3 ms·

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

nkozyra 9y ago
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?
- Lordarminius 9y ago
  deleted
  - nkozyra 9y ago
    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.
    - Lordarminius 9y ago
      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 ?
      - tysonzni 9y ago
        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.
      - nkozyra 9y ago
        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.
fhars 9y ago
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?

Lordarminius 9y ago
deleted
- nkozyra 9y ago
  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.
  - Lordarminius 9y ago
    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 ?
    - tysonzni 9y ago
      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.
    - nkozyra 9y ago
      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.

fhars 9y ago

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.)