Why Do We Have Blood Types? (2014)
mosaicscience.com
mosaicscience.com
Hypothesis given: "So it’s possible that each strain of norovirus has proteins that are adapted to attach tightly to certain blood type antigens, but not others. That would explain why our blood type can influence which norovirus strains can make us sick."
I remember reading somewhere that blood can have more than just the regular ABO antigens. I wonder how that plays into that gene theory.
The concept of hybrid vigor (Expressing two different alleles expressed may yield a competitive advantage over expressing a single allele twice) has always interested me in regards to blood, though I haven't gone digging for a basis for that being a driving force.
https://en.wikipedia.org/wiki/Human_blood_group_systems#Bloo...
And organ transplantation has demanded an even greater understanding of tissue compatibility than blood transfusions.
I thought I read a while ago that there's a theory that different blood types started out with O-, and evolved as a way to be more resistant to certain diseases, but that there were downsides to the other types (certain health problems or less efficient use of energy, I forget now).
I'm not a biologist so I might very well be wrong about that, but it seems that one possible explanation is that the question has no meaningful answer.
It is clearly possible that random genetic changes happen with no impact on fitness at all. They just are.
Secondly, one would expect a neutral mutation to eventually be present in 50% of the population and homozygous in 25%. Or for three variations, we'd expect 1/9th of people to be O, 1/3rd A, 1/3rd B en 2/9ths AB. We've had blood types for millions of years, and no population has anything close to the distribution, which makes me believe there is some kind of evolutionary pressure.
0: https://en.wikipedia.org/wiki/Hemolytic_disease_of_the_newbo...
Also, if there is evolutionary pressure, given that we know blood groups of millions, it shouldn't be that hard to find some correlation between blood group and life expectancy, number of kids, etc. Are you aware of any?
For modeling purposes, I'll start with 50000 people, set the generation span at 20 years, and on average, each female will have 2.004 surviving children. Well, then the mutant population grows at the same rate as the general population, so remains at a tiny fraction.
So I update the model to provide a tiny advantage to the mutant by giving the mutant phenotype more surviving children per generation.
If I set up the model to start with 49998 OO, 1 AO, and 1 BO, set type O reproductive success at 2.004, type A at 2.013, type B at 2.012, and type AB at 2.013, and let it go for 2500 generations (50k years), the ending population is about 20M total, 41% O, 42% A, 11% B, and 4% AB.
That amounts to a relative advantage of only 0.45%. Obviously, the A and B mutations are very unlikely to have occurred at the same time, but it looks like both may have occurred after humans had already migrated from Asia to North and South America, as natives of South America are almost entirely type-O, and the presence of type A in North America may be explainable by Clovis migrants from Europe. So a 50ky timespan is actually a bit too long.
It seems as though there must be a selective advantage to A and B antigens, or that they be linked with an advantage, otherwise, they would not be observable as a significant population now.
[Edit:] Note that this only applies to pre-medicine. Blood type compatibility for the purposes of transfusions is definitely a survival advantage now. If current technology and politics were fixed for the next 50ky, it is likely that the "O" gene variant would become rare, and AA, BB, and AB genotypes would dominate.
It would be extremely hard to find a statistically significant indicator of increased fitness. Evolution is really good at amplifying a 0.1% advantage over countless generations to dominate a population, but to distill that signal from the noise you'd need a study with hundreds of thousands of participants.
Another problem is that the advantage from certain blood types might have only been relevant in prehistoric times, i.e. resistance to diseases that we now can easily treat and avoid. The norovirus mentioned in the article was quite dangerous back then, and still is in developing countries, but is little more than an annoyance here.
Lastly, blood type is correlated with ethnicity, which is correlated itself with life expectancy and resistance to various ailments, making it even harder to unentangle statistically.
"While group A was found to be more common in malaria cases than in normals, the reverse situation was found for group O."
and https://www.eurekalert.org/pub_releases/2015-03/ki-hbg030515...:
"It has long been known that people with blood type O are protected from dying of severe malaria." https://academic.oup.com/jid/article/195/7/1014/800831/Blood...:
"Blood Group AB Is Associated with Increased Risk for Severe Dengue Disease in Secondary Infections"
Not statistically significant? The malaria protection, in particular, seems well known (that doesn't make it true, but I find several papers in what look like respectable sources making such claims) or is severe malaria so rare that being protected against it isn't worth much?
To me, that's a shocking statement. So you're here by accident?
http://www.mosquitoreviews.com/blood-type.html
No idea why mosquitoes would have a preference, but mosquitoes and mosquito borne diseases have had a huge influence on humanity.
Namely that blood types are playing rock-paper-scissors against bacteria / viruses. Pathogens can learn to target a single blood type if it's predominant (just like you can learn you should play Paper if your opponent usually goes for Rock). So it's better to have a population of mixed blood types, and anytime it starts to get out of whack, disease exerts a force that disproportionately takes the newly popular blood type out of the gene pool, pushing back toward equilibrium. Just like the Nash equilibrium RPS strategy is rand().
How to test this experimentally? I'm no molecular biologist, but maybe let viruses reproduce in an environment where one antigen is present for enough generations for them to mutate to have increased effectiveness attacking it (maybe you can determine this from an increasing viral reproduction rate?), then a testable hypothesis that would confirm the theory is the mutation also caused the viruses to lose efficiency at attacking another blood type's antigen.
Random mutation is a cornerstone of evolution. Where those mutations are not being naturally selected the randomness builds into a greater number of types. If we didn't see that, if genes not tied to survivability were homogeneous, then we would need to reevaluate core theory.
This is an example of a non-tech-related article that's perfect for HN because of the "intellectual curiosity" guidelines.
TLDR: Who knows...
https://www.cookielaw.org/faq/#WereoutsideoftheEUareweaffect...