetic disease will be eradicated, we are told, and the more well-heeled in our societies will be able to specify designer babies or pick a clone off the shelf.
Prenatal diagnosis and genetic counselling services for lethal and serious genetically determined blood disorders have been around for some time and make an enormous difference to the lives of individuals. They have had a major influence in countries such as Cyprus, which suffers high rates of beta thalassaemia mutations as a result of previous malarial selection. Such ethically motivated interventions will continue to prevent individual
misery.
However, what genetic intervention cannot do is increase our collective genetic diversity. Putting aside the ethical and technical problems, the fact is that genetic intervention can only reduce diversity. This applies equally to the abhorrent concept of culling the more subjective ‘undesirable’ genetic elements, as practiced by the Nazis on a variety of patients with mental and other disease as well as on Jews and gypsies, and to the Brave New World concept of designer humans. Even if a new breed of geneticists were able to design an especially ‘good model’ that found a large market among potential parents, the exercise would be self-defeating. A clone of such superhumans expanding in our midst would reduce our herd diversity, thus increasing our herd susceptibility to new infectious diseases.
Interestingly, the two characteristics of our species which interest us most, our brain size and our longevity, are potentially amenable to simple genetic interference. The former more than the latter. It seems likely that if scientists were allowed to, they could ‘make’ a human with an even larger cerebral cortex within decades, based on present knowledge. This could be either by manipulating single homeotic genes (genes that control the organization of the embryo and body organs) or more crudely by injecting the product of that gene at an appropriate time in embryonic development. Whether a genetically engineered ‘big-brain’ would be wiser or more intelligent, I do not know. I hope not to survive long enough to see it.
As far as longevity for the rich is concerned, there may be some business opportunities . . . – but there are also warnings. Ira Gershwin had a nice, though politically incorrect, take on Methusaleh’s longevity in the lyrics of the song ‘It Ain’t Necessarily So’ (from George Gershwin’s Porgy and Bess): ‘But who calls dat livin’ / When no gal’ll give in / To no man what’s nine hundred years?’ And there is the risk of overcrowding. According to a Vietnamese origin story, humans originally gained immortality by burying their dead under the tree of life. One day the lizard, who was fed up with having his tail trodden on by the crowd, suggested burying the dead under the tree of death. Life became easier after that.
Has evolution stopped?
Some geneticists argue that natural human evolution has stopped now that medicine allows the less fit to survive thanks to extraordinary advances in disease control and genetic interventions such as counselling and prenatal diagnosis. This seems absurd. Most of the world has limited access to such luxuries, and their influence on diversity of the world’s population as a whole is relatively small. Prenatal diagnosis is in any case intended mainly for single-gene disorders, causing life-threatening disease when inherited from both parents, sufferers from which would usually have had a major reproductive disadvantage if they had survived.
As long as we continue to die, during our fertile period, from diseases that can be affected in any way by our genes, evolutionary selection will continue to operate. Apart from infection, other killer diseases, which carry a genetic predisposition, such as cancers are unaccountably on the increase. Male sperm count is also falling. While these pressures may result from chemical pollution of our environment and food, our susceptibility to them varies and is again genetically determined. As far as human biological evolution is concerned, it has not stopped, merely slowed down.
In the end, humans are the products of the same evolutionary forces as all other animals and will continue to be so. Hopefully, we will come to appreciate this before it is too late. We might even lose our species’ arrogance and accept that we share a thin smear on the surface of a small planet and depend more on our non-human colleagues than many of them depend on us for survival. Only then can we allow our world to recover from the damage caused by our success.
My son once asked me whether a new species of human will evolve – or be artificially evolved. Well, the standard parental answer was that ‘it depends’. I guess it will depend immediately on what our various cultures drive us to do to ourselves and to our environment. Our aggressive behaviour, aided by the demands our growing populations make on our environment, give us the unwanted capacity to impose stress or even to extinguish our species. Our white-hot modern technology would not be able to burn an escape hole from the impoverished prison our small planet might become for the majority of its inhabitants. How we adapt to our fouled nest, and avoid fouling it further, again depends on our immediate capacity to evolve our culture. If we do survive another near-extinction, self-imposed or otherwise, our successors may be biologically different, but there is no doubt that they will be culturally different.
APPENDIX 1:
THE REAL DAUGHTERS OF EVE
The two following pages: Names used for mtDNA lines. This table is intended as a quick reference to naming conventions of the commoner mtDNA lines outside Africa used in the text.
Pages 368 and 369: The full world mtDNA tree. Mitochondrial Eve ultimately has many daughters. The oldest branch is around 190,000 years. All non-African branches derive from two daughters, Manju and Nasreen, of L3 (Out-of-Africa Eve) who dates from 83,000 years ago. From 70,000 years ago there was a worldwide dramatic increase in daughter branches, occurring after the great Toba volcanic eruption. Specific regional distribution is shown at the foot of branches. (Branch dating by the author, where possible using complete sequence data; see Chapter 122).
APPENDIX 2:
THE SONS OF ADAM
The two following pages: Names used for Y-chromosome lines. This table is intended as a quick reference to naming conventions of the commoner Y-chromosome lines outside Africa used in the text.
Pages 374 and 375: The world Y-chromosome tree. African Adam ultimately had at least as many sons as African Eve had daughters. All non-African branches derive from M168, the Out-of-Africa Adam and his three sons Cain, Abel and Seth. Specific regional distribution and nomenclature are shown at the foot of branches. Branch dating is not shown since there is no consensus on method or calibration. The Y-tree shown here is a fusion of Underhill et al. 2000 [Chapter 13] and the Y Chromosome Consortium [Prologue37].
NOTES
These notes are intended as a facility to readers, academic or otherwise, seeking technical clarification and sources of evidence. They contain technical terms and detail which, in the space available, cannot be explained to the same level as in the main text. Multiple citations are merged at the end of a paragraph in many cases, to reduce total numbers of notes. In these cases each citation is keyed by a relevant text string (in bold).
Preface
1. Cann, R.L. et al. (1987) ‘Mitochondrial DNA and human evolution’ Nature 325: 31–36; Vigilant, L. et al. (1991) ‘African populations and the evolution of human mitochondrial DNA’ Science 253: 1503–7; Watson, E. et al. (1997) ‘Mitochondrial footprints of human expansions in Africa’ American Journal of Human Genetics 61: 691–704.
2. Richards, M. et al. (2000) ‘Tracing European founder lineages in the Near Eastern mitochondrial gene pool’ American Journal of Human Genetics 67: 1251–76.
3. That story was told in S. Oppenheimer (1998) Eden in the East (Weidenfeld & Nicolson, London); see also: Oppenheimer, S.J. and Richards, M. (2001) ‘Fast trains, slow boats, and the ancestry of the Polynesian islanders’ Science Progress 84(3): 157–81.
Prologue
1. Some have suggested: Senuta, B. et al. (2001) ‘First hominid from the Miocene (Lukeino Formation, Kenya)’ Earth and Planetary Sciences 332: 137–44. This paper controversially argues that a newly discovered hominid, Orrorin tugenensis, is at 6 million years ancestral to the Homo genus, displacing the current contender Ardipithecus/Australopithecus ramidus (at 4–5 million years: White, T.D. et al. ‘Australopithecus ramidus, a new species of early hominid from Aramis, Ethiopia’ Nature (1994) 371: 306–12) onto the Pan (chimpanzee) branch. The implication is that the Pan/pre-Homo split is put back to 8 million years. first clear evidence for bipedalism: see the fine pictures of a hominid knee joint on pp. 44–5 in Leakey, M. (1995) ‘The farthest horizon’ National Geographic 188(Sept.): 38–51.
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sp; 2. Wheeler, P.E. (1993) ‘Human ancestors walked tall, stayed cool’ Natural History 102(2): 65–7.
3. Elton, S. et al. (2001) ‘Comparative context of Plio-Pleistocene hominid brain evolution’ Journal of Human Evolution 41: 1–27; see p. 19 for Paranthropus and stone tools and p. 21 for Paranthropus and meat. For additional original data for hominid brain size comparisons used in this chapter, see Ruff, C.B. et al. (1997) ‘Body mass and encephalization in Pleistocene Homo’ Nature 387: 173–6.
4. Elton et al., op. cit.
5. even into the modern size range: Saldanha 1 and Kabwe (Broken Hill 1) had brain volumes of 1,225 and 1,280 cm3 respectively, and were both Homo rhodesiense. Their dates have recently been re-assessed stratigraphically to 1.07–1.3 million years – see McBrearty, S. and Brooks, A.S. (2000) ‘The revolution that wasn’t: A new interpretation of the origin of modern human behavior’ Journal of Human Evolution 39: 453–563 pp. 461, 468, 482.
6. Aiello, L.C. and Wheeler, P. (1995) ‘The expensive tissue hypothesis: The brain and the digestive system in human and primate evolution’ Current Anthropology 36: 199–221.
7. Elton et al., op. cit. p. 23.
8. Elton et al., op. cit.
9. 1.07–1.3 million years ago: McBrearty and Brooks op. cit. p. 482.
10. Elton et al., op. cit. pp. 19, 21.
11. Foley, R. and Lahr, M.M. (1997) ‘Mode 3 technologies and the evolution of modern humans’ Cambridge Archaeological Journal 7(1): 3–36; see also Lahr, M.M. and Foley, R. (1998) ‘Towards a theory of modern human origins: Geography, demography, and diversity in recent human evolution’ Yearbook of Physical Anthropology 41: 137–76.
12. another terrible series of ice ages: This was during Oxygen Isotope Stages (OISs) 35–32, see Rossignol-Strick, M. et al. (1998) ‘An unusual mid-Pleistocene monsoon period over Africa and Asia’ Nature 392: 269–72, Fig. 1b. Homo rhodesiensis: very similar to European Homo heidelbergensis; the terms are sometimes used synonymously (for more clarification, see McBrearty and Brooks op. cit. p. 480). a brain volume of as much as 1,250 cm3: Ruff, C.B. et al. (1997) ‘Body mass and encephalization in Pleistocene Homo’ Nature 387: 173–76. op. cit. about half a million years ago, and carried the Acheulian technology with them: Foley, R. and Lahr, M.M. (1997) op. cit., Fig. 5.
Out of Eden: The Peopling of the World Page 35
