Ok, i can buy that. And I do understand it. But I think what you are saying is that if the trait isn’t harmful in some way, that it can/will be propagated without issue, which I have no problem with. It’s the eye color discussion. however, if the trait IS harmful in some way, and causes failure of the carrier of the gene, it will die off eventually. If not, it will condemn the species.
As already mentioned upthread, it is not limited to Asians. The Khoi-San of sub-Saharan Africa often have epicanthic folds, it shows up in the Americas, and it’s also found in Northwestern Europe among the Irish and other Celts.
There is also something called “founder effect” when someone in a small group enjoys disproportionate reproductive success, leaving a trait or two among their many descendants that is basically there by luck rather than it being useful. If in ancient times a group with epicanthic folds, dark hair, and dark eyes did particularly well in Asia and expanded greatly in number those traits might become extremely common even without being advantageous. After enough time, people who didn’t have them might be considered such oddballs as to be at a disadvantage in reproducing, in which case we’re getting into sexual selection.
Just to go full-on crazy talk, how much influence from Genghis Khan is there?
I have never been able to figure out exactly what the epicanthal/epicanthic fold actually looks like. I’ve studied loads of Google Images supposedly illustrating them, with arrows and everything… and they just look like eyes to me! I must be really unobservant…
A few things:
Neutral alleles are just that - neutral. Thus, they are predicted to persist at roughly the same frequency from generation to generation (assuming Hardy-Weinberg equilibrium). The only way that an allele’s frequency can predictably change over time is through selection, either positive or negative. Without selection, nothing changes.
That said, this is biology, so of course there are exceptions. Without selection, the propagation of an allele is dependent on randomness. It’s like flipping a coin. You expect to get 50/50 heads/tails over long trials, but each flip is a random chance. If you only do, say, 10 flips, there’s a pretty good chance you won’t get 5 and 5. Similarly, in a small population size, alleles can become more or less common simply due to random chance. This is called genetic drift. You can even genetic drift to fixation, which is where every gene in the population is of the same allele.
It’s important to understand that not each and every feature of a human population - even physical, genetic traits - are necessarily the direct result of evolution by natural selection. That is, just because everyone in Asia has the epicanthic fold doesn’t mean that it provides some sort of survival benefit. I want to clarify at this point that I have no idea what the current research actually is on this topic - I’m merely listing alternative explanations that may or may not apply.
Genetic drift is one way in which this trait could have arisen. A small population containing people with and without the fold first spread into Asia. Over time, through random chance, the epicanthic fold trait went to fixation.
Sexual selection is another, related, possibility. That would be where the fold trait went to fixation not through random chance, but because it was considered sexually attractive. Those without the fold were perceived to be ugly, and were bred out of the population. Again - no actual physical adaptive advantage was conferred.
Founder effect, which has been mentioned, is another idea related to genetic drift. If the small founding population all happened to have the epicanthic fold, then all of their descendents would also have it.
Slightly more complex is the idea of a selective sweep. In this scenario, one person in the population was born with an advantageous mutation that happened to be physically located on the chromosome very very close to his epicanthic fold gene, but which is in a completely unrelated gene. It could be, I don’t know, a handy liver enzyme, or a healing factor, or whatever. The key is just that it’s physically linked to the epicanthic fold gene. Over time, this new beneficial mutation will be selected for and spread rapidly through the population. As it does, the epicanthic fold gene is sort of hijacked and carried along with it, and also spreads through the population to fixation. Over long periods of time, the beneficial mutation could be separated from the epicanthic fold gene through recombination, but if the two are very close to each other, those recombination events will be very very rare, and could be expected to take longer than the sweep to fixation.
Minimal. I know that he had lots of children, and most Asians can expect him to be in their genealogy, but he’s still a single ancestor out of many. The idea that he would be responsible for a widespread trait like this is implausible.
A “gene” is really just a nickname for a given sequence of genetic code that creates a given predictable result in the organism. Evolutionary “direction” is driven by only one thing: Does a chance variation of sequence create more successful reproduction?
However, highly penetrated genetically-driven characteristics are not necessarily highly penetrated because the genetic sequence coding for that exact characteristic created the successful reproduction. As mentioned above, maybe that part of the gene (or even the whole “gene”) is just hitching a ride on a more important part (where “important part” means sequences that do drive more successful reproduction). Or maybe the number of alleles in a founding population was so small and the reproductive advantage so slight that genetic drift drove frequency by random chance instead of evolution’s “directional” preference.
If a founder of a given group of descendants has a sequence coding for an outcome that is linked to a sequence that’s important for successful reproduction, then the trait will be highly penetrated even if it’s not itself important. For these kinds of reasons, we don’t know if epicanthal folds are incidental, or selected for because they are functional. (And of course, one kind of “functional” might happen if a given group decides epicanthal folds look great, so appearance itself rather than physiologic function is driving the successful reproduction.)
Some mathematical modeling effortshave been done to sort out evolutionary (“Darwinian” in the paper I link) selection from effects such as a population bottleneck that creates a paucity of founders and therefore a paucity of genetic architectures to pass on.
It seems intuitive to me that a more protected inner canthus is a good idea, but I don’t think it’s much more than speculation to say so. As Colibri points out, reasonably prominent epicanthal folds are found in pretty ancient lineages. If its such a great idea, why isn’t it more highly penetrated everywhere?
Well, a trait can be harmful without being fatal. Our bodies and brains are full of flaws that can cause us harm now and then but haven’t killed us off as a species yet.
Because it’s not the only good idea. Someone a long time ago was born without one, but with other traits that enhanced survival, so the eye thing was left behind. Or perhapts it’s a trait that only makes a difference in certain parts of the world.
BTW, Dr. Langston Down, the guy for whom Down syndrome is named, thought that Asians (“Mongols” to him) and people with Down syndrome were somehow related, not just similar. He based this on the fact that (in his typical Victorian racist view) both have such limited intelligence as well as similar physical characteristics.
Such a harmful trait may die off eventually.
Or environmental changes could happen that will turn the tables and later favor that trait.
Or a trait that is harmful in the homozygous recessive may actually be advantageous in the heterozygous state. This is assumed to be the case with the CFTR loci with multiple such alleles that have been stable for many generations.
Observations on an Ethnic Classification of Idiots.
He also recognized Ethiopian and Malay idiots, as well as those resembling American Indians.
Note that “idiot” once referred to a specific grade of mental retardation, below "moron"and “imbecile.”
It’s an extra fold around the corner of the eye (the corner closest to the nose), that creates a more hooded upper eye, and in more extreme cases such as north-east Asians, completely shielding the upper eyelid.
If you wanted to give someone without the fold the appearance of one, you’d gather some skin slightly away from the corner of the eye, on the bridge of the nose, and “pin” it to the corner of the eye. You’d see, with a little imagination, how this would create another fold radiating from the tear duct, and “hooding” the upper eye as in natural epicantic folds.
Hope that helps some.
Few traits are universally good or bad. Example: sickle cell trait. Can be potentially very bad (especially at high altitudes). It’s not bad for areas with malaria.
Even outside the tropics in areas where it is more negative than positive, there’s no real reason it should “condemn” the carriers by its presence.
I do note you modified this statement with “causes failure of the carrier of the gene”. Well, that’s an awfully high bar, and a much higher one than you originally set. Few genes make that much of a difference on their own.
Yes, and to put a finer point on it, “mental retardation” was the term used to replace those…until it became bad and was replaced again…and on it will go.
Genghis Khan is too recent. My guess is that the wide geographic spread of the East-Asian “look” comes from the first development of agriculture in east Asia. A small group of people with a fairly uniform set of physical characteristics experienced a population explosion and spread their genes throughout the region and beyond.
Not necessarily. Remember, not all genes are a simple as the examples we are given in grammar school.
A gene that ‘causes failure of the carrier’ under certain circumstances might be advantageous under others.
Also:
Few genes ‘cause failure’; most have little effect on survival; most of those that do have marginal effects.
Genes can be recessive.
Genes may not be expressed.
Genes may have multiple phenotypic effects - genotype does not effect survival, phenotype does, I want to stress this, although you do not argue otherwise, because a lot of people don’t think of this.
Then you’ve got your epigenetics, which massively complicates things, and is also mind-blowing when you first learn about it.
Thank you for the clarifications. I know I HAVE simplified my questions/comments. However, this is far from a simplistic subject. I think your notes (as well as the notes of others) have demonstrated that the success or failure of a gene, its retention in the genetic code and its ability to propagate throughout a population relies on a number of factors.
Only if it is “harmful” wrt to reproduction. It’s quite “harmful” for a male peacock to have a ginormous tail, but that’s outweighed by the advantage said tail gives him in wooing females and spreading his genes.
Aside from direct attractiveness to females, features such as the peacock’s tail are often considered to be expressions of the “handicap principle”: if a male can survive despite having to drag around that enormous tail, he must be exceptionally fit in other ways, and hence represent a good bet for a female.