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Comment by danieltillett | Hacker News Reader

Some West Africans captured in the slave trade brought the sickle cell mutation to the Americas. But in places like the United States, where malaria was uncommon or nonexistent, the mutation offered less of an evolutionary advantage. As a result, African-Americans have a lower rate of sickle cell anemia than Africans today.

I can't beleive how wrong the journalist got this paragraph. The whole reason for the African slave trade was Malaria as the European "slaves" (poor indentured workers) could not survive in the US south because of Malaria which was very common until the 20th C. Also the reason the rate of Sickle Cell is lower is USA is there has been a significant amount of European geneflow (~30%) into the African American population.

I should add that while the selection pressure has been lower in the USA, this has not been the major reason for the lower rate.

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>The whole reason for the African slave trade was Malaria as the European "slaves" (poor indentured workers) could not survive in the US south

Do you have any references for that?

Apparently the European slave owners survived

It is not just a matter of survival, but being able to perform hard physical labour when carrying a high load of malarial parasites. Europeans in areas of high malarial load just could not sustain the workload that west africans could. Lots of slave owners died of Malaria (particularly their children).

This is why the indentured servants were shipped to the North and the West African’s to the South. Western African slave labour was not able to compete against the lower cost indentured European workers in the North.

Still waiting for those references..

Here [1,2]. I have to say this is very well known to anyone who has studied the history of Malaria.

1. http://cadmus.eui.eu/handle/1814/36118

2. http://historyrevived.blogspot.com.au/2014/09/did-malaria-cr...

Don't quote wrong parts. I read the quote and now it's stuck, well, I can suppress the memory, but not forget ... At least, if it's wrong it's really not worth reading.

Use the article to explore the topic. The whole area of human adaption to infectious disease is fascinating.

Neither I nor you wrote that the whole article would be bogus ..?

I should read articles before commenting, sure, but then I would already know the line and you still wouldn't need to quote it, is all I'm saying.

By the way, I read comments to decide whether to read an article or not, mostly because i could read a few comments before the article has loaded anyway. And I do prefer to read (and take part in) dialog, instead of reading monologues.

I agree with you, clearly the writer has got his science mixed up.

I think you do not quite understand the statistical properties of the evolutionary mechanisms. The ravaging sickle cell disease you describe is the form patients develop if they carry two copies of the gene, which happens to one in four children of pairs where both parents carry one copy (it is not relevant to think about pairs where at least one parent carries two copies, these individuals usually do not reach reproductive age and are commonly infertile if they do).

Assume that 10% of a population carry one copy of the gene, and a carrier has a child with a random partner.

Then 10% of the children will be from partners also carrying the gene, with 2.5% inheriting no copy, 5% inheriting one copy, and 2.5% inheriting two. The other 90% will will be with partners without the gene, with 45% inheriting one copy, and 45% no copy. Absent other illnesses and medical care, 97.5% of the children will survive.

For a parent without the gene, 5% of the children will inherit a copy of the gene from the other partner, and 95% will inherit none. Absent other illnesses, 100% will survive and a person without the gene will on average produce slightly more viable offspring, slowly driving the gene out of the population.

I don't have the actual numbers, but assume that malaria kills 10% of the children without the gene, but only 5% of those with one copy.

Now the expected percentage of viable offspring for a carrier is 0.9 * (2.5 + 45) + 0.95 * (5 + 45) = 90.25, as it is for a non-carrier, since 0.9 * 95 + 0.95 * 5 = 90.25, too.

So with these hypothetical numbers, the partial malaria resistance does cancel the negative effects of the sickle cell gene and the 10% prevalence of the gene is stable. If the prevalence goes down, the gene starts to confer a benefit to the carrier (as the chance of meeting a partner that is also a carrier goes down, and fewer of the children of non-carriers will be carriers), and if it rises, it becomes a liability.

Other numbers will move the equilibrium point, but as long as the gene confers even the slightest advantage, it is expected to stay in the population at a rate that makes it sufficiently improbable for two carriers to meet and have children. (If the rate is low enough it may still be eliminated by pure chance.)

But aren't you describing a statistical side effect? It's not as though this mutation imparts a 100% chance of having sickle cell anemia. If 87.5% (carriers and non carriers) survive significantly longer due to malaria resistance and 12.5% lack that extended lifespan due to anemia, isn't it still an advantage overall?

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What I'm saying is even if it was 100% infant mortality, the statistical odds of getting it still leaves the malarial resistance as a genetic advantage.

Sorry. I don't get your point.

Assuming 100% mortality, how could there possibly be an advantage if the genes of the afflicted cannot be propagated ?

People who have sickle cell anemia still have a life expectancy of years (>40 in US). On the other hand, getting malaria usually means you mortality is measured in days not years. Everyone has a "100% mortality" but the window of survival differs between diseases.

Because not every person with the mutation gets sickle cell anemia. There is essentially a genetic burn rate that is less than the fitness imparted via malarial resistance.

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