Homosexuality – Truths Revealed

There are several different recognized sources that are often claimed as scientific proof that the origins of homosexual behavior are caused by genetic makeup instead of a choice that each individual makes.

This article is simply taking a look a look at some of the research done on whether or not homosexuality is genetically caused. We will be focusing most of our time on three of the more common studies claimed as proof of genetic causation of the homosexual orientation. This is not a “gay bashing,” session nor do I intend to enter into a discussion or debate of the politics for or against LGBT community activists in this article. The purpose here is simply to analyze the claims that homosexuality is genetically caused.

The studies looked at in this report were selected because of they are some of the most commonly cited as solid, evidentiary proof of a genetic component in the causation debate.

Before we get too deep, we should look into the clarification of several commonly used terms when this topic is brought up for discussion. I wish to specifically identify certain words that are more commonly recognized than actually understood. I do not mean to imply that the most of us intentionally misuse these words although the same cannot be said of certain, more supposedly professional, sources. Due to what I have found to be a common misunderstanding of the applicability of these terms, I simply have chosen to go over them before beginning so as to try and minimize confusion.

Heritability
Heritability is a value calculated from zero (0) to one (1) and is most commonly reported as a percentage value. For this explanation we will use the value of 0.35, or 35%. This is the point where, as I understand it, much of the confusion occurs: what exactly do these percentages mean? or else, what do they not mean?

A calculated heritability value of 35% does not mean that there is a 35% probability that the item or trait under scrutiny is purely genetic in nature.

It DOES mean that there is a 35% chance that there may be a genetic component for the trait in that specific individual that is under observation at the time.

When used in a study of multiple individuals, the values are often averaged to gain a generic idea of the overall sample of the participants in that, specific study. But this introduces another commonly misunderstood word or, more accurately in this case, a phrase: Genetic Component.

Genetic Component
Another commonly misunderstood and overused phrase is, ‘Genetic Component.’ People commonly (mis)believe that a genetic component means a Genetic Cause and therefore come to the conclusion that nothing can be done about whatever risk factor is being looked into (don’t worry, I’ll get back to this word “risk” in a minute). However, very few things in our lives and bodies involve one such purely central piece of information that sets so many other things into motion. A Genetic Component is not the same as saying genetic necessity or causation.

Correlation
Something is thought of as corollary (a correlation) when it appears in multiple scenarios but is more of a happenstance than an actual cause. For example, runners tend to have a very good lung capacity; however, having a good lung capacity does not automatically make one a runner. In other words, if something is thought to be a correlation it simply means that it may be consistently present but not thought of as a necessary cause.

Risk
Something that is at risk in this, sense, is not necessarily referencing a danger – it is simply stating a possibility (and/or the likelihood of a possibility) that the component under inspection may occur. For example, an individual standing at a corner may be at risk for crossing the street. The statement  does not assume a danger to the action, it simply is stating that the action may be something to be considered.

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A More General Introduction
Scientifically speaking it is very hard to define things as caused purely by genetic code, especially when it is a well-known fact that habitual behavior changes the brain’s wiring. Sexual intercourse is one such well-known behavior. Science has proven many times over through many different studies that all forms of sexual activity, regardless of gender, heavily affects all parts of brain chemistry, including core structure, active portions, and hormone release.  A person’s sexual activity remolds the brain into new patterns. Part of the brain’s rewiring happens in habit loop forming; this duality may be a part in what makes destructive habits related to sexuality (such as personal abuse or pornography) so hard to break.

Once we begin to combine this knowledge with a proper understanding of the difference between a genetic component and genetic cause, we have a platform to begin our study. Add in the known factors of heritability and that sexual activity itself heavily affects the brain patterns and even the brain structure of each individual, and one may begin to comprehend the scope of the hurdle that those who desire to claim that homosexuality is genetic must jump. But this looks towards the concluding arguments and we should first look into the evidences.

A Brief History – Dr. Spitzer, 1973 and 2003
There are several points where we could go to define the ‘beginning’ of the debate of the sexual preferences point of origin, for this study we are going to go back to 1973 with Dr. Robert Spitzer. As of 2003 a Columbia University Professor of Psychiatry, Dr. Spitzer is known for being an important component of having homosexuality removed from the American Psychiatric Association’s list of mental disorders in 1973 — for those unaware or misinformed, yes, homosexuality was at one point in the recent past thought to be a mental disorder, not a choice or something genetic, but a disease of the mind.

In October of 2003, Dr. Spitzer wrote a study that was published in the “Archives of Sexual Behavior” in which he cited interviews he had conducted with more than 200 people claiming to have been of a homosexual persuasion. In this publishing, he argued that it was possible for an individual to alter their sexual orientation. This claim was based on the fact that most of the 200+ people he had interviewed claimed to be of a homosexual persuasion and had, through reparative therapy counseling, either changed to a completely heterosexual orientation or at least had a dramatically reduced desire for a partner of the same gender.

It probably comes as no surprise that Spitzer’s view and report was attacked rather venomously for making such claims as one of the biggest drives for the “acceptance” of the homosexual community is based on the idea that they are just born this way and not only have no say in the matter, but neither should anyone else hold any differing opinion. What makes these claims by Dr. Spitzer even more potent is that he is a known homosexual advocate. In other words Spitzer strongly supports the gay community movement and really had quite a bit to lose in terms of support for his reporting the facts that his study had uncovered.

The Hypothalamus – Simon LeVay, 1991
The earliest widely publicized claim to evidence of a genetic cause of homosexuality came in 1991 from a Dr. Simon LeVay of the Salk Institute. LeVay evaluated the brains of 35 individual deceased men, 19 homosexuals (confirmed) and 16 heterosexuals (claimed), and claimed that he had found a difference in the size of the hypothalamus. He drew the conclusion from his studies that the sexual orientation of an individual was rooted from biological factors, specifically that his findings, “suggest that sexual orientation has a biologic substrate.”

The media was quick to jump on this, ‘proof’ of one’s sexual preference being biologically encoded and therefore outside of an individual’s personal control. However, in its enthusiasm to put down the opposition it failed to take into account several facts of LeVay’s studies and reports.

For starters it is interesting to note that LeVay was not the first person to discover an altered brain chemistry and construction. The previous year a group reported in the Brain Research that they had found a similar difference in the volume and number of cells in another area of the brain. Oddly enough this report ran rather unnoticed. Why? It is likely because Brain Research is a publication read mainly by and for neuroscientists who actually understand the limitations of the findings that had been discovered and as such, unlike the media, felt no reason to distract and misinform the populace towards the end of altering general opinion and mentality. LeVay told Newsweek that he believes that Americans must be convinced (note, ‘convinced’, not proven to) that one’s sexual preference is determined biologically instead of cognitively stating, “It’s important to educate society, I [LeVay] think the issue does affect religious and legal attitudes.”

But of course, if LeVay’s research legitimately gives a biological answer for the issue then all of this is irrelevant. Very well, let us look at his findings. Conveniently enough, the media avoided some clarification LeVay himself gave of his work (emphasis added):

“It’s important to stress what I didn’t find. I did not prove that homosexuality is genetic, or find a genetic cause for being gay. I didn’t show that gay men are born that way, the most common mistake people make in interpreting my work. Nor did I locate a gay center in the brain. …Since I looked at adult brains, we don’t know if the differences I found were there at birth, or if they appeared later.

Interesting, so although his research is readily touted as proof of biologically/genetically caused homosexuality, LeVay rather explicitly states that his studies decidedly did not, in point of fact, prove any such theory. As if this wasn’t enough to at least curb the enthusiasm with which LeVay’s work is commonly hailed there are many other problems with his study at least some of which LeVay readily admits. For Example:

–   All 19 of the known homosexuals in his studies died of issues tied to AIDS, which also could have caused alterations to the hypothalamus

–   Six of the supposedly heterosexual men studied also died of AIDS, a disease that, at the time anyway, almost no heterosexual men contracted, especially in San Francisco.

LeVay has since admitted that he didn’t actually know if any of the samples in the Heterosexual group were actually heterosexual, but that they were, “presumed [to be] heterosexual.” Considering the previous point, this was a rather personally biased and tremendously irresponsible and unscientific assumption on LeVay’s part.

–   There were at least 6 major exceptions in the study  (6 out of 35 is about 17% of variance):

  • 3 of the homosexual men had clusters of cells larger than the average (presumed) heterosexual sampling
  • 3 of the (presumed) heterosexual men had clusters smaller than the average homosexual sampling

Levay acknowledged and responded to these exceptions by stating that they, “hint at the possibility that sexual orientation, although an important variable, may not be the sole determinant of INAH3 [hypothalamus] size.”

These details in and of themselves are enough to bring LeVay’s so-called research under

heavy scrutiny, but there is more; Dr. E Byne argued in Scientific America that:

“[LeVay’s] inclusion of a few brains from heterosexual men with AIDS did not

adequately address the fact that at the time of death virtually all men with AIDS have decreased testosterone levels as the result of the disease itself or the side effects of particular treatments. … Thus it is possible that the effects on the size of the INAH3 [hypothalamus] that he attributed to sexual orientation were actually caused by the hormonal abnormalities associated with AIDS.”

Additionally, Marc Breedlove (a University of California at Berkeley psychologist) stated of LeVay’s study:

“These findings give us proof for what we theoretically know to be the case—that sexual experience can alter the structure of the brain, just as genes can alter it. You can’t assume that because you find a structural difference in the brain, that it was caused by genes. You don’t know how it got there.”

It is even more interesting to note Breedlove’s commentary because he does believe that there is a genetic component (currently unknown) and is focusing his own research towards finding that entity, but even he recognizes that LeVay’s study is fundamentally weak, flawed, and full of holes.

Chromosome Xq28 – Dean Hamer 1993
In 1993 Hamer and his group of researchers began his own study in which he and his team selected and studied a group of 114 families of homosexual men consisting of 76 individual men and 40 brother pairs. In several of the families studied there was found to be a homosexual link on the maternal side and so Hamer and his team decided to begin looking for a genetic answer on the X chromosome utilizing the correlation of a maternal link. Their studies found that out of the 40 brother pairs, 33 had a marker in the DNA region known as q28, a region of the X chromosome at the tip of long arm. This discovery led them to claim that:

             “The linkage to markers on Xq28, the subtelomeric region of the long arm of the sex chromosome, had a multipoint lod score of 4.0, indicating a statistical confidence level of more than 99 percent that at least one subtype of male sexual orientation is genetically influenced.”

As referenced earlier, what is reported and what is reality tends to become a little skewed at this point. What exactly did Hamer’s study claim and what did they find? What is commonly reported is that they found proof that homosexuality is genetic but is that actually true?

What did Hamer actually claim? That the score indicated, “a statistical confidence level of more than 99 percent that at least one subtype of male sexual orientation is genetically influenced.” In other words, Hamer did not identify or even claim to identify that he had found a “gay gene” but that he felt he had found evidence that highly suggested there was such genetic influence. Some may argue the semantics here, but the difference is actually rather vital once clarified.

Additional research into Hamer’s work reveals some several interesting facts. Popular belief and (mis)understanding is that Hamer and his group found identical sequences, that is that the Xq28 sequence was the same on the 33 pairs of homosexual men. What Hamer really found was that each of the 33 pairs had individually matching sequences; that each brother’s sequences matched the other brother NOT that all 66 (33 pairs) of the Xq28 sequences matched each other, but that every two (between brothers) matched. Interestingly enough Hamer also failed to check the Xq28 sequence in the non-homosexual (heterosexual) brothers to see if they also matched up with or were different from their homosexual counterparts claiming that including that data would have confounded his study.

Now assuming the claims and findings were completely legitimate why would inclusion of this important data be determined to be a factor of confusion? If the Xq28 sequences truly points towards a genetic component being involved, then identifying and including such data from the heterosexual counterparts should only aid in affirming the findings, not confounding the entire study. If this were a minor issue and the only problem to be considered then it would be possible to overlook it as a coincidence, exuberance, or possibly just an oversight and afterthought response on Hamer’s part. However, the failure to even examine the heterosexual brothers’ Xq28 sequence (or at least the failure to record any findings) is not only an outright botching of the job in the proper handling of such a study, but also puts Hamer on the business end of a two-edged sword. Why? Because Hamer’s actions also showed a distinct biasing in the information that he and his group reported, a selective biasing, and a biasing that, if his theories were accurate, should have returned a 100% success rate. Instead, with a completely controlled and selected group he was only able to attain a 52% (some sources claim 53%) success rate. As if that were not enough, recall at this point that we are discussing a heritability factor which, as was discussed earlier, is only applicable to the specific group under observation at the time.

In other words, with a completely homosexual group with no countering agents to check continuity and consistency Hamer, cutting out all competitive data, only managed to net a roughly 50% probability that there may be a genetic component involved in the sexual orientation and made no advances whatsoever as to identifying this supposed agent.

Two basic, similar, and required components and concepts of scientific research are experimentation and repeatability. Even assuming that all was straight up (no pun intended) and fair, the data could have been a fluke, therefore the experiment must be replicable so others may check and recheck the process and findings, not out of distrust for the original experiment or any of its proponents, but to ensure quality and accuracy on all fronts. Attempts to repeat Hamer’s studies and findings have been completely unsuccessful at this point in time. Hamer himself has done some repeating of his own studies with new modifiers including the inclusion of women as well as including the heterosexual sibling’s Xq28 sequences the data of which was turned over to the journal Nature Genetics. Additionally there are at least two other teams of researchers attempting to replicate his initial results, though as of yet (from what data I have available at this time) those replications have not been successful

So once the facts are actually considered it is readily seen that while there is a common claim that Hamer’s research proves a biological link the actual facts give quite a different report. Outside of the unprofessional aspects of his failures in proper research and methodology, the decisions Hamer made in his studies show a clear intent of proving a personal agenda over proving actual fact. This is an issue on two fronts. It not only represents an unscientific approach in general but also shows a severe researcher bias. Contradictory factors in the study that might oppose the desired outcome are ignored, as in the case of the intentional negation of the heterosexual Xq28 sequences in the original study. This further separates the reported outcome from reality because there is no solid basis on which to validly compare the data since the information was biased from the beginning of the study and/or report. It is additionally interesting to note that at this point all Hamer will say about his latest data set is that the data has not discouraged him from pursuing his project.

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I will openly admit I am about to make an assumption or two, so take the following comment with that grain of salt: If Hamer’s findings were in favor of his desired outcome would it not be fair to assume that there would have been quite the media circus to that end? Furthermore, if his research supported his claims then why claim a lack of discouragement from pursuing the project as opposed to being thoroughly ecstatic in the pursuit of further proof of one’s hypothesis?

I think it is fair to assume – but it is still only an assumption – that Hamer’s follow up studies and research did not shine a favorable light on his desired outcome. Rather, it is highly likely that the information gathered did even more to refute the plausibility of a genetic component to one’s sexual preferences. All things considered I feel that this assumption is a safe one, but still wanted to be sure to present that it was an assumption. Now let us continue…

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Twin Studies – Bailey and Pillard, 1991
Several Twin Studies have been conducted over the years but one in particular tends to rise above the others in this particular area of study. In 1991, J. Michael Bailey and Richard C. Pillard put together a study of identical twins, fraternal twins, non-twin biological siblings, and adoptive siblings. One reason this study is frequently cited is due to the higher percentages gained as opposed to other studies. According to Bailey and Pillard, they found that:

Male Data, 1991
52% of identical (monozygotic) twins of homosexuals were homosexual
22% of fraternal (dizygotic) twins were also homosexual
11% of adoptive brothers of homosexual were homosexual
9.2% of non-twin biological siblings reported homosexual orientations
(another, similar study on females was done in 1993 with an even lower percentage value recorded for these areas)

Often, the proponents supporting genetically caused homosexuality zone in on the seemingly large 52%, but even when separating this value from the rest of the study we run into a problem. Genetically speaking (for the purpose of twin studies), identical twins are considered to be carbon copies of one another; if homosexuality were a genetically caused phenomenon then 100% of the identically twins should be homosexually oriented. At the chance of sounding redundant, this poses a serious issue in claiming a hereditary link, however it poses no issue in linking environmental factors as well as one’s sexual preference being based on a decision or series of decision made by the individual.

But perhaps this is a fluke, let’s consider the rest of the data. 22% of the male and 16% of the female fraternal twins in the studies were also homosexuals. It is possible that I am being a bit nit-picky here, but for a genetic link one would think the expectation would be a bit higher than 25%, not lower. Another interesting fact is the in the males studied the percentage of homosexual adopted siblings was higher than that of non-twin, biological siblings. This, again, points to a conclusion of environmental over genetic causation. So to put the actual data into perspective with the facts of the study, while Bailey and Pillard claim that, “Our research shows that male sexual orientation is substantially genetic,” their own data and study actually strongly suggests a more probable tie to environmental influence over genetic cause for homosexual orientation.

There are a few more nails to this particular coffin to be considered. First, Bailey and Pillard’s sample set was not a randomized grouping which would give a more accurate overall view. Instead the participants were recruited through advertisements that were selectively placed into homosexual based publications. Generally speaking this type of selection immediately narrows the field of applicants to a sampling lot that is more likely to give ‘favorable’ results to the study: in this case a higher percentage of homosexual participants. If this seems a little ambiguous or like a red herring to you, consider this:

A local radio station puts out a poll and asks its listeners to weigh in on the topic of discussion. What do the results of the stations poll accurately represent?

The people most likely to respond are those that feel strongly either for or against the topic, those of a mediocre interest are much less likely to take the time and effort to give their thoughts or opinions. So by default the data, from the get go, is going to be a representative of the extremes, not of the mean, the outcome will be determined by whether more that felt strongly opposed to or strongly for supporting the topic were able to weigh in their thoughts.

Now, for this example, let’s say that station only allows the poll request to be played at certain times of the day when they know it is common for one particular group of listeners it feels are on the same page as those controlling/requesting the poll are most likely to be available. It does not hinder or attempt to hinder the discussion of the study with others, but neither does it make any attempt to notify those outside of its specific desired target group of anything to do with the poll. Now to clarify, I am not trying to say that selecting a target group for a study is necessarily wrong.

Assuming this is how the polling situation were set up, what information does the poll represent? The information only represents the opinions and thoughts of the carefully targeted group. However, for this example to fit the claims of Bailey and Pillard’s study, the station would have acted in this fashion and then proceeded to make the claim that that their poll was representative of not only the entirety of their listener base, but also that of the entire populace of the planet.

Now I am guessing that most are reading this thinking something to the tune of, “Come on, that is a bit of a stretch don’t you think?” and my answer to that is a simple one. No. This is exactly what this study has done. Specific data was collected from a grouping that was already biased towards a desired end and then that same data was extrapolated into a much larger grouping and claimed to be definitive proof that a supposed finding (that is not even solidly supported by the biased study) was a universally determining cause.

So again, once the actual facts are considered, there really is no solidly supportive proof whatsoever; if anything, the data collected goes a long way towards supporting the opposing view of what the study was intended to support, that one’s desire or intent on being homosexually oriented is actually heavily influenced by environmental factors and not genetically encoded in each individual.

Other twin studies have been performed with similar (though numerically much less impressive) results over the years. In fact, as some of the readers may recall, some of Hamar’s work was also based on twin studies even though his initial work and data compilation was incomplete.

There are many other studies and methods that have been run with the intent of proving or disproving a genetic link for homosexuality. As of yet, none have proven any more successful in their endeavors than those looked over in this report. Granted, several have claimed to have some grand finding of this-or-that component that ‘further proves’ the genetic tie-in, but these are either, once again, over blown and overrated or just outright lies stretched across a pretty paper to make it sound good and look legitimate. Digging into any one of these studies will very quickly show that the data just is not there to support the claim. When there is no valid claim to facts and especially when the supposed existing facts actually support the opposition more firmly in many ways, it’s generally a good idea to sit back and cool your jets a bit until everything can be worked out, clarified, and corrected. Instead the media, and LGBT community spins these hyper-generalized and overblown claims as solidified “fact” to the general public.

A Quick Review
LeVay.
While commonly hailed as definitive proof, a little digging shows his study to be riddled with basic technical problems, grandiose and unbased assumptions, personally biased data and a failure to replicate either the study or the findings among other technical problems. In short, a lot of unbacked assumption and no solid proof whatsoever to support his claims. Additionally, negating the above entirely, we find that, at best, LeVay’s findings may be able to be tied together correlationaly but are still woefully short when one attempts to tie them in as causation.

Hamer. Largely acclaimed for having found the ‘gay gene,’ closer examination shows a largely biased study that intentionally ignored potentially contradictive data in favor of promoting the hypothesis. When later studies came in containing that (the missing) data and resulting in much lower values, Hamer simply claimed that he was undeterred from his intended goal of study.
Again, no solid facts to support the claim but cited as one who has proven the issue beyond any and all doubt.

Bailey & Pillard. Accredited with using twin studies to definitively identify that homosexuality is indeed genetic, a closer look at their studies and data reveal a very different claim. Far from proving a genetic component, their data actually strongly supports the idea that one’s environment is likely to play a large and definitive role in sexual identity. Findings were misrepresented to the lay people that would not necessarily know the appropriate and accurate use of the terminologies to lead them to believe that something had been found when in fact the opposite of the desired outcome was discovered.

Additionally, each of these individuals at some point or another and in one fashion or another has admitted that there was probable selection biasing in their studies, either of the individuals that participated or of the data itself.

Further discrediting the mentality that homosexuality is prerecorded in one’s genes are the number of acclaimed homosexuals who, through various forms of therapy, have changed their sexual preference and orientation either in part or entirely, and lead very happy, non-oppressed lives after that fact. If one’s sexual orientation were set in genetic code before they ever had a chance to make a call, then this simply would not occur. Some claims have been made that individuals that have altered the orientation through therapy were never really truly homosexuals to begin with, but those claims have no backing behind them whatsoever and are simply a self-protective mechanism based on pure conjecture.

There are a number of other studies that have been done over the years and a handful at least that are being conducted even as you read this report into this topic, but to date, none of them have come any closer to identifying any possible “sex gene” that controls one’s orientation. What has been found is genetic causes for individual conditions and personalities that may place someone at a higher risk (see definition of at risk at beginning of this document) to be homosexually driven or to fall prey to homosexual advances, but even these are all eventually psychologically related and tie heavily into one’s environmental experiences. Again, knowing and considering the difference between correlation and causation is very important when looking at these cases.

Conclusions
For some of us, this debate has been going as long as we can remember, quite possibly our whole lives. Claims have been made for at least the past two decades that definitive proof either had already been discovered or else was just around the corner just waiting to lay the argument to rest in favor of genetically caused homosexuality.  Yet as we have seen, not only does evidence not exist to support this claim, if anything the actual facts point more and more towards the probability that such evidence does not exist (again, correlation verses causation). Dr. Francis S. Collins, head of the Human Genome Project states,

“An area of particularly strong public interest is the genetic basis of homosexuality. Evidence from twin studies does in fact support the conclusion that heritable factors play a role in male homosexuality. However, the likelihood that the identical twin of a homosexual male will also be gay is about 20% (compared with 2-4 percent of males in the general population), indicating that sexual orientation is genetically influenced but not hardwired by DNA, and that whatever genes are involved represent predispositions, not predeterminations.”

Dr. Collins additionally noted that environmental factors, especially one’s ability of free will and one’s childhood, play heavy roles in one’s development.

This is one area where the supporters of genetically caused homosexual tend to get hung up, focusing on this part of Collins comment, “indicating that sexual orientation is genetically influenced” however they quickly forget, ignore, or else simply don’t recognize or know the rest of the same sentence, “orientation is genetically influenced but not hardwired by DNA, and that whatever genes are involved represent predispositions, not predeterminations” (emphasis added). Really, how can one hope to state it more clearly than that? The data of all the studies, when considered in context, points towards correlation of causation, and if the orientation under question is not forcibly caused by a genetic component then the correlated actions are tied to choices made, even if the individual was unaware that those choices were being made at the time.

This is not to say changing sexual orientation is (generally) as easy as flipping a switch from ‘gay’ to ‘straight’ or vice versa. As mentioned earlier, many studies have been done that show physical and chemical alteration of the brain as sexual activity, and especially repeated sexual activity, occurs. One cannot (again, generally) simply decide, “I’m going to be (insert sexual preference here) today.” The change is going to take time and effort on the part of the individual for going in any direction whether it be hetero-, homo-, trans-, or bi-sexual. Often times our earliest influences go relatively unnoticed unless someone decides to make a point of making an issue about them which is why most don’t recall really ever having, ‘chosen’ their sexual preference and instead just realized that they were one way or another.

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Source Material
Most of my information in this document was obtained directly from the links below. Although I have personally studied this topic off and on for over 10 years I tried to limit my commentary to the information contained in these documents so as to provide specific source material for reference.

http://narth.com/docs/nothardwired.html

http://narth.com/docs/080307Abbott_NARTH_article.pdf

http://www.mercatornet.com/articles/view/facts_not_flattery_about_same_sex_attraction

http://narth.com/docs/whatdofirststages.pdf

http://www.cwfa.org/images/content/bornorbred.pdf

http://www.trueorigin.org/gaygene01.asp

http://www.isds.duke.edu/courses/Fall02/sta240/THmidt.dir/sciencearticle.pdf

http://www.pbs.org/wgbh/pages/frontline/shows/assault/genetics/nyreview.html

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