Wednesday, May 25, 2011

What Causes Homosexuality: And Why It Matters

I submitted this paper to the Stand for the Family Symposium on 19 May, and anticipate presenting it at the same in October 2011. I've posted on this subject before, but I condensed my presentation. 

What Causes Homosexuality: And Why It Matters

A.    Introduction
B.     Sex determination
1.      Epigenetics
C.     Causation
1.      The Parking Lots Test
D.    Conclusion


Misunderstandings about homosexuality frequently strain family relationships.  Accurate understanding about the causes of homosexual orientation can lay a foundation for understanding, reconciliation, and peace in these conflicted families.  Through a scientific inquiry, I grapple with the question: what causes homosexuality? I include analysis of some of the most recent and most significant studies which bear on the question, including the 2010 Swedish twin study, the largest of its kind.


Our response to various bioethical problems often depends not only on a general understanding of the philosophical question at issue, but also on a detailed understanding of the biological organ or mechanism in question, the methods or techniques employed to generate the data, a sense of which data are in fact relevant, knowledge of how to properly interpret scientific results, and a sophisticated appreciation of treatments currently or conceivably available.
– Adina L. Roskies[1]
For decades, a heated debate has raged about what causes homosexuality.  Religions, political parties, and family members have taken sides and aligned themselves against opposing positions, and this fire shows little sign of burning out. 
But why does this debate matter to strengthening the family? 
 I offer two reasons:
(1)   Responses to homosexual orientation frequently result in family conflict (including rejection of gay and lesbian children).  Mental health of siblings, accountability of parents and children, and family relationships are at stake.  More accurate understanding of homosexuality’s causes holds promise for strengthening families by providing a foundation for bringing peace to these conflicted homes. 
(2)   The answer to the causation question bears on the question of changeability.  Homosexual orientation may be changeable (1) sometimes, (2) always, or (3) never.  If #3 is true, the nature and utility of marriage may be best fulfilled by affirming same-sex marriage (SSM).  If, on the other hand, #2 is true, there may be reasons to prefer a norm affirming opposite-sex marriage over same-sex marriage.  Because a
“right” marriage culture is vital to strengthening the family, the answer to the question of “how changeable is homosexual orientation” (and thus, “what causes homosexuality”) proves extremely important.
The paper below will lay groundwork for an ethical response to homosexuality-related questions by examining “the biological organ or mechanism in question, the methods or techniques employed to generate the data, a sense of which data are in fact relevant, knowledge of how to properly interpret scientific results, and a sophisticated appreciation of treatments currently or conceivably available.”  Specifically, the groundwork will be constituted of an answer to the question: “What causes homosexual orientation?”

Sexual Determination

What makes a man a man and a woman a woman?  There are two common ways of causing/determining sex in the biological world: 1) nongenetic factors (such as environmental temperature) and 2) genetic factors.  Humans fall into the latter category, based on the genotype of chromosome 23: XY individuals are male and XX are female.  This genetic difference causes a number of measurably different phenotypes (physical traits)- different shaped faces, different genitalia, different brains, different hands, different hematocrit (red blood cell count), different muscle mass, and different hormone profiles to name just a few.  All right, nothing new here so far.  How does the genotype difference translate into these phenotypes? 
Here the answer begins to get more complex.  The default phenotype in humans is female.  For a short period after an egg is fertilized, the zygote is bipotential, meaning it can become either a male or a female, and has both Mullerian ducts (precursors to the uterus and fallopian tubes) and Wolffian ducts (precursors to the prostate and seminal vesicles).  A simplified, two-step explanation of how the default female embryo is converted into a male:
Step 1: the SRY (Sex-determining Region Y) gene from the Y chromosome is translated into a protein known as TDF (Testis Determining Factor). 
Step 2: TDF causes a consequence cascade, which in concert with hormones causes the phenotypic differences observed between males and females. 
Now, as you might imagine, things can go wrong at a number of points during this process.  In Step 1, the SRY gene could be broken or missing- this results in XY, or X_ persons that are phenotypically female (Turner syndrome).  The SRY gene could be translocated to an X, resulting in an XX person that’s phenotypically male (XX male syndrome).  The SRY gene could be faulty, resulting in an XY phenotypic female (Swyer syndrome).  This is just the beginning, though, as these abnormalities result only from Step 1 problems.
Step 2 problems are even messier.  Step 2 problems also demonstrate why genes are not the whole story when it comes to sex determination.  Before I illustrate some Step 2 problems, let me describe epigenetics[2] by comparing the endocrine system to a football team.


“The construction of a building is as important as the blueprint.”  -Our Stolen Future, page 204
Hormones (such as the androgen testosterone) are like footballs; hormone-producing glands such as the adrenal gland are like the quarterbacks that throw the footballs; and wide receivers are the hormone receptors- proteins embedded in cell membranes or cytoplasm which “catch” the football and pass its signal down into the cell.  After being caught, the hormone football then degrades.  The football’s signal exerts influence upon (epi) the genetic (genetic= hence, epigenetics) expression of the cell.  The most typical cellular responses to catching the football are to up- or down- regulate gene expression: meaning that the number of proteins the cell translates from a particular gene goes either up or down.  If there are too many or too few received footballs, disaster can occur (e.g. testes won’t develop).  Okay, so we’ve got the basics of the endocrine system- what next?
Without the activity of the endocrine system, especially of androgens, an embryo cannot become phenotypically male.  For instance, for a short time embryos have a pair of partially developed organs that if left to themselves will turn into ovaries.  If acted on by “downstream” elements from TDF, however, the gonads will become testes.  Similarly, many typically male phenotypes are dependent, not only on genes, but upon precise dosages and timing of specific hormones.  Though the causes of fetal hormone variance are not substantially understood, their role in sex determination is.  For emphasis, I’ll repeat the bottom line: sex determination is not merely genetic; it relies necessarily on the endocrine system.  Now for why this matters.
Some industrial chemicals are affecting human fertility and sex determination.  The reason?  The industrial chemicals do what some plants have been doing for millennia: they manipulate the human endocrine system to decrease human fertility.  The most common ways chemicals disrupt the endocrine system:
·         They block the ball (for instance, by binding to or disfiguring the hormones)
·         They hold the receiver (by binding to the receivers’ hands so there’s no room for hormones)
·         They throw their own football-like balls into the air (known as hormone mimics)
·         They tackle the quarterback (block the glands from producing or releasing hormones)
These endocrine disrupting effects often take place entirely independent of genes or gene expression.  Because some wide receivers will catch about anything that’s lofted to them, the mimics oftentimes don’t even need to bear a resemblance to an actual football- even a lampshade sometimes does the trick.  To complicate matters, hormone mimics and defensive linemen tend to stick around, rather than degrading like good little footballs do after they’re caught- thus, they can go through the cycle again and again. 
The same effects caused by endocrine disrupters can occur if genes coding for hormone receptors are flawed, or if glands don’t produce hormones in the right conformations (shapes) and amounts and at the right times.  What kinds of effects do we see in the animal kingdom (including Homo sapiens) when these internally and externally induced Step 2 problems occur?
·         Over a single decade, Florida eagles showed a sharply atypical lack of interest in nesting or courtship during the mating season for several consecutive years[3]
·         In the early 70’s, for the first recorded time male-female nesting pairs of western gulls were replaced by same-sex female pairs with extraordinarily large numbers of eggs.  The eggshells were thinner than usual, and the next two decades witnessed the spread of this phenomenon from Southern California to the Great Lakes, Puget Sound, and the coast of Massachusetts[4]
·         CAIS (Complete Androgen Insensitivity Syndrome) – human beings that are phenotypically female but genetically male.  These individuals have gonads inside, but they’re testes instead of ovaries.  The genetic maleness of these people usually isn’t noticed until puberty when menstruation fails to start. 
·         PAIS (Partial Androgen Insensitivity Syndrome)- the phallic structure varies in every degree between a penis and a clitoris.  The genotype is male (XY).  Some have a single orifice connected to both the urethra and the vagina.  These people span the entire range from predominantly phenotypically female to predominantly phenotypically male.
·         The sons of female rats given a small dose of dioxin (a hormone mimic) on the fifteenth day of pregnancy, a crucial window in sex determination, had sperm reductions as high as 56% less than their peers whose mom’s hadn’t been given the dioxin (interestingly, rats have ridiculously more sperm than they need, so even a hit of 56% won’t likely affect their fertility.  Humans, on the other hand, have just barely enough).  Additionally, the sons whose moms were poisoned were much less likely to sexually act like males and much more likely to arch their backs in the typically female response known as lordosis, and allow another male to mount them.[5]
I could go on, but the other effects follow similar lines, i.e. they confirm that sexual differentiation and reproductive problems result from endocrine disruption.  The timing and doses of hormones floating around in the womb during the critical sex determining phases of fetal development are like the small rudders which turn huge ships.  Bottom line of this primer on sex determination?  Both 1) genes and 2) the intra-organismal environment (i.e. the womb) play a huge role in sex determination. 


Now why in the world did I spend all that space giving a primer on sexual determination?  Because it provides vital context to the second of two causation theories that we will test. 

The Parking Lots Test

If John claims that the car is parked in lot C, and his wife Sarah claims that the car is parked in lot D, how do you test who’s right?  The answer: you walk to the two parking lots and see which lot the car is parked in!  This kind of organized common sense is at the root of scientific inquiry, and it is the method we will use to test two competing theories that claim to explain what causes homosexual orientation (HO).  I point out that we will not be testing the causation of homosexual behavior, nor of some mix of homosexual behavior and HO- we will only be testing the narrow question of what causes HO.  The lineup:

Theory 1: MIC

This is the non-biological factors theory.  Though there could be any number of non-biological factors, I have named the theory after some of the popular ones I hear most often: molestation, infection, and choice.  Molestation is the idea is that people become HO as a result of childhood and/or adulthood molestation.  Infection is the idea that people become HO as a result of some kind of contact with someone who’s already HO, such as the way you might get recruited into the NRA, the way you catch a cold, or the way you “inherit” from your upbringing the practice of waiting until prayers are said before you start eating.  This “infection” idea is similar to memetic inheritance, if you’re familiar with the concept.[6]  Under this umbrella you could also place “the way you were raised,” or parenting styles, which have also been proposed as causative factors.  Choice is the idea that a person chooses to be HO.  I’m going to aggregate this constellation of factors such that any one of them, or any combination of them, whichever results in the strongest presumption in its favor, will be tested below (in the parking lots below, we’ll assume whichever combination will help MIC make the best predictions).  I will refer to this set of factors as MIC, which stands for Molestation/Infection/Choice theory.  

Theory 2: GPRE

This is the biological factors theory.  Though there could be any number of biological factors, I have named the theory after the most popular ones: Genes and PRE-natal hormones (GPRE).  Now is where I drive home the relevance of the sex determination primer.  This theory considers sexual orientation to be a subset of sexual development.  The most likely placement of sexual orientation is under the umbrella of prenatal sexual differentiation of the brain.
Okay, so now we have the lineup.    Four problems and two terms before we get started:

Mixed Causation

What if HO is caused by a mix of MIC (molestation/infection/choice) and GPRE (genes/pre-natal hormones)?  This would frustrate our test, which requires exclusive theories. 
For the moment I resolve this tension by imposing a 90% threshold.  The relevant question here is a common statistical one: what % of the variability in trait A is caused by factor X?  The question is usually answered with a confidence interval.  Examples: 90% (or .9) of the variability in autism, +/- 10 percent, is due to heritable factors.  Anorexia is 70% +/- 10% heritable.  40% of the variability in alcoholism, +/- 10%, is due to heritable factors.  Using these three examples as a precedent, I will set both MIC and GPRE to 90% +2%/-2% (meaning 90% of the variability in HO, plus 2% or minus 2%, is due to MIC/GPRE).  This basically means that we will test two hypotheses: (a) 90% of the variability in HO is due to MIC and (b) 90% of the variability in HO is due to GPRE.  Because this standard excludes the opposite theory from having even the possibility of accounting for more than 12% of the variability, our test may proceed- duo non possunt in solido unam rem possidere (two cannot possess one thing each in entirety). 


What about those who consider themselves intermediate between homo- and hetero- sexual orientation?  Depending on where one draws the lines, this bisexual group could account for most of the population.  In the studies where there are only two categories, we assume that individuals reported their predominant orientation.  In studies that do report bisexuals, we consider the implications of bisexual orientation.  As I will explain, the possible errors resulting from assuming that individuals report their predominant orientation cut in favor of MIC.

The Difficulty of Self-Reporting

Many of the parking lots will have a set of data for heterosexual people and a separate set of data for homosexual people.  In most cases the subjects were separated by self-report.  The criticism here is that the reporters could be mistaken or lying.  This difficulty is not fatal to our test.  There are two and only two types of error that could come from self-reporting: false positives and false negatives.  A false positive would be a heterosexually oriented person who reported as HO.  A false negative would be a HO person who reports as heterosexually oriented.  Interestingly, both false positives and false negatives favor MIC and disfavor GPRE, since most of the lots we will visit measure biological phenomena.  Example: let’s say homosexuals on average have bigger toes than heterosexuals.  The false negatives would make the heterosexual toe size mean (average) closer to the homosexual mean, and the false positives would make the homosexual toe size mean closer to the heterosexual mean.  Thus, self-reporting problems favor MIC- meaning a conclusion that MIC is a better theory than GPRE is suspect, but a conclusion that GPRE is a better theory than MIC could only be strengthened by reporting errors. 
The number and magnitude of pathways to HO also cuts in favor of MIC for the bulk of our parking lot tour.  Imagine that some people are raped into HO, while others are merely born that way.  In this hypothetical there are two separate pathways to HO- which again will mean that both the number and size of non-GPRE pathways to HO, if they exist, will further vitiate confidence in a MIC> GPRE conclusion, but serve to strengthen a GPRE> MIC conclusion.

Reliability of Studies

How can the reader know that what we see in the parking lot is legitimate?  The short answer is: she ultimately can’t.  The longer answer is that she can take reasonable steps to become more confident in the legitimacy of the studies.  You will note that with some exceptions, I don’t heavily reference the studies/parking lots we are about to visit. This is a strategic decision.  I feel that the 80+ additional pages I could, by virtue of my academic training in the biological sciences, compose on the nitty gritty of the science would 1) merely replicate what more capable authors have already accomplished and 2) distract somewhat from my intended objectives for the book as a whole.  Most of the studies are readily accessible by anyone with internet access, and each and every study is cited and available in at least one of the two resources: 1) Bill Bradshaw’s analysis and treatment of the studies in a 57-page .pdf entitled The Evidence for a Biological Origin of Homosexuality, which I have made available for the reader[7]; 2) Simon LeVay’s 295-page Gay, Straight, and the Reason Why: the Science of Sexual Orientation, published in 2010.  Using the bibliographies in both of these resources and “peer reviewing” the studies yourself will also help. 

Beginning the test

Okay, now we’re almost ready to embark!  Together we shall make a multi-stop journey through a countryside filled with parking lots.  As we journey, please keep a tally of points.  Example: if we were contrasting “flat earth” vs. “spherical earth” theory, one parking lot might be to get on a spaceship, fly out into space, then turn around and look at the earth.  Flat earth would predict they’d see something like a piece of paper; spherical earth would predict they’d see something like a sphere.  You would likely award -1 (a demerit) to flat earth since its prediction was contradicted, and +1 (a point) to spherical earth for being vindicated.  Similarly, MIC and GPRE will, like John or Sarah above, make a prediction of where the car will be.  As we visit each lot, award a point to either or both theories whose predictions are matched by our observations, and award a demerit to the predictions which are contradicted.  At the end, I will ask you what score you came up with.  Ready?

Parking Lot 1: Gay hands

The hands of men and women are, on average, distinctly different.  Specifically, the 2D to 4D (second to fourth digit, or ring to forefinger) ratio is closer to one in women than it is in men.  MIC would predict that either 1) the male HO population will have the same mean ratio as the male heterosexually oriented population; 2) somehow the choice or infection of HO changes finger length; or 3) a molestation or choice event retroactively changes finger length.  2 and 3 are possible but not particularly likely, which leaves MIC with prediction 1.  GPRE would predict the opposite, namely that the mean ratio for HO men will be closer to that of heterosexually oriented women, and that the mean ratio for HO women will be closer to that of heterosexually oriented men.  What do we observe?  HO men’s ratios are shifted in the direction of straight women, and HO women’s ratios are shifted in the direction of straight men[8]. 
Some scientists would put the matter to bed right here in parking lot 1, claiming that it’s ludicrous to think that MIC causes HO- after all, 1) the differences are significant; 2) these populations were selected on a single variable, HO; 3) self-reporting and multiple-pathway errors cut in favor of MIC; 4) the study has been independently replicated many times; 5) with a little training on taking precise measurements + a large sample, almost anyone can replicate this experiment; and 6) there is no reason why molestation, choice, or infection would alter the length of a person’s fingers (in any case, fingers can be measured in the womb and in early childhood well before either parenting, infection, choice, or molestation have an opportunity to alter the 2D:4D ratio).  So some scientists would say.  I, on the other hand, have promised a parking lot tour, not a one-stop trip- thus, we shall proceed.   

Parking Lot 2: Twins

Will same-gender identical twins or fraternal twins be more likely to share the same sexual orientation?  MIC would predict that, at a large sample size, either type of twin will be about equally exposed to cultural influences, molestation, and choice.  In any case, an individual’s molestation, choice, and infection experiences will be a much better predictor of whether that person is HO than biological factors, since biological factors are not primary etiological factors of HO.  Thus, two brothers or two sisters are neither more nor less likely to share the same orientation as fraternal or identical twin siblings.  GPRE (genes/prenatal hormones), on the other hand, would make two very specific predictions: One, that identical twins will share the same orientation more often than non-twin siblings because they share a greater portion of their genes (and genes are partly the cause of HO).  Two, the identical twins will not always share the same orientation, because that would mean HO is only genetic, rather than being a product of both genes and pre-natal hormones (because the fetal twins develop at different paces and are positioned differently in the womb, we’d expect at least slightly different results if pre-natal hormones are causative agents).  What do we observe?  Same-gender identical twins on average share the same sexual orientation much more than fraternal twins[9].  The author of the seminal study writes: “The evidence we have at present strongly supports the proposition that there are hereditary factors in male homosexuality – the observation that an identical twin of a male homosexual has approximately a 20% likelihood of also being gay point to this conclusion, since that is 10 times the population incidence.[10]  The broadest twin study just came out in 2010:
“We used data from a truly population-based 2005–2006 survey of all adult twins (20–47 years) in Sweden to conduct the largest twin study of same-sex sexual behavior attempted so far. We performed biometric modeling with data on any and total number of lifetime same-sex sexual partners, respectively. The analyses were conducted separately by sex. Twin resemblance was moderate for the 3,826 studied monozygotic and dizygotic same-sex twin pairs. Biometric modeling revealed that, in men, genetic effects explained .34–.39 of the variance, the shared environment .00, and the individual-specific environment .61–.66 of the variance. Corresponding estimates among women were .18–.19 for genetic factors, .16–.17 for shared environmental, and 64–.66 for unique environmental factors. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior…
It has been suggested that individual differences in heterosexual and homosexual behavior result from unique environmental factors such as prenatal exposure to sex hormones, progressive maternal immunization to sex-specific proteins, or neurodevelopmental instability (Rahman, 2005). Although the unique environmental variance component also includes measurement error, the present results support the notion that the individual-specific environment does indeed influence sexual preference.[11] 

Parking Lot 3: Childhood gender-nonconformity

Little boys and little girls differ significantly on their risk taking, looking at their mothers’ faces, and turn-taking behaviors.  They also differ in how much they engage in rough-and-tumble play, how often they convert domestic objects into weapons, and whether they prefer boy or girl clothing.  Are girly-behaving boys or boyish-behaving girls more likely on average than their gender-conforming counterparts to report HO as an adult?  MIC would predict that knowing a subject’s childhood behavior would on average tell you nothing or very little about whether the person is HO, since the MIC factors of choice, molestation, and infection usually exert the majority of their influence in later childhood or afterward.  GPRE, on the other hand, which considers sexual orientation to be largely a brain-located reality whose development is almost wholly complete by six months post-partum, would predict a high correlation between early childhood gender non-conformity and adult HO.  What do we observe?  Over 40 studies confirm a high correlation between childhood non-conformity and adult HO[12].  Remember to tally the points for MIC and GPRE as we go along- I’ll be asking you for the scores you awarded later on.

Parking Lot 4: The older-brother effect

Psychiatrists at London’s Maudsley Hospital predicted in the 60’s and 70’s that later-born boys would be more likely on average to be HO.  Later this prediction was modified slightly: men that have older brothers are more likely than all other men to be homosexually oriented.  What would MIC think of this prediction?  Ceteris paribus (all else being equal), either 1) MIC would conclude that the prediction would fail- after all, what could having older brothers have, on average, to do with infection or choice or molestation?, or 2) MIC would ratify the prediction because older brothers are more likely to molest their younger brothers, but for that same reason would limit the prediction to a weak correlation, as the increased likelihood would be moderate.  GPRE would look again to the endocrine system and genetics for answers, and would find a potential answer in each.  From epigenetics is the hypothesis that a mother’s immune system may conclude that this Y-chromosome-antigen-exposing XY creature inside her XX self is foreign, and will mount a moderate defense in the course of the pregnancy, the residual effects of which may disrupt end-user endocrine action in a subsequent male pregnancy.  From genes the answer may be that maternal line of gay men tend on average to be more fecund (have more kids) than other mothers, or that heritable factors make a fetus more susceptible to a homosexualizing maternal anti-male antibodies response.  Thus, GPRE would not be surprised if the prediction is verified.  What do we observe?  Compared with having no older brother, each older brother increases the likelihood of a subject being HO by 33%[13]. 

Parking Lot 5: Handedness

MIC: handedness will not help you predict whether a subject you’ve never met is HO- only a knowledge of the subject’s environment (molestation and infection) and personal choices will.  GPRE: if handedness is related to the same genes that affect sexual orientation, or if handedness is related to hormone activity, then such a correlation is possible, though not necessarily an intuitive prediction.  What do we observe?  Gay men are on average left-shifted in handedness compared with straight men, and lesbians very shifted toward non-right handedness compared with heterosexual women[14]:
“The authors conducted a meta-analysis of 20 studies that compared the rates of non-right-handedness in 6,987 homosexual (6,182 men and 805 women) and 16,423 heterosexual (14,808 men and 1,615 women) participants. Homosexual participants had 39% greater odds of being non-right-handed. The corresponding values for homosexual men (20 contrasts) and women (9 contrasts) were 34% and 91%, respectively[15]” (emphasis added).

Parking Lot 6: Older-brother effect and handedness

How about another twist on the older brother effect?  Say the London Psychiatrists now claim that the older-brother effect applies only to right-, but not left-, handed men.  MIC’s response: “HO is not caused by biology, it is caused by infection, molestation, and/or choice.  Handedness in concert with the number of older brothers is not going to tell you anything about whether a person will turn out HO.”  GPRE’s response: “If right- but not left- handedness is correlated to the same genes that cause either increased maternal fecundity or male HO, as is suggested by the left-shift in handedness, then such a prediction may be verified.”  What do we observe?  The older-brother effect only applies to right-handed men[16].  

Parking Lot 7: Limb length to trunk length ratio

MIC: the ratio of limb:trunk length will not help you predict a person’s sexual orientation because that ratio is biological, and biology does not cause HO.  GPRE prediction: HO men will have a ratio shifted toward that of heterosexual women, and HO women will have a ratio shifted toward that of heterosexual men.  What do we observe?  HO men have a ratio shifted toward that of heterosexual women, and HO women have a ratio shifted toward that of heterosexual men[17].

Parking Lot 8: Gait and voice-quality

This lot is similar to lots 1 and 7.  MIC prediction: these “gaydar” signals won’t work because, again, they’re biological (though perhaps gaydar signals cause persecution of such individuals, and the persecution makes them gay).  GPRE prediction: gender-atypical intermediate gait and voice quality for HO men and women.  What do we observe?  Gender-shifted gait and voice quality, as well as other aspects of body function, in both lesbian women and gay men[18].

Parking Lot 9: Cross-cultural rates of HO

Because culture and choices vary so widely, MIC would predict that the prevalence of HO will accordingly vary from culture to culture.  GPRE would predict that, absent some regional endocrine influence or lineage-conserved genotypic trend, prevalence of HO will be fairly uniform across cultures.  What do we observe?  Consistent cross-culture prevalence of HO[19]. 

Parking Lot 10: Female to Male HO ratio

Would MIC predict that men or women would more often be HO?  Are men or women molested more on average than the other gender?  If so, the M of MIC would predict the more-often-molested sex.  Are men or women more susceptible to HO infection?  Under the I of MIC, the more susceptible gender would have a higher prevalence.  Are men or women more likely to choose HO?  Under the C of MIC, the “more likely to choose” gender is predicted to manifest a higher prevalence.  Because the answers to this question are unclear, one might reasonably conclude that this parking lot cannot cut for or against MIC.  GPRE, on the other hand, would definitively predict that the default sexual orientation, female-type (towards men), would have a higher prevalence simply because there are more steps that must go “just right” in order to result in male-type orientation (towards women).  What do we observe?  Consistent 1.5 to 2.0 times the rate of gay-to-lesbian HO[20]. 

Parking Lot 11: Personality and gender-associated occupational preference

MIC: there will be no difference between HO and heterosexual populations for either gender as to gender-associated occupational preferences, physical aggressiveness, empathy, expressiveness, and aesthetic/technological interests unless they on average either 1) result from MIC factors or 2) lead to MIC factors.  GPRE: HO men will consider themselves less masculine, and HO women more masculine, than their heterosexual counterparts, including in the listed categories.  What do we observe?  Gay men consider themselves less masculine, and lesbian women more masculine, than their heterosexual counterparts.  Significant gender shifts in physical aggressiveness, empathy, expressiveness, aesthetic/technological interests, and gender-associated occupational preferences are also observed. 

Parking Lot 12: Cognitive traits

Will HO men and heterosexual men score differently on tests where each gender is known to perform differently, such as male-favored mental rotation of objects, targeting, navigation and female-favored tasks such as verbal fluency, letter fluency, synonym fluency, judgment of line orientation, and remembering the location of objects on a page?  How about HO and heterosexual women?  MIC prediction: no.  GPRE prediction: yes, the HO population will perform more like the heterosexual norm of the opposite gender.  With the exception of lesbians who don’t do worse than straight women on object location, the HO subset of both genders does indeed perform atypically on these metrics for their gender (toward the opposite gender). 

Parking Lot 13: Molestation rates

In what way does molestation cause HO?  One hypothesis is that whichever gender a child first has sexual contact with will determine the orientation of that person for life (e.g. if molested by a man or experiments with a male peer, a boy will grow up HO.  If molested by a woman or experiments with a female peer, he will grow up HO, and vice versa for girls).  The less popular theory is that the person will grow up attracted to the opposite gender of their first sexual experience partner/molester.  MIC would endorse at least one of these hypotheses, and absent genes dependent on subsequent external stimulus, GPRE would predict an absence of effect. 
One study indicates that both gay men and lesbians are more likely to have had sexual contact with an older person of their own sex when compared to heterosexual people.  This study requires the assumption that the adolescents and children were sexually passive targets.  Especially for the adolescents, the molester may have either picked up on clues about the target’s sexual orientation from childhood indicators and selected on that basis, and/or the target may have invited or resisted less the molestation than their heterosexual counterparts.  In the study, 68% of the men and 62% of the women subjects identified themselves as homosexual before the molestation took place.  The authors also said: “[Molestation] may not, however, be a causal factor in either gender.  Perhaps children or adolescents with a higher potential for homosexual behavior are more likely to enter a situation that leads to same-sex molestation.”  In similar molestation studies, over 95% of the subjects report being aware of their own HO before the incest or sexual relations with adults. 
Another study reported that molested males, though not molested females, were more likely than non-abused males to form homosexual partnerships in adulthood.  The latter study’s finding could be limited to homosexual behavior rather than HO, and thus might be beyond our scope. 
The fact that most young people in at least America develop an awareness of their sexual orientation while they are still virgins and/or before they’ve have sexual experiences with members of the preferred sex belies the molestation hypothesis.  The reality that one out of three US women is sexually abused before age 18, yet the prevalence of HO in women is far less than 33%, is another factor vitiating the first hypothesis (similarly, the difference between the % of molested men and the prevalence of HO even without subtracting the unmolested HO population argues against molestation as an etiological factor).  Last, the undisputedly high incidence of HO persons who were never molested indicates at the least that there’s more to the HO story than molestation.
Some in the MIC camp predict that sexual abuse of girls by men would cause an increased incidence of HO in women.  GPRE would predict that the abuse would be irrelevant.  What do we observe?  No greater percentage of lesbians than straight women report having been abused. 
In conclusion, I’m not sure how to score this lot- it seems dicey.  You choose for yourself- I’m going to give both MIC and GPRE neither a point nor a demerit. 

Parking Lot 14: Boarding school

Homosexual behavior is common among British children and adolescents who attend single-sex boarding schools.  MIC would predict a higher incidence of HO in this population than the general population.  GPRE would predict no difference.  What do we observe?  Adult Britons who attended these schools are no more likely to engage in homosexual behavior than those who did not.  Once again, this behavior-based outcome may be beyond our “HO causation only” tour.

Parking Lot 15: Systemic cultural molestation

There are a number of cultures with require male youth to engage in homosexual acts, some of them believing that semen improves vitality.  An example of this norm is found in the Sambia tribe of New Guinea.  If indeed molestation causes HO, then MIC would predict elevated levels of HO in the men of this tribe.  GPRE would predict no difference in orientation.  What do we observe?  As adults, these men marry and behave heterosexually.  Again this behavior outcome may be outside our “orientation only” scope.

Parking Lot 16: HO as a subset of gender socialization

If the psychology of gender is socialized (meaning that the mental and behavioral traits that differ between males and females are learned from parents and society more generally), why couldn’t HO be simply a subset of gender learning gone awry?  MIC would predict that if you raise a child as a girl the child will adopt a female gender identity, including an attraction to men.  Biology-bound GPRE would predict that sexual orientation is mostly independent of socializing factors.  What do we observe in this parking lot?  Studies of genetic males who were reassigned as females while babies (due to severe congenital malformations of the pelvic area) report being attracted to females when they reach adulthood.    Additionally:
“In 1995 Diamond reviewed the arguments that homosexuality is an acquired/learned condition. His summary of the earlier work of investigators in both the United States and Great Britain who examined the family and social backgrounds of heterosexual, bisexual, and homosexual adults was “Their basic finding was that no common parameter of family or upbringing could be linked causally to sexual orientation, nor could any link be found between any aspect of an individual’s childhood or adolescent experiences and homosexual or bisexual activities.” Nothing published in the subsequent 14 years appears to contradict this conclusion.[21]

Parking Lot 17: HO as a product of parent orientation

HO could result from a child role-modeling her parents.  MIC would predict that HO parents that raise their own or others’ offspring would have a higher incidence of HO among those raised children.  MIC would further predict that, on average, straight parents will raise fewer HO children.  GPRE would predict than either correlation would be due to genetics and prenatal hormones (biological parentage) rather than how the parent raises the child.  What do we observe?  The vast majority of HO people have straight parents, and according to numerous studies children raised by HO parents don’t differ in sexual orientation from children raised by straight parents (with the exception of the female biological children of lesbians).

Parking Lot 18: Choice

MIC would predict that many if not all HO people chose to be HO.  GPRE would predict that neither HO nor heterosexual people choose which sex to be attracted to.  What do we observe?  Only 4% of gay men and 15% of lesbians say that choice has anything to do with why they are HO.  One may speculate that heterosexually oriented people would on average respond similarly- namely that choice has little to do with why they are heterosexually oriented.   
One also questions here why so many would choose to be HO (homosexually oriented):
“Join us and very possibly break your parents’ hearts, throw the family into chaos, run the risk of intense self-loathing, especially if you are religious, invite the disgust of much of society, give up the warmth and benefits of marriage and probably of parenthood.[22] 
If heterosexual orientation is an available alternative, why are so many otherwise reasonably normal people choosing what many consider an exceptionally difficult life as an HO person?

Parking Lot 19: Animal HO

Some people claim that a number of animals are homosexually oriented.  MIC would predict that animals would not manifest HO because, with a few exceptions (species which can learn from their peers, such as ravens and higher mammals and primates), animals are merely products of their environment and are incapable of sexually abusing, being molested, being “infected” with cultural information, or choosing.  Also, even from an evolutionary perspective, homosexuality will be selected against since it doesn’t produce offspring- right? 
Looking to the substantial prenatal and genetic similarities between ours and other species, GPRE would predict widespread homosexual conduct (which serves as the indicator of HO animals since they cannot self-report) in the animal kingdom.  What do we observe?  More important than the strength of the evolutionary arguments[23] for either side (which are abundant and available) is the reality suggested by our observations.  We observe homosexual, bisexual, and/or transgender courtships, sex, affection, pair bonding, and/or parenting in about 1,500 species, with substantial documentation for 500 of those 1,500.  Examples: 8% of male rams behave only homosexually (turns out the sexually dimorphic nucleus of the medial preoptic area is half the size in the gay than in the straight sheep); one report is that 9 of 10 giraffe pairings occur between males; in some penguin species same-sex individuals mate for life and refuse to mate with females even when given the chance; and many others (gulls, mallards, dolphins, elephants, lions, bison, bonobos, and hyenas to name a few).  Speaking of same-sex penguin pairings, Carol Lynn Pearson wrote:
“I have followed the charming story of Roy and Silo, two male penguins who met in a zoo holding tank in 1998 in New York’s Central Park.  They became inseparable, built a nest, defended it from others, and “engaged in what zookeeper euphemistically call ‘ecstatic display.’”  They showed signs of wanting to be parents, so the zookeepers gave them a dummy egg, which they successfully incubated, then gave them an actual egg.  When the baby chick was born, Roy and Silo cared for it, fed it, kept it warm, and successfully launched it into maturity.  Years later, the couple is still going strong and is regarded as just another couple by their heterosexual penguin peers.[24]
“Sexual behavior is clearly under genetic control in animals. A single gene… controls male and female sexual behavior in fruit flies. When the female route of expression of the gene is experimentally induced in genetic males, they do not exhibit male courtship movements and sounds. When the male route of expression of the gene is experimentally induced in genetic females, they behave sexually like males. It is not valid to dismiss evidence obtained from non-humans with the rejoinder that, “But, of course, people are not fruit flies.” Evidence continues to mount that the biochemical mechanisms that operate during embryonic life are remarkably similar, in general outline, among animals, and a large number of the genes that control development in fruit flies and people (and worms, and frogs, and mice) are the same.[25]
Another observation- remember the rat sons referenced in the sex determination primer?  The landmark study on the rat genome noted: “the rat genome contains about the same number of genes as the human and mouse genomes. Furthermore, almost all human genes known to be associated with diseases have counterparts in the rat genome and appear highly conserved through mammalian evolution, confirming that the rat is an excellent model for many areas of medical research.[26]  Our reliance on mice and rats for experimenting with new drugs evidences our trust in the biological similarities between rats and humans.  In the experiment referenced above, a single dose of a known endocrine disruptor was given to mothers.  MIC would perhaps concede that HO in animals is biological, but inasmuch as HO in animals is similar to that in humans, a biological factor such as an endocrine disruptor won’t affect HO.  GPRE would predict hyper-masculinizing or feminizing of the sons, depending on the effective direction of the endocrine disruption.  What do we observe?  The small dose of endocrine disruptor was enough to turn the rat sons to homosexual behavior.  Other studies, such as one where moms were exposed to plant estrogens, resulted in sons who show less mounting behavior and fewer ejaculations.  The latter study shows that the first ten days after a rat’s birth (rats aren’t as developed as humans at parturition) constitute the critical period for development of those areas of the brain linked to sexual behavior.

Parking Lot 20: Congenital adrenal hyperplasia (CAH)

CAH “refers to any of several autosomal recessive diseases resulting from mutations of genes for enzymes mediating the biochemical steps of production of cortisol from cholesterol by the adrenal glands.”  Individuals (usually women) with CAH frequently had too little or too much of sex steroids such as testosterone, progesterone, and estrogens during development.  MIC would predict that there will be no difference between HO and heterosexual populations as a result of the biological factor of CAH presence.  GPRE would predict masculinized or feminized orientation, based on which steroids were present at altered levels, and the magnitude of alteration.  Because very elevated testosterone is the most frequent occurrence, GPRE would predict increased incidence of HO.  What do we observe?  No less than 19 studies evidence that CAH women are on average very significantly shifted in the direction of HO.

Parking Lot 21: Auditory pathways

Did you know the cochlea makes sounds in addition to sensing them?   It’s true- and the sounds are called oto-acoustic emissions (OAEs).  A sensitive microphone placed inside the ear can detect the OAEs frequencies.  Any particular person will have between zero and about a dozen different OAEs.  It turns out that the number and volume of these OAE varies predictably by gender (women have on average more and louder OAEs).  This sex difference also exists in monkeys and sheep.  MIC’s prediction: HO and heterosexually oriented individuals from either gender will not differ in their OAE’s because anyone can choose/become infected/be molested into HO, and none are significantly biologically predisposed.  GPRE: HO males will be shifted toward the heterosexual female norm, and HO females toward the heterosexual male norm.  What do we observe?  HO men show no difference from heterosexual men, and HO women are shifted towards the heterosexual male norm.
Additionally, men and women differ in their prepulse inhibition (PPI), which is the degree to which they are startled by a loud sound stimulus if they are exposed earlier to a weaker sound.  This non-learned behavior is measured via eye blink, and is lower in women than it is in men.  MIC would predict no PPI differences; GPRE would predict gender shifts for this sexually dimorphic trait.  What do we observe?  Homosexual women manifest a significantly masculinized PPI. 

Parking Lot 22: DES exposure

What is DES?  “Diethylstilbestrol (DES) is a synthetic nonsteroidal estrogen that was first synthesized in 1938. Human exposure to DES occurred through diverse sources, such as dietary ingestion from supplemented cattle feed and medical treatment for certain conditions, including breast and prostate cancers. From about 1940 to 1970, DES was given to pregnant women under the mistaken belief it would reduce the risk of pregnancy complications and losses.[27]  DES is also a known estrogen mimic.  MIC would predict that DES exposure would not affect the likelihood of either gender’s HO, since the pre-natal hormones aren’t causes of HO.  GPRE would predict a discernible difference between DES-exposed and non-exposed people.  What do we observe?  There was no indication that DES influences the sexual orientation of sons.  Out of 30 women whose mothers were not exposed, none indicated either a bisexual or a HO.  Out of 30 women whose mothers were exposed, 24% reported a lifelong bisexual or HO.  When studying sister pairs where one sister had been exposed in the womb to DES and the other hadn’t, 8% of the unexposed sisters reported lifelong bisexual orientation, while 42% of the exposed sisters reported a lifelong bisexual orientation[28]. 

Parking Lot 23: HO running in the family

Additionally, what would MIC and GPRE predict about homosexuality running in families?  MIC might or not predict HO running in families based on how conserved the family culture is through generations, which culture could affect HO incidence in the family.  GPRE would predict a moderate correlation based on the genetic component of HO.  What do we observe?
“Data from random samples show that gay men are about three times more likely to have gay brothers than are heterosexual men (9% compared to about 3% in the general population). Lesbians tend to have a higher incidence of lesbian sisters (6-25% compared to about 2% in the general population).[29]

Parking Lot 24: Androgen Insensitivity Syndrome (AIS)

“In another human intersexual condition called androgen insensitivity syndrome (AIS), the gene that encodes the protein receptor that mediates signaling by testosterone is mutant. Males with this condition cannot respond prenatally to the male steroid hormones and are convincingly female in anatomy. These persons are nearly always raised as women, are no different in psychological well-being compared to control women…[30] 
MIC would predict that AIS would not affect homosexual orientation- after all, the HO is overwhelmingly caused by molestation, choice, or cultural infection rather than biology.  GPRE would predict that fetal androgen sensitivity is vital to converting the default orientation towards men into an orientation towards women, as a lack of prenatal exposure to androgens leads to a sexual orientation toward males- sublata causa, tollitur effectus (the cause being removed, the effect ceases).  What do we observe?  AIS men uniformly exhibit sexual attraction to men. 

Parking Lots 25-32: The brain

This could be the most important lot visited on the tour- as your guide I have “saved the best for last.”  Though brains are plastic in some limited ways until about age 25, most structural aspects are static and measurably different for men and women by a few months after birth, which is before the time that MIC factors could exert influence.  If girl and boy brains are different from each other- how about the brains of HO men and women?  MIC would predict no difference.  GPRE would predict, as it has in the many parking lots before this one, that the brains of HO men and women will be atypical for their gender in the direction of the opposite gender.  Additionally, GPRE would predict marked differences in parts of the brain that are likely candidates as sexual orientation centers.  What do we observe? (award points for each bullet) 
·         HO men are gender-shifted in terms of the relative sizes of the left and right cerebral hemispheres in the direction of the heterosexual female norm. 
·         Both gay men and lesbian women are gender shifted toward the opposite gender in their brain responses to compounds thought to be sex pheromones.  
·         Gay males, like females, have better verbal abilities than straight males.
·         Both gay men and lesbian women are gender shifted toward the opposite gender in the functional connectivity of their amygdalas, the emotional center of the brain, as measured by cerebral blood flow. 
·         The isthmus of the corpus callosum, whose size heritability is a whopping 94%, is different between heterosexual and homosexual men.
·         Viewing a female face produced a strong reaction in the thalamus and medial prefrontal cortex of straight men but not of gay men.  Gay male brains reacted more strongly to the face of a man.
·         The anterior commissure (superfast cables connecting the brain hemispheres) are larger in gay than in straight males. 
·         Significantly, gay men are gender shifted in the size and density of the third interstitial nucleus of the hypothalamus, which is a sexually dimorphic cell group concerned with male-typical sexual behavior. 

The 32-stop parking lot tour is now complete!  Thanks for coming along for the ride- next let’s check the scoreboard.  Now, there could be some error (which could go either way) in assuming each parking lot merits the same amount of points- nevertheless for the sake of convenience, presume each lot can give out no more than two demerits or two points [five possibilities: 1- both MIC and GPRE’s predictions failed (one demerit each), 2- they both succeeded (one point each), 3- one succeeded and the other failed (one point, one demerit), 4- one either succeeded or failed and the other neither succeeded nor failed (one point or demerit), 5- neither succeeded or failed (none)].  What did you get?  My tentative tally is MIC, -22 GPRE, 27.  We must remember that the size and magnitude of multiple pathways, if they exist, will frustrate GPRE’s claims but serve to substantiate MIC’s claims.  Also, if any persons in the sample groups mistakenly reported their orientation or lied, such errors will similarly reduce or eliminate the differences between heterosexual and homosexual norms in the parking lots which measured physical attributes.  To account for these MIC-favoring self-reporting and multiple-pathway errors, I will award a modest one demerit to MIC, leaving MIC -23 and GPRE 27 for a point spread of 50.   


HO is very likely caused predominantly by genes and pre-natal hormones, and not by factors such as parenting, infection, molestation, or choice. 

[1] Adina L. Roskies, Neuroethics Beyond Genetics, EMBO reports 8:S55 (2007).
[2] Note to geneticists- I recognize that epigenetics usually refers to genetic imprinting and methylation, and represents both a field that is both new and, in my view, exciting.  Here I follow Robin Holliday’s precedent  in using the term more broadly- in this case to refer to regulation of gene expression and other downstream effects caused by hormones.  Holliday, R., 1990. Mechanisms for the control of gene activity during development. Biol. Rev. Cambr. Philos. Soc. 65, 431-471.
[3] Theo Colborn, Our Stolen Future. 
[4] Theo Colborn, Our Stolen Future, chapter 1.
[5] Theo Colborn, Our Stolen Future, chapter 1.
[7]  (with permission) at
[8] See Levay, Gay, Straight and the Reason Why: the Science of Sexual Orientation, pg. 138-142.  Some of the primary literature: Hall, L. S. & Love, C. T. (2003). Finger-length ratios in female monozygotic twins discordant for sexual orientation. Archives of Sexual Behavior. 32, 23-28; McFadden, D. & Shubel, E. (2002). Relative lengths of fingers and toes in human males and females. Hormones and Behavior. 42, 492-500; Brown, W. M., Hines, M., Fane, B. A. & Breedlove, S. M. (2002b). Masculinized finger length patterns in human males and females with congenital adrenal hyperplasia. Hormones and Behavior. 42, 380-386; Rahman, Q. & Wilson, G. D. (2003b). Sexual orientation and the 2nd to 4th finger length ratio: evidence for organising effects of sex hormones or developmental instability? Psychoneuroendocrinology. 28, 288-303.
[9] Some of the primary literature: Bailey, J. M. & Pillard, R. C. (1995). Genetics of human sexual orientation. Annual Review of Sex Research. 6, 126-150; Bailey, J. M., Pillard, R. C., Neale, M. C. & Agyei, Y. (1993). Heritable factors influence sexual orientation in women. Archives of General Psychiatry. 50; Bailey, J. M., Dunne, M. P. & Martin, N. G. (2000). Genetic and environmental influences on sexual orientation and its correlates in an Australian twin sample. Journal of Personality and Social Psychology. 78, 524-536.
[10] Dean Byrd wrote an article for the NARTH website dated April 4, 2007 quoting Collins’ book, The Language of God, on genetics and homosexuality. Byrd’s review provided accurate quotes but implied that Collins believes free will is involved in the development of homosexuality. Subsequently, David Roberts at ExGayWatch wrote Collins to find out if Byrd had captured his views properly. Collins responded by saying the quote in an email.  Available at
[11] Eva Carlstrom, Niklas Langstrom, Paul Lichtenstein, and Qazi Rahman, “Genetic and Environmental Effects on Same-sex Sexual Behavior: A Population Study of Twins in Sweden.”  Archives of Sexual Behavior (2010) 39:75–80.
[12] Bailey, J. M. & Zucker, K. J. (1995). Childhood sex-typed behavior  and sexual orientation: A conceptual analysis and quantitative review. Developmental Psychology. 31, 43-55.  See also Katarina Alanko, Pekka Santtila, Katarina Witting, Markus Varjonen, Patrik Jern, Ada Johansson, Bettina von der Pahlen, N. Kenneth Sandnabba, "Psychiatric symptoms and same-sex sexual attraction and behavior in light of childhood gender atypical behavior and parental relationships," Journal of Sex Research, Sept-Oct, 2009 49, 494-504; Ploderl, M. & Fartacek, R. (2008).  Childhood gender nonconformity and harassment as predictors of suicidality among gay, lesbian, bisexual, and heterosexual Austrians.  Archives of Sexual Behavior 38, 400-410; Cardoso, F.L. (2009).  Recalled sex-typed behavior in childhood and sports’ preferences in adulthood of heterosexual, bisexual, and homosexual men from Brazil, Turkey, and Thailand.  Archives of Sexual Behavior 38, 726-736.
[13] See Levay, Gay, Straight and the Reason Why: the Science of Sexual Orientation, pg. 260-270.  Some of the primary literature: Blanchard, R. & Bogaert, A. F. (1996). Homosexuality in men and number of older brothers. American Journal of Psychiatry. 153, 27-31; Bogaert, A. F. (2003a). The interaction of fraternal birth order and body size in male sexual orientation. Behavioral Neuroscience. 117, 381-384; Bogaert, A. F. (2003b). Number of older brothers and sexual orientation: new tests and the attraction/behavior distinction in two national probability samples. Journal of Personality and Social Psychology. 84, 644-652; Bogaert, A. F. (2006). Biological versus nonbiological older brothers and men's sexual orientation. Proceedings of the National Academy of Sciences of the United States of America. 103, 10771-10774.
[14] Though one study detected the shift in women only: Mustanski, B. S., Bailey, J. M. & Kaspar, S. (2002). Dermatoglyphics, handedness, sex, and sexual orientation. Archives of Sexual Behavior. 31, 113-132.
[15] Lalumiere, M.L., Blanchard, R. and Zucker, K.J. Sexual orientation and handedness in men
and women: a meta-analysis. Psychological Bulletin, 126, 525 (2000).
[16] Blanchard, R., Cantor, J. M., Bogaert, A. F., Breedlove, S. M. & Ellis, L. (2006). Interaction of fraternal birth order and handedness in the development of male homosexuality. Hormones and Behavior. 49, 405-414; Bogaert, A.F., Blanchard, R. & Crosthwait, L.E. (2007).  Interactino of birth order, handedness, and sexual orientatino in the Kinsey interview data.  Behavioral Neuroscience 121, 845-853; Blanchard, R. & Lippa, R.A. (2008).  The sex ratio of older siblings in non-right-handed homosexual men.  Archives of Sexual Behavior 36, 163-176.
[17] Martin, J. T. & Nguyen, D. H. (2004).  Anthropometric analysis of homosexuals and heterosexuals: implications for early hormone exposure.  Horm. Behav. 45, 31-39.
[18] Johnson, K.L., Gill, S., Reichman, V. & Tassinary, L.G. (2007).  Swagger, sway, and sexuality: Judging sexual orientation from body motion and morphology.  J Pers Soc Psychol. 93, 321-334; Rieger, G., Linsenmeier, J. Al, Gygaz, L., & Bailey, J. M. (2010).  Dissecting “gaydar”: Accuracy and the role of masculinity-femininity.  Archives of Sexual Behavior 39, 124-140.
[19] Whitam, F. L. (1983).  Culturally invariant properties of male homosexuality: Tentative conclusions from cross-cultural research.  Archives of Sexual Behavior 12, 207-226; Wellings, K., Field, J., Johnson, A. M. & Wadsworth, J. (1994). Sexual Behavior in Britain: The National Survey of Sexual Attitudes and Lifestyles. Penguin Books.
[20] See Levay, Gay, Straight and the Reason Why: the Science of Sexual Orientation, pg. 13-15.  Some of the primary literature: Laumann, E. O., Gagnon, J. H., Michael, R. T. & Michaels, S. (1994).  The social organization of sexuality: Sexual practices in the United States.  Chicago: University of Chicago Press; Statistics Canada, (2004) Canadian Community Health Survey 2003.  Available at accessed January 14, 2010; Smith, A. M., Rissel, C. E., Richters, J., Grulich, A. E. & de Visser, r. O. (2003).  Sex in Australia: sexual identity, sexual attraction and sexual experience among a representative sample of adults.  Australia New Zealand Journal of Public Health 27, 138-145.
[21] Bill Bradshaw, “The Evidence for a Biological Origin of Homosexuality,” available at pg. 14.
[22] Carol Lynn Pearson, No More Goodbyes: Circling the Wagons Around Our Gay Loved Ones pg. 16. 
[23] See e.g. Jeff Kirby, “A new group-selection model for the evolution of homosexuality,” Biology and Philosophy 18:683-694, 2003.
[24] Carol Lynn Pearson, No More Goodbyes: Circling the Wagons Around Our Gay Loved Ones pg. 16. 
[25] Bill Bradshaw, “The Evidence for a Biological Origin of Homosexuality,” pg. 7.
[26] NIH New Release, National Human Genome Research Institute, March 31, 2004, "Scientists Compare Rat Genome With Human, Mouse: Analysis Yields New Insights into Medical Model, Evolutionary Process," available at
[28] Theo Colborn, Our Stolen Future, pg. 65.
[29] Bill Bradshaw, “The Evidence for a Biological Origin of Homosexuality,” pg. 6.
[30] Bill Bradshaw, “The Evidence for a Biological Origin of Homosexuality,” pg. 12.

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