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Just as a comment for further discussion, I did hemoglobin research for about 4 and a half years. I recall a conversation (ca 1993 or 1994) with Professor Gary Ackers (at the time, chair of biochemistry and molecular biophysics at Washington University in St Louis Medical School, and one of the leading experts on hemoglobin cooperativity) about a paper, in which they mapped the site of action of the digestive enzyme the malaria parasite used on hemoglobins (as Hb is what they eat). It turns out that in the process of polymerization (HB S now, the sickle cell Hb), the polymerization caps the site of digestion, making Hb a poor meal for the parasite. That, to my understanding, was the way that in heterozygous individuals the mutation had selective pressure against the parasite. It slowed the rate of growth, because they couldn't feed as effectively on heterozygous individuals. Inter-cell death seems to be a poor mechanism for selective pressure, as few cells are sickled in heterozygous individuals. dwmyers
I read this in a test on genetics in GCSE Biology. If a sample of a carrier's blood is kept in low oxygen conditions, a few cells with become sickle shaped. This is roughly what the test said:
A couple are worried that they might pass on sickle cell anaemia to their children, so they had blood samples taken for a test. The father's sample developed sickle cells in low oxygen conditions whereas the mother's didn't. What does this mean?
Of course, it meant that the couple's children would a half chance of becoming a carrier, but won't develop the disease. But since I can't obtain the paper, I can't prove that it was there, but I doubt that it's a lie.
I don't see where Eurocentrism comes into play, but if you read any of the article you'd see that infarcts to vital organs, severe pain, a shortened lifespan, and the fact that most people in the world do not have sickling cells would likely be the reason sickle cells are considered abnormal.MartinezMD (talk) 23:05, 17 January 2014 (UTC)