quote:
I disagree. The majority of affected people come from African decent. Lets say we have 100 carriers, 50 male, 50 female. Then we have 100 with full-blown SCA, 50 male, 50 female. All it takes is for these people to get it is to procreate in order for it to proliferate in their progeny. Heterozygous becomes homozygous in the offspring and that's when people start dying.
How do you get your 100 individuals with full-blown SCA ? From the figures which you agreed with only 25% of the offspring would have full-blown SCA. Are you assuming that each couple has an average of 4 children ? If so why don't you mention that you should also have 200 new carriers and 100 people without the SCA gene at all ?
If you actually do a proper analysis you will see that if your initial population is entirely heterozygous for the SCA gene then the next generation will also have an average of 1 copy of the gene per individual (the distribution wills change so that many will have 2 copies or none). The only way for that to change is if the individuals with 2 copies are more successful at breeding ("fitter") then those with none. i.e. only if full-blown sickle-cell is better - or less bad - than the lack of malaria resistance in the "normal" population.
(And, of course, out of malarial areas the lack of resistance is not a disadvantage at all - while full-blown SCA is unambiguously bad).l