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Author Topic:   A question about evolution
caffeine
Member (Idle past 1024 days)
Posts: 1800
From: Prague, Czech Republic
Joined: 10-22-2008


Message 22 of 70 (798443)
02-02-2017 2:43 PM
Reply to: Message 20 by Coyote
02-01-2017 11:38 PM


Eskimos have relatively dark skin because no matter how much nude sun bathing they did they couldn't get Vitamin D from the sun--they had to get Vitamin D from their environment, so skin color didn't matter.
I heard a different hypothesis for this one - basically that the Inuit's vitamin D requirements are amply met by their diet, so there is no selection pressure on skin colour. Arctic peoples tend to eat diets full of fatty meat and fish; since there is not much else to eat in the Arctic. Blubber and fish are both rich in vitamin D; so there's little need to synthesise your own; unlike someone living in temperate Europe eating a lot more plant food.

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 Message 20 by Coyote, posted 02-01-2017 11:38 PM Coyote has replied

Replies to this message:
 Message 28 by Coyote, posted 02-02-2017 7:26 PM caffeine has replied

  
caffeine
Member (Idle past 1024 days)
Posts: 1800
From: Prague, Czech Republic
Joined: 10-22-2008


Message 23 of 70 (798444)
02-02-2017 3:06 PM
Reply to: Message 5 by Theodoric
02-01-2017 4:37 PM


A little bit hairy
That took 3 minutes.
3 minutes that would be have been better spent asking a question in a forum, since this:
quote:
Mongoloids evolved hairlessness to keep clean while wearing heavy garments for months without bathing during the Ice Age.
is nothing but unevidenced speculation that does little to address the question. European populations are some of the most hirsute in the world; so any explanation that relies on evolution at high latitudes is incomplete at best. I've no idea why Europeans are hairier than east Asians, but I don't think it necessarily needs an adaptive explanation.
If it does, then asking why Asians have less hair than Europeans seems to be approaching the question backwards. Looking at human diversity as a whole; it seems that east Asians are more likely to be closer to the plesiomorphic condition - the hairiness of European and Semitic men is the outlier. If this is adaptive; and not just the result of drift; it seems more plausible that this is due to sexual selection; or is a side effect of selection on hormone production for some other reason - since an explanation based on response to cold or somesuch doesn't explain the enormous difference between men and women.
The first answer you find through Google or Bing is usually not going to be a good one unless your question is very simple.

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 Message 24 by Theodoric, posted 02-02-2017 4:22 PM caffeine has replied

  
caffeine
Member (Idle past 1024 days)
Posts: 1800
From: Prague, Czech Republic
Joined: 10-22-2008


Message 25 of 70 (798459)
02-02-2017 5:09 PM
Reply to: Message 24 by Theodoric
02-02-2017 4:22 PM


Re: A little bit hairy
The ability to follow the sources is always there.
The ability, yes, but not the will to pay in order to read a chapter of an obscure 20-year-old anthropology book in order to find out if it says the same thing a wikipedia editor claims it does and, if so, whether their argument is any good.
The point is that the original post was intended as a gotcha against atheists
But if you think someone's trying to 'getcha'; then why not either a) ignore them; or b) subvert their attempt by starting an interesting discussion about the evolution of pigment and hair variation in humans. Unless you get enjoyment out of calling out those whose motives you find dubious, I can't see the point. It just looks a bit petulant.
Pigment variation is a much more interesting topic than why creationists argue the way they do. The below is actually not the image I'm looking for, but it's the closest I could find for now. The one I wanted shows the correlation between average melanin levels and insolation - because there are a few bits of the world where the insolation level differs from what you'd expect from the latitude, for reasons I dont know. The correlation is strikingly close; and the bits that don't match all fit with large migrations either historically attested or hypothesised for different reasons (like the Bantu and Austronesian expansions).

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caffeine
Member (Idle past 1024 days)
Posts: 1800
From: Prague, Czech Republic
Joined: 10-22-2008


Message 35 of 70 (798553)
02-03-2017 11:44 AM
Reply to: Message 28 by Coyote
02-02-2017 7:26 PM


Caffeine--You said essentially the same thing I did.
If you think so, then I expressed myself poorly, since these seem like different ideas to me.
You suggested that there was no selection for lighter skin because insolation was so low that this would not have helped with vitamin D production anyway.
I suggested that there was no selection for lighter skin since vitamin D requirements were already met by diet.
They're not mutually exclusive, but they're not the same either.

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caffeine
Member (Idle past 1024 days)
Posts: 1800
From: Prague, Czech Republic
Joined: 10-22-2008


(1)
Message 51 of 70 (799261)
02-08-2017 3:37 PM
Reply to: Message 46 by CRR
02-08-2017 6:31 AM


The theory that best fits the facts is that Adam and Eve were created with 2 alleles for each of these genes so they had the genetic potential for all skin colours. Their children would have had a variety of skin colours. Some black, some white, some in between. Assuming random pairing in this generation some couples would have had both black, both white, or some mixture. This would then have created families where some had skin colour predominately at both ends of the range.
So how did we get races with different skin colours? Perhaps an event that divided the population into family groups, some white, some black, most in between. The Tower of Babel meets that requirement. The new languages groups would have kept families together and locked skin colours into language groups. As these groups spread out they took their new languages and skin colours with them.
I see two primary flaws with your model.
Firstly, Adam and Eve's alleles are not enough. Take the MC1R gene. The 'M' stands for melanin, and this is a gene we know plays a role in pigmentation in mammals, including humans. Now, in your model, there are at most four alleles of MC1R in humans - two each from Adam and Eve. In the real world, we know there are many many more. Here's a study looking at the role played by some variants of MC1R in skin cancer risk. They genotyped less than 2000 people, all of them in eastern Spain, and identified 53 variant forms of the gene.
The second problem is that skin colour is not randomly distributed around the world as if it was some historical accident. Rather, skin colour is strongly correlated with levels of UV radiation. There is no reason for this to be the case in your model; but it is elegantly explained as an evolutionary adaptation.
Edited by caffeine, : No reason given.

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caffeine
Member (Idle past 1024 days)
Posts: 1800
From: Prague, Czech Republic
Joined: 10-22-2008


Message 65 of 70 (801211)
03-04-2017 8:53 AM
Reply to: Message 62 by AZPaul3
03-03-2017 7:13 AM


Re: Step 2
A different allele of the same gene. No information loss. An information difference. Different proteins resulting from the different nucleotide sequences.
CRR is not completely off on this one. The known mutations which lead to the 'red hair' alleles of MC1R are all loss of function mutations. They produce a receptor protein which is broken, in a sense, and so where the wild type would perform its role of promoting melanin production, the red hair variants don't.
However, we know that loss of function mutations are not the only ones that can happen to MC1R. In those mice that are dark on old lava flows and light elsewhere, some of the darker mice pigmentation seems to be due to MC1R mutation (but not all - different populations of melanistic mice acheived dark fur through different pathways). I don't think the functional basis is understood in the mice; but it can't simply be breaking the receptor like the mutations which contribute to lighter pigmentation in humans.

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 Message 62 by AZPaul3, posted 03-03-2017 7:13 AM AZPaul3 has replied

Replies to this message:
 Message 66 by AZPaul3, posted 03-04-2017 10:12 AM caffeine has replied

  
caffeine
Member (Idle past 1024 days)
Posts: 1800
From: Prague, Czech Republic
Joined: 10-22-2008


Message 70 of 70 (801371)
03-05-2017 4:06 PM
Reply to: Message 66 by AZPaul3
03-04-2017 10:12 AM


Re: Step 2
Or, do the major variants of MC1R cause the melanocortin 1 receptor to stimulate the melanocytes into eumelanin production while the minor variants of MC1R block the melanocortin 1 receptor from stimulating eumelanin production causing the melanocytes to make mostly pheomelanin instead?
Do you really consider the minor variants of MC1R to be "broken, in a sense"?
Yes, I would. The loss of function alleles of the MC1R gene produce a protein that functions less effectively or, in a few cases, does not function at all. The phenotypic effect is an individual with higher proportion of pheomelanin than eumelanin; but the point is the way that this is acheived - it's acheiving by 'breaking' the protein. This, I believe, is what the wiki author was trying to say. The variant MC1R alleles are not dysfunctional in the sense of the individual's overall phenotype - they are dysfunctional in the sense of coding for a dysfunctional MC1R protein.
And, no, I do not believe you would call this a "loss" of genetic information. So, again, no information loss. An information difference. Different proteins resulting from the different nucleotide sequences. Different proteins having different effects upon the system.
And, as often happens with evolution, some of the minor variants convey some advantage in an environment and become the major variants in a population.
Information theory is not something I ever got my head around, so I would steer clear of such things. However, I can understand (in a non-formal sense) how a mutation that led to a protein which doesn't 'work' can be described as information loss. There are many different ways you can stop a protein from functioning effectively, which is why there are so many different loss-of-function variants of MC1R known.
I'm not claiming that CRR is right in general, of course. There are other ways to acheive lighter pigmentation. ASIP is the gene which makes agouti protein; which inhibits the MC1R protein from stimuating the production of eumelanin, and there are known variants of this gene in populations with lighter skin. This seems to me like two different mechanisms to acheive lighter pigmentation - one by making a protein which more effectively inhibits eumelanin production; and one by breaking the protein which should stimulate that production.
I am probably just adding to confusion here though, so maybe I will stop typing.

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