[QUOTE=Blake]
I already explained this. The hair in the beard is no more dense than the hair anywhere else on the body. In contrast the human bear is notably more dense than hair elsewhere on the body, and for that matter denser than the hair of other apes.
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I assume you mean that ape hair is no denser in the beard region than in other places. When you say denser, what do you mean? Hairs per cm2, or thickness/coarseness of the hair? Again, men and women have the same number of hair follicles on their faces. I bet that apes have fine villous hairs on their upper lips and cheeks that don’t show up in photos, just like modern humans do. So the hair of the beard is coarser than the hair of the scalp or forearms - so what? Its growth is under a different set of controls, so it’s not surprising that it would turn out differently. Pubic and axillary hair are coarse, and they are under the control of circulating androgens, too.
[QUOTE=Blake]
No, it isn’t. As you already noted we need two mutations: one that make s facial hair sensitive to androgens for no apparent reasons. That then has to be either followed or preceded by a second mutation that produces a protein that binds up androgens. Those are two distinct processes: one that makes the hairs sensitive to androgens, and one that stops them being sensitive to androgens.
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No. Again, just one process. I have no idea what the signal is that tells an ape’s cheek hair to be a terminal hair, any more than I know what the signal is that makes your scalp hair become terminal hair instead of villous hair. Let’s assume that it’s some combination of local growth factors, or sunlight, or cortisol, or insulin, or whatever. The point is that every follicle has a control mechanism in place that determines what sort of hair it will make. The control system may have multiple inputs, but it probably funnels down through one or a few common pathways at the end, as is the case for many biological systems. All cells also have receptors for testosterone, pre-existing, for other metabolic purposes. The mutation in question would have been to link the pre-existing testosterone receptors in the cheek follicle to the control path for hair differentiation. Now the default for the cheek cell is to make a villous hair unless testosterone levels rise above a certain value: not zero, but some critical threshold. This is not an impossible task; pubic hairs are villous until testosterone levels start to rise in both males and females at the start of puberty, at which point those same follicles produce terminal hairs instead. Note that pubic hair is more sensitive to androgens than facial hair is.
My definition of an androgen-sensitive beard follicle is one that makes villous hair unless it is stimulated by androgens, at which point it makes terminal hair instead.
[QUOTE=Blake]
If an individual woman evolved hair that produced the androgen binding protein before she had evolved facial hair sensitive to androgen then it would be an unexpressed mutation, hence no selective pressure. But if a woman evolved the androgen binding protein for other causes first (as I suspect you are arguing), and then later evolved facial hair sensitive to androgens she would never have developed facial hair because she would never have had circulating androgens.
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[QUOTE=Blake]
This still doesn’t address the criticism that if this protein preceeded androgen sensitive beards then fertile women would exhibit no change and hence the trait is purely negative, and if it followed androgen sensitive beard devlopment then there was no selective advanatge in developing androgen sensitive beards to begin with since all men and women would be equally hairy.
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Sex Hormone Binding Globulin (SHBG from now on) does not make circulating androgen levels go to zero in women. There is always some circulating level of androgen. If androgen production rises, or SHBG levels fall, the circulating level of androgen rises. SHBG helps to regulate circulating hormone levels by serving as a buffer of sorts. There is a complex interplay between estrogen production, androgen production, and SHBG production. There is plenty of selective pressure to have a SHBG system - it helps in the regulation of fertility, for one thing. We evolved SHBG way before we were primates.
[QUOTE=Blake]
In short you are back at your starting point. Your hypothesis makes no sense because if women always had the androgen absorbing protein being expressed then no fertile woman would ever have expressed facial hair. The only women who would ever have displayed increased facial hair are those who were infertile. IOW the mutation would actually reduce mate selection and reduce reproductive fitness in any woman carrying the mutation. As such the mutation would rapidly be weeded out and never get passed on.
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I don’t understand your reasoning here. I’m saying that a trait developed that made some fertile females’ faces less hairy overall than all the other females.
[QUOTE=Blake]
This is the flaw in the hypothesis you are running. It relies on the fact that the first women with this trait women are carrying a mutation that only ever gets expressed to advertise their lack of fitness.
[/QUOTE]
No! The trait is that instead of automatically having terminal hair on the face in whatever the previous pattern was, some of that hair will now remain villous unless stimulated by an arbitrary level of testosterone. Fertile females can advertise their fitness by their smooth faces.
[QUOTE=Blake]
If we assume the ancestral woman has beard hair of density X. Then this woman evolves beard hair sensitive to androgens. She will still produce beard hair of density X because that is the default condition, i.e. it is the condition that exists in all men, women and children regardless of androgen levels.
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No, if she’s fertile (or at least has low circulating androgen levels - the two are linked, though) she will have facial hair of X-1. She still has the same number of hairs on her face, but more of them are villous and fewer are terminal.
[QUOTE=Blake]
It is hair that is not a secondary sexual characteristic. Only if the woman is infertile will the androgen levels cause beard hair to increase to density X+1. IOW the trait only becomes expressed when the woman is advertising her own lack of fitness. Such a trait can’t get passed on.
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If the woman has elevated androgens, her hair may end up back at X, or X+1, or Z. It really doesn’t matter whether the ‘hairy’ state matches the original state or not. Just that the non-hairy state is visibly different than the original state. Since more females are fertile than not, most females with the trait will be barefaced, not hairy. More will be helped by being able to signal fertility than will be harmed by signaling their infertility.
[QUOTE=Blake]
No, it doesn’t. Think about it for a second. Imagine if we genetically engineered a chimpanzee troupe to produce a patch of testosterone sensitive hair on the backs of their hands.
The fertile female chimps won’t produce any less hair on their hands just because the hair is now testosterone sensitive. They will produce exactly the same amount they always did because they have a protein that absorbs most testosterone in circulation. So fertile female chimp hands will look exactly like they always did: ie indistinguishable from the hands of pre-pubescent chimps.
However the infertile female chimps will produce more hair on their hands. Only in these infertile chimps will the gene ever be expressed. As such any female carrying the gene only gets two possible outcomes: non-expression if she is fertile, or expression as an advertisement of infertility. Since a non-expressed gene can’t be selected for the only possible selective pressure is negative.
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One last time: you can engineer the pre-existing terminal hairs on the hand to default to villous hairs unless there is a high enough level of testosterone around. The fertile females will produce smaller, paler hair on their hands, because their circulating estrogen levels are high enough to stimulate the production of enough SHBG to keep their circulating levels of androgens low enough (but not zero) to keep the hand hair from turning dark and thick. They will produce the same number of hairs, but of a different type. The prepubescent chimps of both sexes will also have hands with short, thin, pale hair, because they don’t have much androgen circulating either. In pubescent males the villous hair will differentiate into coarse, pigmented hair as androgen levels rise.
Female chimps with common endocrine problems that lead to infertility will have elevated circulating androgen levels, either due to excess production or due to low SHBG due to low estrogen levels. The fine, pale hair on the hand that they had before puberty went awry will now darken and thicken, forming terminal hair. This may or may not resemble the hair on the hand of an unmodified chimp; it doesn’t really matter. Maybe the hair looks more like human pubic hair than the silky terminal hair of a normal chimp. Both fertile and infertile chimps are showing the effects of the engineering. Mix a few engineered females into a group of normal chimps, and at first the males will mate with all females equally. Soon, however, it will fall out that mating with a barehanded female gives you a 95% chance of an heir, but mating with a hairyhanded female, either wild type or engineered, gives you only a 90% chance. Thus the trait is selected for. If you want a brute analogy, think of sickle cell trait. One copy of the mutant gene gives you relative immunity to malaria; two copies give you sickle cell disease. Yet this trait has not died out, because on a population level it saves more people in malarial areas than it kills.
And now, to bed. I’d appreciate it if others could tell me whether I’m being clear or not.
