A test for the pathogenic theory of homosexuality?

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Compare monochorionic to dichorionic twins. If there’s a teratogen causing homosexuality then it should show up as a statistical difference in concordance for homosexuality.

Of course this would only tell us whether there is a prenatal pathogen. It wouldn’t rule out the possibility that there is a pathogen that only strikes later on.

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68 Comments

  1. Interesting to study sheep, too. Since there are no other animals where exclusive homosexuality is common, if pathogens are at work in both man and sheep they are rather likely to be close relatives. 
     
    How bout pooling some tissue homogenates from gay sheep and injecting it into sheep embryos. Been done? 
     
    Next on the list would be adoptive transfer of lymphocytes to gestating SCID sheep or neonatal sheep; this can help test for autoimmune causes.  
     
    Actually, it would be interesting to simply maintain a SCID sheep colony and see if the sexuality outcomes varied. It’s probably impossible to keep SCID sheep, though; or anyway far harder than keeping SCID mice.

  2. Good luck getting past the review board, even providing that you fund those proposals yourself. I think this topic is going to be institutionally grounded for many years. That isn’t to say that I don’t agree with everything you’ve stated.

  3. I don’t quite follow the logic. Why would there be a statistical difference in concordance?  
     
    If the theory is that some maternal infections may cause the fetus to develop homosexuality, what difference does it make if they are mono- or dichorionic twins? They still share the same mother and both fetuses will presumably share the exposure to any maternal infection (unless we are positing a freak uterine infection, already a rare occurence during pregnancy, that only infects one amniotic sac and spares the other… in which case the rarity of such a clinical scneario makes it extremely unlikely a study with sufficient power to prove any statistically significant effect would be at all feasible).

  4. The more the hypothesis is put out there as a possibility, one with which a growing number of people become familiar, the more likely reluctance to test it will eventually weaken.  
     
    While right now academia may not feel free to take the leap, what about the sheep ranchers? 
     
    After all, they spent money, as I understand it, for people like Roselli up in Oregon to try to figure out why so many of their rams are duds, but his studies on hormones, as far as I know, haven’t given them any returns. 
     
    Surely the ranchers have heard of Cochran’s hypothesis, don’t you think? Come to think of it, maybe not. Maybe that’s the problem.  
     
    However, if they have, why haven’t the ranchers’ associations pressed for testing the pathogen hypothesis, unless someone has steered them away from it. They lose a lot of money with those duds.  
     
    I know nothing of the politics of the associations representing the multimillion dollar industry of sheep ranching, but surely they are a big enough group and well-funded enough to do something about it if they were told what might be causing so many of their rams to turn out as duds. So, maybe there is the possibility they don’t really know of GC’s idea all that much. 
     
    There was a ridiculous PETA uproar in which an even more ridiculous lesbian former pro tennis player got involved, but everyone I know (I live in a liberal area of CA with friends in non-scientific fields)was laughing at both PETA and the tennis player. They thought it ridiculous that research about what makes rams or people gay should be stifled.  
     
    Hopefully we are growing a bit less PC.  
     
    There are so many studies out there linking chronic illnesses and mental illnesses to pathogen attacks on the brain that I’d think sexuality could be just one more thing researchers examine. 
     
    Perhaps we simply need to entitle the study “The etiology of heterosexuality.”

  5. Isn’t a genomic study of the gay sheep in order as well?

  6. In my opinion the the reason so many gay/homosexual peoples hackles are raised when the idea of these kind of studies are raised is the ‘mental illness’ stigma related to homosexuality that we have lived with for many decades.  
    Perhaps the study should just be titled ‘The Etiology of Sexuality’ which would cover all orientations? I mean, do we even know how heterosexuality develops? 
    I’ve always been unconvinced by the whole ‘birth order’ hypothesis – although I admit this is probably coloured by my own experience as I am in a male/male relationship and I am the oldest of four offspring with three younger heterosexual brothers, while my partner is the youngest of ten (five male, five female) which include identical twin sisters who are lesbian. The reproductive fitness of my partners family as a whole has probably been increased as the homosexual family members have raised some of the children of heterosexual family members (and one of the lesbian sisters has two daughters and nine surviving grandchildren), so I do tend to buy into the whole ‘gay genes benefit kin’ argument.

  7. craker, 
     
    as i understand it whether two twins share the same placenta or not effects how concordant they are in their exposure to teratogens. 
     
    i haven’t read enough research on this, but that’s the impression that i currently have. someone who knows better is very welcomed to correct me.

  8. ben g, 
     
    Think anatomically. If we are discussing the potential developmental impact of a maternal infection, then let’s consider how the fetuses are subsequently exposed to the teratogen. In most instances – other then the hypothetical I posed above of an infection that affects one amniotic sac and spares the other – the infectious agent is present in the maternal bloodstream and passes across the placenta to infect the fetus.  
     
    So, why would it matter if the twins are monochorionic or dichorionic when the fetuses share exposure to the same maternal circulatory system?

  9. Regarding the older brother/mother’s immune response theory– googling, I found an abstract of an 2008 Emory University study by an Andrew Francis. It’s a demographic study that pokes a lot of holes in that theory. I haven’t figured out how to link on this site, but you can google it. 
     
    The point about the mental illness stigma is well taken, but the pathogen hypothesis doesn’t suggest mental illness; furthermore, people have come a long way in how they view gay people. Straights might view the sexual preferences of gay people as odd, even incomprehensible, yes, but the vast majority don’t think of gays as mentally ill. 
     
    Also, other studies continue, some searching for hormonal in-utero causes while a few are still looking at genetics or epigenetics. So, whatever the cause, as long as it turns out to be biological in origin, don’t you think once the cause is identified, there’ll be research to prevent its occurrence? Yes– because there will be a demand from parents-to-be, worldwide. That may not be a pleasant thought to some, but it’s what is inevitable. 
     
    Thus, when you think about it, Cochran’s hypothesis should pose no more a “threat” to gays than any other hypotheses. I mean, how do gays react to theories that posit that their brains were not sufficiently bathed in testosterone, not masculinized, that they were effectively feminized or left feminized in utero? *If* that were proven, the next step would be to research what caused the hormonal action or inaction, and the next step would be to do something about it.  
     
    I just can’t stand the idea of scientific inquiry being quashed by fat-cat administrators and brown-nosers protecting their feathered nests, afraid of the truth, whatever that truth is.  
     
    Having worked in the public school system for over 30 years, I saw the “re-invention of truth” in action over the last 15 or so years of my career, and it’s ugly, really, really ugly– a combo of Big Brother and political correctness– and it’s scary. Look at what it has produced.

  10. Ahem. As a gay person AND a sheep farmer, let me set a couple of things ‘straight.’ First off, sheep are not the only animals that show exclusive homosexual behavior. There are well documented life-long homosexual pair bonds in a number of bird species. A number of other wild ruminants related to sheep exhibit same-sex orientations – it’s just harder to study in the wild (Wildebeests X & Y in a herd of 1,000 are gay – how you gonna prove that?). 
     
    Second, gay sheep studies may have been cloaked with an ‘economic’ rationale originally – perhaps as a means of justifying the grant to study homo sheep, but to suggest that there is ANY economic impact on the sheep industry at all because a percentage of rams are getting it on with each other rather than the ewes is laughable in the extreme! That’s out-of-touch academics grasping desperately for a real-world impact for their research.  
     
    The 2% to 4% of rams that are gay have zero impact on any sheep operation’s bottom line – No one, I repeat, no one, “loses a lot of money on those duds.” It is a non-issue in the industry. There are roughly the same percentage of rams born with only one descended testicle. No one is worried about the economic impact of monorchidism.

  11. Presumably if your prize ram won’t perform, you can milk him anyway. Or are sheep the only animals that can’t be subjected to AI?

  12. Alan,  
     
    As a non-sheep rancher, I only know what I’ve read. I’ve been conned? Sad, then, for there should be no reason at all to find an “excuse” to study sexuality, no reason at all. If what you say is true, that’s one more example of what can happen when scientific inquiry is quashed for political purposes. Gee, the medieval church would love such a practice, wouldn’t they? We ought to let the extreme left and the extreme right duke in out in the ring until they destroy each other and leave the rest of us to pursue what is, whatever it is. 
     
    As for gay behavior in other animals, I’ll let the experts in animal behavior speak to that. I’ve read conflicting info, but I don’t profess to know if what has been observed in other species is what we’ve observed with sheep and humans. I’ve read “yes”; I’ve read “no.” 
     
    However, as for studies on the cause of sexuality, hetero or homo–science should not be  
    subjected to this. Period.  
     
    Aside from the idea that censorship itself is downright dangerous, that it spreads from one field to another, it’s great that humanity is now benefitting from studies into pathogenic causes of all kinds of things, and the brain has become the next frontier.

  13. Alan – your points on other mammals make sense. I guess we don’t know for sure about all of them. When it comes to highly sex-dimorphic passerine birds with small breeding territories, it’s easy to see when they are gay, and lots of birders would notice. The thing is, I believe it is extremely rare in most of those birds (this is covered in Ehrlich et al’s “The complete birder” but I lost mine). What’s odd, evolutionarily, is for it to be both common and exclusive or nearly exclusive. Do you know any animals where more than 1 in 10,000 or so individuals are estimated to swing that way? 
     
    I too was wondering what is so costly about gay rams – seems like you would just use the straight rams for studs, and no shortage would result. I guess there could be a small loss in that if you have a superb gay male that you want to breed, you can’t do so cheaply.  
     
    Craker – check out some vertically transmitted parasites, you’ll see that they aren’t necessarily transmitted with 100% efficiency.

  14. Oh, something I wanted to add. 
     
    The reproductive fitness of my partners family as a whole has probably been increased as the homosexual family members have raised some of the children…. 
     
    The math just doesn’t support this kinship support theory, Kermadecer. Anecdotally, we can all come up with examples of aunts, uncles, brothers, sisters, etc., gay or straight, who’ve raised family members, but not to the degree that the fitness question of homosexuality is solved, not even close.

  15. The only reason a concept as shabby as the “Gay Uncle” theory survives is because it is never compared to anything else. 
     
    Historically speaking all people have been expected to contribute and that includes the handicapped, infirm and infertile. Imagine the reaction if a researcher hypothesized that nature selects for eye damaging genes so that blind people can stay home and raise their relatives children. That hypothesis would be considered cosmically stupid.  
     
    Anybody can create an “x is busted Uncle” Theory and apply it to almost any disability. Does anyone know if a mainstream scientist has tried to use this general hypothesis in an attempt to explain any known disorder in humans?

  16. I think it persists because most people don’t know anything quantitative about kin selection. But then, what _do_ they know anything about?  
     
    I’ve seen people opine that heterosexuality is just as much as mystery as homosexuality. I’ve had a halfway competent evolutionary biologist tell me that homosexual probably _is_ caused by some pathogen, but that we should, if we ever definitely establish that as fact, keep it secret forever to avoid hurting people’s feelings.  
     
    I’ve had someone [a grad student in anthopology] argue that male dogs _do_ exhibit parental care, like wolves, only they do it secretly, so that no one has ever noticed it over thousands of years. I’ve heard someone [a tenured professor in biology) argue with me about Jewish medieval history, using _Fiddler on the Roof_ as his historical source. And admit it.  
     
    I’ve had referees for PNAS suggest that there is probably no such thing as positive selection. 
     
    I could go on, but suddenly I need a drink.

  17. In answer to David B’s and Eric Johnson’s queries, the sheep industry doesn’t use A.I. to the extent it is used in the cattle industry. In cattle, a superior bull can be used to sire thousands of offspring and his semen is shipped everywhere. In sheep, however, owning to a slightly different cervical structure it is extremely difficult to fertilize trans-cervically (i.e., the turkey baster method). Almost all sheep A.I. is done surgically using a laproscope (a much more invasive and costly procedure), so the potential to use any one superior sire on thousands of ewes is just not practical. I use A.I. regularly since I import semen from the top rams in the UK to the US (I’ve got several guys on ice at UC Davis right now). But it’s not cost-effective by any means. Certainly semen from gay sheep can be collected just as easily as it can from straight ones (perhaps even more easily….given the method used to obtain a specimen ). But the reality is, any top ram that’s gay, probably has about a dozen or so straight brothers hanging around that are just as good, so why bother worrying about it?  
     
    Also, more to the point, almost all livestock breeding involves one male with a group of females. If he’s solo, and there’s no other rams around to take out to the local disco, he’s going to do the job – it may not be his sexual ‘preference’ but hey, it’s breeding season, and the testosterone is running high…. In the middle of rut, most ruminants will boink anything (surely you’ve see the you tube clips of sex-crazed moose mounting statutes, etc).  
     
    In a range situation (on a Western ranch or an Ozzie or Kiwi sheep station) with multiple males running unsupervised with lots of females, sure, the gay rams will be off on their own listening to the Pet Shop Boys or whatever, but their straight brothers will be only to happy to fill in for them. So, again, there’ no economic need to study homosexuality in livestock. Interesting topic, though, nevertheless.

  18. gcochran 
     
    Those are some sad examples. Have you ever considered why mankind might select for stupidity? 8-) 
     
    BTW, even if nobody determines what causes homosexuality science is advancing so rapidly that someone will eventually reverse it by accident. Once that happens scientists might have the political cover to look for the cause. 
     
    Brain Birth Defects Successfully Reversed Through Stem Cell Therapy 
     
    These cells migrate in the brain, search for the deficiency that caused the defect, and then differentiate into becoming the cells needed to repair the damage. 
     
    The scientists are now in the midst of developing procedures for the least invasive method for administering the neural stem cells, which is probably via blood vessels, thus making the therapy practical and clinically feasible.

  19. I could go on, but suddenly I need a drink.  
     
    I know that feeling. My colleagues and I needed lots of drinks when high school administrators and so-called “experts” insisted that kids reading on the sixth grade level could and SHOULD BE in the same English/literature/composition classes with those reading on the college level. It was bad enough that they actually spouted that idiocy, but worse that they had the power to force it to occur– and that they did. We protested mightily for years, but the PC Beast is mighty. Their answer was always the same: “Experts say…”. No such experts existed, of course. Plenty of frauds ,though, con artists willing to sell their next book, flim flammers willing to be used by interest groups with an agenda, cons who’d figured out the way the political winds were blowing. It’s amazing and depressing the number of people who don’t give a damn about real kids and their educations. Their professed concern is phony. 
     
    Thus, today the practice has spread to other states that were sane at one time. Once again, the state that just keeps giving, California, has spread its lunacy to the other 49 or most of the other 49.  
     
    Returning a bit closer to the topic–there’s an early view in Psychological Science of a study done by Auyeung and Baron-Cohen (he of autism studies) entitled, “Fetal Testosterone Predicts Sexually Differentiated Childhood Behavior in Boys and Girls.” 
     
    They took samples of amniotic fluid from amniocentesis tests, then later administered a questionnaire to parents seeking to discover if gender atypicality correlated to the earlier measure of fetal T. They claim, “Thus, our data are the first documentation that androgen exposure prenatally relates to sexually differentiated play behavior in boys and girls.” 
     
    Since gender atypicality is the only known predictor of eventual homosexuality in some, they see this an important. The study isn’t out yet.

  20. I’ve had referees for PNAS suggest that there is probably no such thing as positive selection. 
     
    OMG, I know you’re serious. We ARE in trouble.

  21. GB 
     
    PCB exposure does the same thing
     
    Boys with higher PCB exposures are less likely to engage in masculine patterns of play, and girls with higher exposure are more likely to engage in masculine play. 
     
    Even so I don’t think this has much to do with sexual orientation, at least in males. Roselli has been trying to create gay (and straight) sheep for years by altering prenatal hormone levels. He can make them more or less masculine but he hasn’t had any luck with orientation.  
     
    If homosexuality was caused by a hormone surplus or deficit it would be obvious because it would affect the body as well. If gay men were deprived of the right amount of prenatal testosterone they’d probably have a high rate of undescended testicles and things like that.  
     
    Ok, now in the case of “Butch” lesbians you might have a case. Their physiques are significantly more masculine than the average.

  22. Just out of curiosity, if gay rams are not used for AI, why would farmers keep them? I thought rams (adult uncastrated male sheep) were only kept for breeding. The great majority of male sheep are castrated or slaughtered as lambs.

  23. Without endorsing blockage of scientific research, this comment thread itself indicates one of the problems, in that people are moving “naturally” to the language of disorder. The history of religious oppression same-sex activity (and thus same-sex orientation) has suffered down the centuries inevitably colours reactions. (Is priestly celibacy a “disorder” for example? It is certainly reproductively disfunctional.) 
     
    That same-sex orientation–in a situation where people are not strongly pressured to have children, even if only as pension plan–inhibits breeding is presumably true: but not so much where social expectations were different. (Indeed, there is evidence that the conjunction of Catholic dogma with priestly celibacy has meant that the Catholic priesthood has always been disproportionately same-sex oriented: if you were not allowed to have the sex you wanted, you may as well get as much social kudos for not having sex as you can.) 
     
    I would have thought one of the difficulties for the pathogen theory is that male sexuality seems to be predominantly “bimodal” (i.e. interested in either men or women) while female sexuality appears to be more fluid. Male sexuality has primarily visual/physical triggers (“men’s eyes are secondary sex organs” as a romance-writer of my acquaintance puts it) while female sexuality has primarily emotional triggers may explain the difference but I don’t know how that would then sit with the pathogen theory.  
     
    A lot of animal homosexual activity has been documented. Though social expectations (typically with a religious origin)–that sex “just is” reproductive, and only reproductive, so of course the two individuals are not the same sex/it is some strange aberration we can ignore/not embarrass ourselves reporting–have seriously got in the way of building up accurate data. 
     
    But dubious empirical claims abound–no same-sex orientation among hunter-gatherers, for example. When it has been documented among Amerindians (admittedly often ex-farming cultures), Australian Aborigines (emphatically not) and (I understand) Siberian cultures.  
     
    Even more basically, do we understand the mechanism(s) that establish sexuality? It is surely hard to work out mechanism(s) for deviation from the norm if we do not know the mechanism(s) which establish the more normal pattern.

  24. Alan: 
     
    Of course, you know of the ram that went over the cliff because he didn’t see the U-turn? Or 
     
    Mary had a little sheep 
    And with her sheep she went to sleep. 
    The sheep turned out to be a ram 
    And Mary had a little lamb.

  25. Here is what I would like to understand: what is it, exactly, that causes straight people to be attracted to the opposite sex? I mean, we appear to have lost the ancient and unambiguous scent clues. So how do we know who we are supposed to be attracted to? 
     
    To motivate the question, imagine taking a large group of male infants and having them raised by men on an island without any females (or vice versa). It seems to me that they would all have to end up gay – what else could possibly happen once the hormones kicked in? Yet in real life the vast majority of human beings pick up on the fairly subtle differences between males and females (they’re shaped a little differently, they behave a little differently, their voices are a little different, etc.) and somehow manage to figure out nature’s intended plan. But how does this work? 
     
    If we understood this, wouldn’t we gain insight, not just into the question of homosexuality, but into the full range of human sexual behavior? After all, it can’t all be genetics (or even epigenetics)! Are there specific genes (or specific pathogens, to cover that theory) for sadomasochism? Transvestism? Bestiality? Necrophilia? If not, then it has to be some sort of environmental influence, acting at a young age, that steers people towards such behaviors. And if that’s how you explain the less common fetishes, why not homosexuality? 
     
    It’s this line of reasoning that makes me a somewhat suspicious of the emphasis currently placed on genetics as an explanation for homosexuality. What is really needed is a unified theory that explains all human sexual behavior – heterosexuality, homosexuality, plus the various paraphilias – in a single framework. It seems clear to me that, in such a theory, genetics cannot be the whole story, and in fact may not play as big a role as is generally argued for today.

  26. Lorenzo 
     
    Nobody knows why some men are gay. However if in ten years time researchers discover that it’s caused by exposure to a microbe during early childhood would it be a huge surprise to anyone?

  27. craker, 
     
    isn’t one of the functions of the placenta to protect the fetus from possible infection via filtering out bad substances? this implies that a maternal infection is not enough by itself for the gay pathogen to infect the fetus. it must make it through the placental barrier as well. so we’d expect some difference in exposure to teratogens between monochorionics and dichorionics, right?

  28. A few points– 
     
    “Without endorsing blockage of scientific research, this comment thread itself indicates one of the problems, in that people are moving “naturally” to the language of disorder.” 
     
    1. Don’t know what you mean by the language of disorder. 
     
    2. So far, yes, research seems to support that of those who have had same-sex experiences, men are more exclusively homosexual than are women. 
     
    However, I don’t think women have been studied very much, so it’s hard to draw conclusions about them. After all, in one of the studies, women reacted to bonobos getting it on while neither gay nor straight males did. I can’t account for that other than to say it comes as no surprise to anyone on this board that the male brain and the female brain are different. Who knows? Maybe something that makes us laugh causes a physiological reaction that got measured as a sexual reaction, or maybe something that makes us laugh–I think watching bonobos fooling around might make me laugh– puts us in the mood. You know, there’s a tip for the guys–humor indeed is a way to a woman’s heart. Then again, maybe we women are just a bit more voyeuristic than the guys.  
     
    3. I’d like an evolutionary biologist/anthropologist to tell me how likely it is that one reason women may not be as “visually” stimulated as quickly and to as great a degree as men is that we have had built into us a natural wariness, a guard that allows us to first size up the guy, to take measure of him, to decide if is he “safe.” After all, think how vulnerable a woman is. She can’t match even a small male in strength and guess what? Sex can hurt, you know? Hurt badly if she isn’t ready for it, and/or if her partner doesn’t take care (which means he must care enough to take care). Thus, she is physically in danger and is always aware of this. Put simply, we have defense mechanisms. Somewhere in our make-up must be the instinct to proceed carefully.  
     
    4. I have read people who offer all sorts of comparisons of animal behavior to human homosexual behavior; they even include the fact that newly hatched birds can imprint on humans or inanimate objects. 
     
    Anything I have read about imprinting that applies to birds doesn’t apply to people, according to the experts I’ve read. 
     
    Furthermore, I think someone said it above in a post–most animal “gay” behavior is not exclusive and some of what is perceived and labeled as “gay behavior” is not sexual at all.

  29. Anonymous,  
     
    Examples like Lesbos when the men were depleted by war and the same sex that took place in Roman and other armies throughout history can be explained by the absence of the opposite sex. Guys in prison today get out and revert to heterosexual sex the minute they leave the place. Almost all human inhibitions/taboos can be tossed aside under the right circumstances.  
     
    The more difficult question is why some boys/men have no physical attraction to women. They’ve never been interested–zip, nada, zilch. The female form just doesn’t do it for them, and some have a real physical revulsion thinking of women in a sexual context, the same way straights thinking of gay sex feel revulsion. So, lots of gays had some sexual experience with women but report having to jump through mental hoops to perform/enjoy/want to continue, etc. It’s the male form they want. I’ve never been able to understand why you’d want something you’ve already got yourself, but hey, that’s the mystery of all this. 
     
    The fetish stuff is a great question. I wouldn’t be at all surprised to find that the really strange ones (I mean, what the heck’s up with “water sports,” for example)are the result of brain damage/malfunctioning of some sort. Has to be. 
     
    If attraction to one or the other sexes is located in one small part of the brain (and not the result of the interaction of a jillion places located here and there)then finding the neurons involved would be a start, right? I’d think that it would be centered in one part and not that complicated or else too many things could have gone wrong and we’d not have survived. 
    But, I realize…I know nothing.

  30. Ben g, 
     
    No, it does not follow that there would necessarily be a difference between exposure if we compared monochorionic and dichorionic twins.  
     
    I suggest looking at an anatomical figure of the placenta. Just to review, oxygenated maternal blood perfuses the placenta via leaky, open endometrial arteries (named spiral arteries). The chorionic villi from the fetus are bathed in the maternal blood within the placenta. As you correctly stated, there is an epithelial layer covering the fetal blood vessels that acts as a barrier preventing direct contact of the maternal and fetal circulation. Oxygen and nutrients can pass across this barrier, as well as some teratogens. 
     
    Now, let’s assume the hypothetical “gay pathogen” teratogen we’re considering can only pass into the fetal circulation if there is a compromise of the filtration function of the chorionic villi. Okay, why should there be a difference between monochorionic and dichorionic twins in this instance? For simplicity, let’s also specify that we are only considering the case of monozygotic mono- vs. dichorionic twins (to remove genetic variation as a confounding variable).  
     
    Even in the case of the monochorionic twins the blood vessels for any given twin will be distinct. Certain chorionic villi will supply the circulatory system of one fetus, and other chorionic villi will supply the circulatory system of the other fetus. So, theoretically it is entirely possible there could be a compromise of the placental barrier for the chorionic villi supplying one fetuses circulatory system while maintaining the barrier for the other fetus, even in the monochorionic case.

  31. craker, 
     
    i don’t know the anatomy here. before posting i was aware of two things: 1) that the behavioral genetic literature shows significant differences between mono and di-chorionic twins on a variety of psychological traits, and 2) that the placenta prevented teratogens from reaching the fetus. i put 1 and 2 together and came up with the test idea in this post.  
     
    if you’re correct in saying that the chorionic villi are the only bottleneck for teratogens between the mother and the fetus, then my test idea would not work.

  32. Craker – purely speculative but possible, at least a priori, is that some parasites adept at vertical transmission try to replicate/flare in placental cells (starting with cells facing the maternal serum/humor) to facilitate invasion of the fetus. But sometimes maternal immunity succeeds in suppressing the incursion / flare / staging activity in the placenta. Thus, single shared placenta = greater concordance for infection in the twins, since dual placentas can sometimes themselves be discordant for the “flare.” 
     
    Work on the monochorionic/dichorionic concordance theme, relating to schizophrenia in MZ twins, was cited by Ewald &/or Cochran’s long paper on schizophrenia. (I haven’t read what they cited.)

  33. Eric, 
     
    It’s not outside the realm of possibility, however it seems highly unlikely. The fetuses are sharing the same uterus and the maternal endometrium is fairly uniform. Also, any immune response will be systemic (i.e. once the immune response is activated by either of the sites of infection, any antibodies and activated lymphocytes will circulate through the bloodstream and encounter both placentae). If it were the case though we could look at the placentae and presumably find some histopathological evidence of this “flare” up in the placental tissue.  
     
    Btw, if you have access to the paper you referenced, can you send me the citation? This discussion has piqued my interest and I’d like to read up a little more on the literature.

  34. ben g,  
     
    One quick question about the mono- and dichorionic twins studies you’re referring to: Do you know if the studies further specified whether they were only investigating the differences between mono- and dichorionic monozygotic twins? 
     
    It seems that is the essential point. If they are comparing dichorionic dizygotic twins to monochorionoic monozygotic twins then I would suspect there would be quite a few significant differences because of the genetic differences.

  35. Whoops,  
     
    To Lorenzo I said, “Don’t know what you mean by the language of disorder.” 
     
    Jeez..dumb, I know, but the word disorder I took to mean “chaos,” or “confusion” which is why I was confused. Sorry, my fault.  
     
    Disorder? Well, yes, actually, as long as we don’t get too picky about terminology If I’ve only one functioning kidney, or lung, or eye, or ear, then each of those that doesn’t work is malfunctioning. Is a malfunction a “disorder”? Why not? 
     
    I’ve been given a mouth in which to place food, teeth with which to chew that food, a digestive system that breaks it down further, absorbs nutrients, and sustains the body by converting that food to energy. If for some reason I choose to put that food some place other than my mouth, like sticking it in my ear instead, or maybe letting it lie on my stomach where I simply contemplate it, then I’d say I had a disorder. If I didn’t eat, like an anorexic, I’d say I had a disorder. If I repeatedly ate, then vomited, I’d say I had a disorder. 
     
    The structures of the body pretty much reveal function, don’t they? An erect penis is a pretty good delivery apparatus for sperm. The vagina is a pretty good receptacle for that sperm delivered by that penis.  
     
    However, before that sperm can be delivered where it’ll be useful there needs to be desire to so deliver. That desire must lead to a pleasurable experience so that the deliverer wants to make deposits again and again.  
     
    When there’s an operable penis and healthy sperm in the semen but no desire to deposit that sperm where it’ll have any use, serve any purpose, I’d say there’s a system’s malfunction–otherwise there’d be no need for the sperm. In other words, the design and the operation seem to be at cross purposes. Malfunction, disorder….yes.

  36. It’s almost certainly cited by this paper, which I don’t have access to at the moment. There’s a small chance it was some other Cochran & Ewald paper rather than this one: 
    Genes, germs, and schizophrenia: an evolutionary perspective. PMID: 12878806 
     
    > Also, any immune response will be systemic (i.e. once the immune response is activated by either of the sites of infection, any antibodies and activated lymphocytes will circulate through the bloodstream and encounter both placentae). 
     
    True. Or it may already have been activated long before. In either case, stochastic events could still determine the fate of particular foci of parasite activity – or at least that’s what I’m proposing.  
     
    > If it were the case though we could look at the placentae and presumably find some histopathological evidence of this “flare” up in the placental tissue.  
     
    Yes I agree. Assuming we know what sequence to look for, FISH should do the job even if there is no inflammation. Today you don’t even have to know what to look for as you could start out with the ViroChip, or PCR on 16S rDNA, though I’m not sure those are guaranteed to work. 
     
    Actually, I just checked and there are very few papers yielded by pubmed[monochorionic schizophrenia]. The paper cited by Cochran/Ewald is very likely to be this one: 
     
    http://schizophreniabulletin.oxfordjournals.org/cgi/reprint/21/3/357 
     
    I’m halfway through it right now and it is quite intriguing. As for mechanism they suggest what I suggested; they also suggest that 85-100% of monochorionic pairs exchange some blood (presumably it’s a small leak usually?). What’s truly amazing is that they claimed concordance of 60% in pairs with markers of monochorionism, and only 10% in those without. Now, that is some pretty intense stuff, by my lights. I’ll certainly be looking at these numbers for other diseases. I would have looked this up a long time ago if I knew the differences claimed were so big.

  37. Philosophically speaking, we aren’t here to be organisms – not anymore. Ergo, as has been pointed out, there are two different definitions for disease. Sometimes a fitness-reducing phenotype may be conducive or irrelevant to human aims, while it’s also possible for a fitness-enhancing or neutral phenotype can be pathological to human aims.  
     
    Thus, being gay might not be a disorder. If a whole society were gay it would obviously be a disorder. If only 3% of the society is, maybe not. I don’t really see what the big problem with it is, personally.  
     
    In the future, many people with no negative feeling about homosexuality might nevertheless choose to have their children be straight if it becomes possible to do so, just so their lineage will be likelier to continue (especially if they are planning to have few children). Or maybe not, if in the future gay people have more children than they do now.

  38. Does one have a hearing disorder if one can only hear out of one ear? If one is blind but is quite fulfilled living without sight, is his blindness a disorder? Are one’s feelings about a condition or state of being the only determiner of what might be a disorder? That’s pretty much why I said, “If we don’t get too picky about terminology.” 
     
    To clarify, I’d say that if my ear doesn’t hear, there is an auditory disorder. If my eyes don’t see, I have a visual disorder no matter how much I might be quite happy and content with my state of being and others happy with me.  
     
    A gay man wanting to have his own children w/out using clinical help requires he have sex with a woman. There are some gay men who can’t achieve this.  
     
    A gay friend and colleague of mine wanted kids desperately but two things prevented it: one, he didn’t want to use insemination for a host of reasons, all of which seemed reasonable at the time; two, when he and his partner considered adoption, he argued endlessly with himself about whether a child should have both a mother and a father. I thought him quite unselfish for giving it the thought he did, but it didn’t surprise me, for he was a very unselfish person.  
     
    When his paternal desires kicked in, at that point, I wonder what word might he have thought fitting. I know he wouldn’t have used “disorder” because he was quite the activist and of course he didn’t feel there was anything wrong with being gay, but I do know he was full of conflict and doubt about adoption and full of longing for what wouldn’t be.  
     
    Having left behind the anxiety and hurts of his youth, a struggle it would seem almost all gay people faced during the years in which he grew up, he went through his twenties and very early thirties quite happy and carefree. Then as his future lay before him and the reality of age set in, according to him, he viewed his gayness in a bit of a different light, something he had not foreseen. He had thought the days of wishing he had been born straight were over long ago, but the child situation had caused fleeting thoughts that disturbed him. 
     
    Turns out best that they didn’t have the kids. Neither he nor his partner made it past the age of 35.  
     
    “What’s in a word?” some bard asked.

  39. Can’t see my post. I think I typed, “What’s in a word?” Correction. “What’s in a name?”  
    Time for bed.

  40. The only reason a concept as shabby as the “Gay Uncle” theory survives is because it is never compared to anything else. 
     
    I don’t think strong convictions are warranted given the state of the data on this subject, but the busted uncle theory has two important strengths in comparison to pathogen theory (as fine as it is among the few circulating hypotheses):  
     
    1) It at least attempts to square the circle that there is a nontrivial genetic component to homosexuality while selection should strongly work against this. Some theory needs to account for this, and there are only a limited number of ways to approach it. 
     
    2) There is at least some empirical support for it from Samoa, which is more than we can currently say for pathogen theory. 
     
    Vasey, P. L., Pocock, D. S., & VanderLaan, D. P. (2007). Kin selection and male androphilia 
    in Samoan fa?afafine. Evolution & Human Behavior, 28, 159?167.  
     
    Vasey, P. L., & VanderLaan, D. P. (2008). Avuncular tendencies in Samoan fa?afafine and 
    the evolution of male androphila. Archives of Sexual Behavior. doi:10.1007/s10508-008-9404-3.  
     
    Vasey, P. L., & VanderLaan, D. P. (in press). Materteral and avuncular  
    tendencies in Samoa: A comparative study of women, men and  
    fa?afafine. Human Nature.

  41. Jason Malloy 
     
    Can you think of even one other phenomenon where scientists use a “Busted Uncle” hypothesis to explain it? 
     
    It could be a blind uncle, deaf uncle, infertile uncle, hopelessly unattractive uncle, any kind of uncle that has little chance to produce his own offspring.  
     
    I don’t think this concept has ever been used to explain anything in humans.

  42. I’ve got a new hypothesis, I call it the “Straight Uncle Theory.” 
     
    Throughout prehistory straight uncles were more likely than gay or transgendered uncles to be chieftans or warriors. The higher status conferred upon elite tribal members decreased the mortality rate of their offspring and close relatives. Lower mortality increased the spread of genes related to heterosexuality. 
     
    Bonus Point: 
    Anyone who questions my hypothesis is a hater.

  43. Check out Hamilton’s rule.

  44. Can you think of even one other phenomenon where scientists use a “Busted Uncle” hypothesis to explain it? 
     
    It’s just kin selection. So, sort of: insect eusociality, altruism, kin altruism, etc. 
     
    The three genetic explanations for homosexuality are overdominance, frequency dependent selection via kin selection, and sexually antagonistic selection. 
     
    Recent evidence for the third one strikes me as the most convincing.

  45. Keller and Miller’s paper also seems apropos here. RE: the persistence of some genetic diseases: Resolving the paradox of common, harmful, heritable mental disorders: Which evolutionary genetic models work best? 
     
    Do gay men tend to have older fathers?

  46. Recent attempts to test the gay germ theory with the GSS here, here, and here.

  47. Jason Malloy 
     
    From Keller and Miller’s Paper 
    Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? 
     
    I feel compelled to add that there don’t appear to be any common Schizophrenia genes. Any harmful Schiz mutations that crop up are rapidly put under by natural selection. The Keller/Miller paper appears to be 68 pages of, “I know this idea doesn’t work in practice but what about in theory?” 
     
    Feb 12, 2009: New Direction In Search For Genetic Causes Of Schizophrenia Proposed 
     
    “The literature is replete with dozens of genes and SNPs identified as associated with schizophrenia,” says first author Anna Need, PhD, a postdoctoral associate in the Center for Human Genome Variation at the Duke Institute for Genome and Sciences Policy. “But we systematically retested all the leading candidates and concluded that most, if not all of them, are false positives.”

  48. Jason Malloy 
     
    Thanks for the Congenial Times links. 
     
    A large, Danish study found the same thing as the GIS. Urban birth in Denmark is strongly associated with gay marriage.  
    Childhood family correlates of heterosexual and homosexual marriages: a national cohort study of two million Danes.

  49. The three genetic explanations for homosexuality are overdominance, frequency dependent selection via kin selection, and sexually antagonistic selection. 
     
    1. As to overdominance– a study disputing that is offered in Journal of Sex Research, “Family and Sexual Orientation: The Family Demographic Correlates of Homosexuality in Men and Women” by Andrew Francis, October, 2008.  
     
    2. Kin selection–is there evidence that gay men in non-island populations nurture brothers, sisters, extended family, or other community members enough to pay their evolutionary way? I can see that in an isolated area almost anyone who doesn’t have his or her own offspring to care for would be likely to contribute to the care of others as long as physical or mental incapacities don’t prevent it. If this is an evolutionary strategy, it would seem that nature would have devised other similar stategies.  
     
    For instance, is unatractiveness in women a strategy to insure they remain unsuitable marriage partners and so are used to take care of others? Hmmm. But, that’s also a waste of a uterus, isn’t it?  
     
    Is infertility in women a strategy for survival of the group? After all, not tied down to taking care of her own children, she can care for other’s kids and the old people? This is essentially the case for gay men in this kin selection hypothesis of homosexuality. It’s a kind of infertility.  
     
    Of course, the loss of a fertile female would have been more serious than the loss of an occasional rare male who didn’t reproduce except when the population of males was threatened by any reason.  
     
    However, thinking about gay men in more heavily populated, non-isolated areas, (just thinking aloud here- I have no study that either suppports or refutes this,)it seems that once they reach a certain age, they leave for greener pastures, an area which is much more populated. There seems to be no obvious evidence that they stick around to raise family members to insure their survival or well being any more than their straight siblings do.  
     
    3. Sexually antagonistic selection–this is the model proposed by Ciani. Yes, he’s come up with a model which, he argues, is the only way homosexuality in men could have survived in fairly “stable, low frequencies.” 
     
    Do we know, however, in what frequencies homosexuality has existed and where it has existed? What are our sources? All we know is there are references to it from a long, long time ago, but apparently no references to it in some places nor knowledge of it among some groups. How reliable is our info about its occurrence and the rate of its occurrence among this group or that?  
     
    With this sexual selection hypothesis, aren’t there simple, non-invasive, inexpensive tests that the sisters of gay men could undergo that gives at least a hint of their fertility? A test of their mothers would be unhelpful because by the time these gay men are identified, their mother’s fertility has begun to decline. But what of their same-age or near-age young sisters? I mean, even a test of estrogen levels can give some indication unless I am way off base here. I realize hormone level measurements don’t predict that a woman will conceive and deliver a child w/out incident, but it’s some place to start.

  50. Back to the sexually antagonistic selection hypothesis–I realize we can look at how many children the mothers of gay men have had and compare those numbers to the number of kids mothers with non-gay sons have had, but that strategy wouldn’t account for modern decisions about child bearing, with birth control so available and so many people choosing to have fewer kids. 
     
    That’s what I was thinking when I asked about simple tests that give at least some hint of fertility.

  51. Jason, 
     
    I too find that Slate article on Sexual Antagonism most convincing, for anecdotal reasons. 
     
    In my family I don’t know of any homosexual men – up to 3rd cousins – but there are many homosexual women, and the men outproduce the women in number of offspring completely. For instance my paternal grandfather was a larger than life character, a military man and great athlete and intellectual. He had 7 children, 5 female – 1 married with 3 kids, 4 unmarried and childless, possibly 3 lesbians – he had 2 sons, one with 5 children, and one with 6 children – my Dad. So the sons on average had 5.5 children, and the daughters 0.6. 
    I have 4 sisters, 1 lesbian, 1 bi-sexual, who have a total of 3 children, and it seems like I myself will outproduce them.  
     
    So here you would have some factor making male offspring more fecund, but making females less so and more likely than average to be lesbian.

  52. pconroy 
     
    Do you see that the same hypothesis could just as easily apply to Autism, Psoriasis, Acne or pretty much anything? 
     
    Something along the lines of… 
    “In family X most of the boys have severe depression but the girls tend to have lots of kids. So my hypothesis is that the gene that causes depression in boys also produces extra fertility in women.” 
     
    If someone applied that logic to anything but homosexuality people would not take them seriously. 
     
    The MZ concordence rate for homosexuality is only like 20% or 30% and scientists haven’t found any pattern of inheritance. If it was caused by a fertility gene or gay uncle gene shouldn’t it be as obvious as Sickle Cell?

  53. There does seem to be some clustering of homosexuality in families, but I also remember Paul Ewald stating that it’s not unusual for pathogens to cluster in a family, with carriers passing bugs along from one generation to another. Families share exposure and susceptibilities. Food for thought. 
     
    I too am reminded of stories that anecdotally show the clustering, in this case, a friend of my mother. She had three sons, one straight, two gay (well, the youngest is bi, if we accept bi as a category–he does have daughters), but the two non-straight sons come from two different fathers. It was that which first made me interested in the subject. As a kid, I assumed that meant it was genetic, but now it appears it’s not so simple as all that.

  54. Craker, 
     
    From my psychology book: Even identical twins may receve not-so-identical prenatal nurture. Two-thirds of identical twins share the same placenta, and thus a more similar prenatal environment (although one might get a richer blood supply and weigh more at birth). Other identical twins have separate placentas. In this arrangement, one placenta sometimes has a more advantageous placement that provides better nourishment and a better placental barrier against viruses. Early indications are that, compared with same-placenta identical twins, those who develop with separate placentas are somewhat less similar in their psychological traits, such as self-control and social competence (Phelps & others, 1997; Sokol & others, 1995) — pg. 114 of Psychology (8th Edition) by David C. Myers 
     
    And here are the full references: 
     
    *J.A. Phelps, J.O. Davis, and K.M. Schwartz, “Nature, Nurture, and Twin Research Strategies,” Current Directions in Psychological Science, Vol. 6, No. 5 (October 1997), pp. 117?121. 
     
    *D.K. Sokol, C.A. Moore, R.J. Rose, C. J. Williams, T. Reed, and J.C. Christian, “Intrapair Differences in Personality and Cognitive Ability among Young Monozygotic Twins Distinguished by Chorion Type,” Behavior Genetics, Vol. 25, No. 5 (September 1995), pp. 457?466.

  55. A theory I heard once to explain a number of disorders is that while a single mutation should only show up rarely, if a number of different mutations all lead to the same result then sheer chance could result in a higher than 1% rate (if n mutations have p probability of arising the phenotype should occur at 1-(1-p)^n). I don’t know if that holds any water, so I’m asking the experts here.

  56. “I wouldn’t be at all surprised to find that the really strange ones (I mean, what the heck’s up with “water sports,” for example)are the result of brain damage/malfunctioning of some sort. Has to be.” 
     
    Has to be? I don’t think so. Simple conditioning provides an elegant explanation. 
     
    A lot of fetishes involve things that, for one reason or another, generate feelings of shame, disgust, or fear. The various types of arousal are so similar that it’s mostly our contextual awareness that distinguishes them. 
     
    Was there something wrong with the brains of the dogs who salivated at the sound of a bell?

  57. Was there something wrong with the brains of the dogs who salivated at the sound of a bell? 
     
    Nope, nothing wrong with those dogs– they just knew the old bell meant food. Food is good! Drinking urine and wallowing in it isn’t.  
     
    The question raised is really how much of what is termed “abnormal psychology” has its roots not in the “psyche” (whatever that is) but in the good old electro-chemical brain. In other words, aren’t we finding more evidence that there is a biological root or trigger to so much of this type of behavior? 
     
    Years ago, a person who found it nearly impossible to navigate life’s daily obstacles w/out falling apart, or who may have been so bad off he or she found it hard to get out of bed, was thought to be either emotionally weak, extraordinarily lazy or manipulative, or flat-out crazy, and people tried to explain either the weakness, the laziness, the manipulation, or the craziness with events in the person’s past. In other words, they sought a strictly psychological explanation. Then, we began to learn about the chemical state of depression.  
     
    Long ago they threw some people who acted weird into asylums. They had undiagnosed diabetes. 
     
    Aren’t we finding out that those who are really “out there” with such practices are likely to have something that isn’t operating properly in the brain? That the behavior is not just the result of the “psychological?”  
     
    I don’t even know anymore how we can separate the psychological from the biological.  
     
    I admit that the connection between staph infections and PANDAS has made me hyper-mindful of the possibilities that bugs, parasites, or autoimmune reactions may be at work in so many of these cases where behavior is odd and self-destructive. And, that’s the category into which watersports fall. 
     
    Guess I’m just not so sure anymore that we can chalk up all the weird things people do to this nebulous thing we call the mind.

  58. the connections between staph infections and PANDAS 
     
    Check–it’s a strep infection that’s been identified w/ PANDAS.

  59. One last thought–I found it fascinating that among all the tics and/or odd compulsions associated with PANDAS are separation anxieties, bedwetting, excessive urination and unusual interest in urination. 
     
    I remember the poor kid I grew up next to–he got dragged to a child psychologist for his bedwetting. I wonder now if his problem was PANDAS. Who knows? Studies show that the strange behaviors in these kids abate, in some faster than in others, then stop altogether, but return when the kid has had another strep infection.

  60. Urine is sterile. What’s really dangerous is coprophagia.

  61. PANDAS: A link between strep throat and OCD 
     
    “Though it is not known why, PANDAS patients overwhelmingly obsess about urination, which is not an especially dominant obsession in other OCD cases.”

  62. Google search: Pandas OCD Urination 
     
    Go through the links and you’ll find dozens of mentions like this 
    “This is a report of an 11-year-old, prepubertal boy with acute-onset urinary urgency and frequency, obsessions and compulsions related to urination…” 
     
    I don’t think the smart money bets on Freud.

  63. “Then, we began to learn about the chemical state of depression.” 
     
    No, we didn’t. We have no more idea of what depression or schizophrenia – or for that matter, virtually any other mental disorder – are than we ever did. What we know is what they aren’t, not what they are. 
     
    There are only a few exceptions, and the exceptions are usually quite different (in more than the obvious way).

  64. Caledonian, you’re more right than wrong about depression, but the way you put it is arguably a little extreme. The depressogenic effects of exogenous pro-inflammatory cytokines are repletely confirmed by roughly a dozen works or more, at least some of which use stringent logic (I haven’t read em all), with few or no failures to replicate reported to date. The attempt to show that cytokines are actually elevated in depression has been much less consistently successful, though the recent salvo from Harvard (PMID 17681762) was particularly impressive because of its highly significant differences from normals in something like 20 different cytokines. It’s a fairly strong hypothesis, anyway. 
     
    I know less about the details of the monoamine hypothesis.

  65. Caledonian, 
     
    “Then, we began to learn about the chemical state of depression.” 
     
    That sentence doesn’t say we know what the triggers/causes of so-termed “chemical imbalances” are or even that we know what those levels ought to be in individuals, but we do know neurochemicals are involved, don’t we? That’s a great deal more than concluding people are weak or lazy. I thought I was sufficiently general in saying we’ve “learn[ed] about.”  
     
    How involved are personal experiences or other other environmental factors as triggers? Genetic susceptibility factors? We can only stay tuned.  
     
    That being said, your point about knowing what they aren’t is well-taken.

  66. Eric J. Johnson  
     
    I read about that just a few months ago and it’s pretty interesting. Evidence is mounting that depression can be triggered by an immune response. 
     
    Bacteria, Serotonin, and Depression: A Possible New Approach to Treating Mood Disorders

  67. > but we do know neurochemicals are involved, don’t we?  
     
    Not that I know of. But I’m not a big expert.  
     
    Cortisol is supposed to be elevated in about 1/2 of depressed subjects. I’m not sure what percentile “elevated” means, what p values are on record for differences from normals, or whether the finding has been disputed. (A single study with p barely under 0.05 does not mean much to me in most contexts.) 
     
    I don’t know why this hasn’t provoked a larger “whoa depression is often an organic disease!” epiphany. For one thing, if you assume there is a single pathogenesis, then obviously cortisol cannot be an important cause, since 1/2 of subjects are normocortisolemic. However, it’s also possible cortisol is the sole cause of depression in those in whom it is elevated, and the other cases are caused by something else. The way to address this possibility is to experiment by (temporarily) raising the cortisol of normals and lowering the cortisol of depresseds. I’m not sure if this has been done. Cortisol at very high levels (Cushing’s disease) is indeed depressogenic but I’m not sure those levels aren’t higher than those found in primary major depression.  
     
    I’m not sure if any replicated results have come out about monoamine levels; that’d be the other place to look. As I mentioned the work on cytokine levels has been frustratingly inconsistent, with roughly as many disconfirmations as confirmations. 
     
    My opinion is that a significant percentage, at least, of primary depression cases are organic. But by “opinion” I mean I am permitting myself certain intuitive leaps or whatever, rather than sticking strictly to the strict stuff.

  68. Eric J. Johnson: 
     
    Fair enough. Let’s say instead that we know of mechanisms which are likely involved in at least some diagnosed cases of depression. My point is that we have no general theory that holds water, and even in specific cases, we usually can’t demonstrate a clear physiological problem or show that any particular mechanism is involved. We don’t even have convenient ways of measuring some of the factors, and the ones we do have are often too invasive to be of much use. 
     
    As for the monoamine hypothesis: It’s complete nonsense which is repeated (and sometimes believed even by people who should know better) because of its utility in getting people to accept treatment and view that treatment as beneficial or necessary. Examination of the relevant evidence shows that the most common claims regarding “chemical imbalances” are obviously wrong, and the more subtle arguments are insufficiently supported to stand as truth claims. It makes as much sense as saying that someone has too much black bile – it’s humour theory given modern clothing. 
     
    >”My opinion is that a significant percentage, at least, of primary depression cases are organic.” 
     
    I don’t possess a strong argument against that, although given the ubiquity of depression (and the difficulty of clearly distinguishing between clinical and subclinical cases) I suspect that the majority do not represent a malfunction of any kind, physiological or psychological. 
     
    >”but we do know neurochemicals are involved, don’t we? That’s a great deal more than concluding people are weak or lazy.” 
     
    Well, of course neurochemicals are involved. Thought doesn’t take place without them. We just don’t know that they’re part of whatever’s responsible for the conditions. 
     
    Postulating ‘psychological’ causes doesn’t require that we assert people are weak or lazy, either. Part of the reason pseudoscientific biological just-so stories are currently popular is the reaction to the old pseudoscientific psychological just-so stories. 
     
    Most people would rather have an explanation that’s wrong but says implies their problems are well-understood and beyond their ability to influence than an explanation that’s wrong and says their problems are the result of personal failures. 
     
    The pendulum swings between two extremes of nonsense, and at present we’re at the biological-causation side.

a