Many years ago, my then-wife’s adoptive mother snapped at me about the topic of Sickle-cell disease (SCD). She told me that she had SCD, and that it was an example of how the government of the United States had silent intentions on killing off blacks because they’re very susceptible to SCD and there was no studies being done to find a cure. At the time, I didn’t have any real knowledge on the subject and wound up essentially listening to her but knowing she was mistaken on the subject. However, it’s an interesting example of one of the aspects of evolution that I wanted to jot down a few thoughts about, so it serves as a good starting point.
SCD is a genetic issue, and it’s an adaptation that has a seriously positive payoff. You see, people with only a single sickle-cell gene are much better equipped to survive malaria. Sure, your lifespan gets cut shorter and there are some serious health issues that go hand in hand with it, but it’s a hell of a lot more genetically advantageous than dying in childhood with malaria, and from a pure evolutionary perspective, people who die as children do not have the potential to be parents. If a genetic abnormality causes death in middle age and prevents death in childhood, then the odds are greater that the person in question can live long enough to pass on their genetics.
But people sincerely don’t understand genetics and evolution. There’s this notion out there that everything is an individual bit in the genome that we just need to tweak and all will be well. That’s not really how things are.
When we think about genes as laypeople, we are usually not thinking about genes. We are thinking about phenotypes. A phenotype is basically some attribute we can observe about a thing, such as whether the peas were round or wrinkled, green or yellow, big or small, etc. But these traits should not be considered independent of one another. A single gene could impact many phenotypes, and a phenotype could be the visual result of many different genes working in concert. And before we go messing around phenotypes, we really need to know what we are actually altering. For example, if we created a process to cure malaria by altering genes to ensure single sickle cell genes, which would inadvertently give rise to massive incidents of SCD. Another example comes from reading about the research of Dimitri Belyaev on the tameness of silver foxes. I’m mid-way through Dawkins’ latest book, which drew this to my attention, and according to what I’ve read (I’m no expert on this work) we see that the tameness he was breeding for had unexpected corollary impacts on fur color, ear shape, and a variety of behaviors to name but a few.
Evolution has a few billion years head start on us. We’re still new to genetics. Gregor Mendel did his experiments on peas between 1856 and 1863. In 1859, Charles Darwin published On The Origin Of Species. Walther Flemming reported his discovery of chromosomes in 1882, a mere 128 years ago. Watson and Crick proposed their double helix DNA model in 1953. We’ve only just mapped the human genome, and we don’t really know what all the bits we’ve mapped actually do yet. But we’re making progress. My point is that understanding more about the nature of genetics will only help us in understanding ourselves.
Jim