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.
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?
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.
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.
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.
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.)
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.
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.
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.
It turns out that if you want to correct sickle cell disease, you (just) have to revert the single the bit of genetic instruction that permits hemoglobin proteins to atomically interlock like legos. The aggregation only occurs when the protein structures are well-suited to aggregation. A single atomic 'feature' on the protein is the difference between a protein that aggregates easily and one that does not.
Further, there is actually a separate mutation to the hemoglobin protein that actively disrupts the interlocking of even those hemoglobins that would otherwise do so. So the presence of an additional atomic feature or bump on the protein actually inhibits aggregation when intermixed with proteins that would otherwise aggregate.
Companies [1] are right now developing gene therapies [2] that introduce that 'upgraded' version of hemoglobin in patients. The upgraded hemoglobin has a mutation from a threonine to a glutamine at position 87 of wild-type human hemoglobin:
https://serotiny.bio/notes/proteins/hbb/
Hemoglobin is an interesting molecule. There are a lot of variations, and even the 'bad' variations aren't always 'bad' for everyone. I believe there is a significant portion of those with homozygous sickle cell trait (meaning they ought to have full on sickle cell anemia) who don't show any symptoms. I have thalassemia (a similar hemoglobinopathy), but I also carry the hereditary persistence of fetal hemoglobin (I basically have baby blood), which means -- if i were to have sickle cell anemia -- it wouldn't affect me as much, and my anemia symptoms from the thalassemia are greatly lessened.
There's a ton of other variations that can ameliorate all these things too. That's just my knowledge on one. In fact, for those with full-on thalassemia (or sickle cell too), they frequently give hydroxyurea, which causes the bone marrow to produce fetal hemoglobin, to aleve the anemia symptoms.
It's another example of odd evolution, people with Thalassemia minor were able to survive malaria, and because they were able to remain alive, they spread their genes, increasing the pool of people with Thalassemia
The thalassemias are also common in south and southeast asia and the middle east (I guess it must have been an Indo-European trait?). It's like 20-40% of people.
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[ 2.8 ms ] story [ 61.2 ms ] threadI 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.
Assuming 100% mortality, how could there possibly be an advantage if the genes of the afflicted cannot be propagated ?
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.)
Do you have any references for that?
Apparently the European slave owners survived
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.
1. http://cadmus.eui.eu/handle/1814/36118
2. http://historyrevived.blogspot.com.au/2014/09/did-malaria-cr...
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.
Further, there is actually a separate mutation to the hemoglobin protein that actively disrupts the interlocking of even those hemoglobins that would otherwise do so. So the presence of an additional atomic feature or bump on the protein actually inhibits aggregation when intermixed with proteins that would otherwise aggregate.
Companies [1] are right now developing gene therapies [2] that introduce that 'upgraded' version of hemoglobin in patients. The upgraded hemoglobin has a mutation from a threonine to a glutamine at position 87 of wild-type human hemoglobin: https://serotiny.bio/notes/proteins/hbb/
[1] https://www.bluebirdbio.com/our-focus/severe-diseases/
[2] http://www.nejm.org/doi/full/10.1056/NEJMoa1609677?query=fea...
There's a ton of other variations that can ameliorate all these things too. That's just my knowledge on one. In fact, for those with full-on thalassemia (or sickle cell too), they frequently give hydroxyurea, which causes the bone marrow to produce fetal hemoglobin, to aleve the anemia symptoms.
It's all very interesting
It's another example of odd evolution, people with Thalassemia minor were able to survive malaria, and because they were able to remain alive, they spread their genes, increasing the pool of people with Thalassemia