Sickle-cell anemia does not prove evolution!
by Felix Konotey-Ahulu
Sixth-graders I have lectured on genetic counselling invariably pop some questions
such as:
‘Is it true that the sickle-cell phenomenon has established Darwinian evolution
as fact?’
Behind the question, of course, lies the assumption that observing selection/adaptation
involving a mutation (an inherited random change or defect) somehow implies that
the more complicated forms seen today arose from simpler forms traced back ultimately
to one-cell organisms.
The answer is of course ‘no’. In the early 1950s I did a course on evolution
and metaphysics at the feet of Professor J.Z. Young, perhaps the greatest evolutionist
of recent years. Nothing has happened during the past 30 years in molecular biology
in general, and the sickling phenomenon vis-à-vis malaria in particular,
to have raised evolution from theory to established fact.
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 Dr Felix Konotey-Ahulu, M.D. (Lond.), FRCP, DTMH,
is a world authority on sickle-cell disease, with 25 years’ experience as
a physician, clinical geneticist and consultant physician in Ghana and subsequently
in London. He is a visiting professor at Howard University College of Medicine in
Washington, and honorary consultant to its Center for Sickle Cell Disease. He is
the author of a major 643-page text, The Sickle Cell Disease Patient
(Macmillan, 1991, ISBN 0333-39239-6; Tetteh-A’Domeno Co., Watford, UK,
ISBN 0-9515442-2-5, 1996).
This article is abstracted with Dr Konotey-Ahulu's permission from pages 106–108
of his book.
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A scientific theory that tackles ‘origins’ must of necessity find that
it is out of its depth. In his 1985 book, The Limits of Science, Nobel
laureate Sir Peter Medawar stated clearly that ultimate questions like ‘origins’
go ‘beyond the explanatory competence of science’. For people to state
that because sickle-cell trait children are resistant to cerebral malaria, therefore
the whole neo-Darwinian scenario is fact, is like saying that my black skin’s
ability to withstand the tropical sun establishes an evolutionary process, starting
perhaps with a ‘big bang’, leading to single-celled organisms, multicelled
organisms, invertebrates, vertebrates, and on up to man. In any case, although malaria
would certainly seem to be a major factor in maintaining a high frequency of such
inherited red cell defects, the real situation concerning their distribution also
involves a complex interaction of viral infections, dietary habits and social factors.
There is not the random mating which Western population geneticists often assume,
and African anthropogenetics cannot ignore the effect of marriage customs, and social
and religious habits that lead to in-breeding, for example.
Stuttering facts
The hypotheses of some anthropologists and theoretical geneticists detract from
more serious work. While natural selection is a fact, attention to selection hypotheses
is frequently overdone and other factors ignored. In one case it was found that
out of 10 West African individuals carrying the sickle-cell trait and living in
the UK, there were five who had the genetic predisposition to stuttering (which
is known to be high in West Africa). The temptation to use natural selection explanations
to link the stuttering gene frequency to child-hood malaria and sickling overlooks
some important sociological facts.
First, most who have the stuttering tendency in Ghana in particular are left-handed,
which is a major social disadvantage. Relatives heckle and bully the left-hander
for doing household jobs with the ‘wrong hand’. The already nervous
left-hander is then forced in the schools to write with the right hand, evoking
a constant state of agitation.
The desire to excel against all odds is great, so left-handers are generally better
at their studies. You will thus find a higher number of left-handers, and thus more
stutterers, in any academic institution. If that institution is in northern Nigeria,
for instance, 30 per cent of these stutterers will also be sicklers, simply because
30 per cent of the rest of the population are sicklers. This has nothing to do with
malaria and selection, nor does the fact that of the five consultants in the haematology
department of a famous African teaching hospital, 80 per cent had the sickle-cell
trait.
I have indicated more than once that African anthropogenetics would be much better
served by thinking along factual lines rather than theoretical evolutionary concepts.
The same could certainly be said for science and medicine in general.
Sickle-cell disease
Sickle-cell anaemia is caused by an inherited defect in the instructions which code
for the production of haemoglobin, the oxygen-carrying pigment in red blood cells.
You will only develop the full-blown, serious disease if both of your parents have
the defective gene. If you inherit the defect from only one parent, the healthy
gene from the other one will largely enable you to escape the effects of this serious
condition.
However, this means you are capable of transmitting the defective gene to your offspring,
and it also happens that such carriers are less likely to develop malaria, which
is often fatal. Being a carrier of sickle-cell disease without suffering it (heterozygosity
is the technical term) is far more common in those areas of the world which are
high-risk malaria areas, especially Africa.
This is good evidence that natural selection plays a part in maintaining a higher
frequency of this carrier state. If you are resistant to malaria, you are more likely
to survive to pass on your genes. Nevertheless, it is a defect, not an increase
in complexity or an improvement in function which is being selected for, and having
more carriers in the population means that there will be more people suffering from
this terrible disease. Demonstrating natural selection does not demonstrate that
‘upward evolution’ is a fact, yet many schoolchildren are taught this
as a ‘proof’ of evolution.
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