Homosexuals Anonymous

Offering Guidance, Fellowship & Care



Some gays or gay-friendly activists cite like-minded psychiatrists to back their cause and put down those, who assist people who do not want to act out their same-sex attractions. So how about it?
I have been taken professional training in psychology for many years now and very much appreciate this science as well as the need for it in therapy and in everyday life. However, what we see today in psychology and psychiatry is a very distorted version of it that has little to do with science and much with politics.
For hundreds of years science has seen "homosexuality" as a "disorder". All of a sudden they changed their view. Now this is nothing unheard of - it is part of science. But, if the change in view has politics as its reason and not science, we have a problem.
Today, statistics show clearly that MSM (men who have sex with men), a tiny percentage in the overall population, have an enormous percentage in the number of STDs (sexually transmitted diseases). Yet, assisting those who do not want to go that way is claimed harmful.
Healing identity problems and fulfilling unmet emotional needs on the inside by mutilating healthy human bodys ("reassignment surgery on transgenders") on the outside while violating the hippocratic oath is seen as "science".
Many years ago I always wondered why so many people (especially men) with same-sex attractions all over the globe (!) have similar life stories - a nonexisting bond with their same-sex parent in childhood, emotional/verbal/physical/sexual abuse and the like. Why they all obviously try to heal their inner wounds and unmet legitimate needs with sex - probably due to lack of a better means or help from others. Just to tell them "well, if you feel like it, just do it then! Have sex with someone your own gender!" is not science, it is irresponsability and total negligence (NOT tolerance!).
Limiting scientific research by forcing a political scheme on it - hereby only allowing politically correct outcome - is not sciencee, but propagande. Yet so many scientists yield to it without having the guts to stand up to the value and standards of their profession. Some use unproven claims, evaluations, personal opinion, politics, propaganda in order to disclaim opposing views. Again: that's not science and you are not doing psychiatry, psychology, neurology or medicine a favor. Science observes and researches and does not judge or even limit observation or research.
So before you quote a psychiatrist or the like in order to back your - political! - theories, think twice if that won't backfire.

Epigenetic theories of homosexuality

Epigenetic theories of homosexuality concern the studies of changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence, and their role in the development of homosexuality.[1][2][3] Epigenetics examines the set of chemical reactions that switch parts of the genome on and off at strategic times and locations in the organism's life cycle. However, epigenetic theories tangle a multiplicity of initiating causes and of resulting final effects and will never lead to a single cause or a single result. Hence, any interpretation of such theories may not focus just one isolated reason of a multiplicity of causes or of effects.[4]

Instead of affecting the organism's DNA sequence, non-genetic factors may cause the organism’s genes to express themselves differently. DNA in the human body is wrapped around histones, which are proteins that package and order DNA into structural units. DNA and histone are covered with chemical tags known as the epigenome, which shapes the physical structure of the genome.[5] It tightly wraps inactive genes on the DNA sequence making those genes unreadable while loosely wrapping active genes making them more expressive. The more tightly wrapped the gene, the less it will be expressed in the organism. These epigenetic tags react to stimuli presented from the outside world. It adjusts specific genes in the genome to respond to humans' rapidly changing environments. The idea of epigenetics and gene expression has been a theory applied to the origins of homosexuality in humans. One team of researchers examined the effects of epi-marks buffering XX fetuses and XY fetuses from certain androgen exposure and used published data on fetal androgen signaling and gene regulation through non-genetic changes in DNA packaging to develop a new model for homosexuality.[6] The researchers found that stronger than average epi-marks, epigenomes that are wrapped tightly around the DNA sequence, convert sexual preference in individuals without altering genitalia or sexual identity.[7] This research gives support to the hypothesis that homosexuality stems from the under expression of certain genes on the DNA sequence involved with sexual preferences. This theory as well as other concepts involved with epi-marks, twin studies, and fetal androgen signaling will be explored here.

Epigenetic marks

Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during gestation and after birth. Moreover, epi-marks are modifications of histone proteins.[8] Epigenetic marks are modifications of the methyl and acetyl groups that bind to DNA histones thereby changing how the proteins function and as a result, alter gene expression.[9] Epi-marks change how the histones function and as a result, influence the way genes are expressed.[1] Epigenetic marks promote normal sexual development during fetal development. However, they can be passed on to offspring through the process of mitosis. When they are transferred from one parent to an offspring of the opposite sex, it can contribute to an altered sexual development, thus leading to masculinization of female offspring and feminization of male offspring.[10] However, these epi-marks hold no consistency between individuals in regard to strength and variability.[citation needed]

Twin studies

Identical twins have identical DNA, which leads to the perceived conclusion that all identical twins are either heterosexual or homosexual. However, it is evident that this is not the case, consequently leaving a gap in the explanation for homosexuality. A "gay" gene does not produce homosexuality. Rather, epigenetic modifications act as temporary "switches" that regulate how the genes are expressed.[10] Of the pairs of identical twins in which one twin is homosexual, only twenty percent of the other twins are homosexual, which leads to the hypothesis that even though identical twins share the same DNA, homosexuality is created by something else rather than the genes. Epigenetic transformation allows the on and off switching of certain genes, subsequently shaping how cells respond to androgen signaling, which is critical in sexual development.[6] Another example of epigenetic consequences is evident in multiple sclerosis in monozygotic (identical) twins. There are pairs of twins that are discordant with multiple sclerosis and do not both show the trait. After gene testing, it was suggested that DNA was identical and that epigenetic differences contributed to the gene difference between identical twins.[11]

Effects of fetal androgen exposure

While in the fetal stages, hormonal influences of androgen, specifically testosterone, cause feminine qualities in regard to sexual development in females and masculine qualities in males. In typical sexual development, females are exposed to minimal amounts of testosterone, thus feminizing their sexual development, while males are typically exposed to high levels of testosterone, which masculinize their development. Epi-marks play a critical role in this development by acting as a buffer between the fetus and androgen exposure. Moreover, they predominantly protect XY fetuses from androgen underexposure while protecting XX fetuses from androgen overexposure.[1] However, when androgen overexposure happens in XX fetuses, research suggests they can show masculinized behavior in comparison to females who undergo normal levels of androgen exposure. The research also suggests that excess androgen exposure in females led to reduced heterosexual interest in adulthood than did females with normal levels of androgen.[12]


New epi-marks are usually produced with each generation, but these marks sometimes carry over between generations. Sex-specific epi-marks are produced in early fetal development that protect each sex from the natural disparity in testosterone that occurs during later stages of fetal development. Different epi-marks protect different sex-specific traits from being masculinized or feminized—some affect the genitals, others affect sexual identity, and yet others affect sexual preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons and similarly a partial masculinization of daughters. Furthermore, the reversed effects of feminization and masculinization can lead to a reversed sexual preference. For example, sex-specific epi-marks normally prevent female fetuses from being masculinized through exposure of atypically high testosterone, and vice versa for male fetuses. Sex-specific epi-marks are normally erased and not passed between generations. However, they can sometimes escape erasure and are then transferred from a father's genes to a daughter or from a mother's genes to a son. When this happens, this may lead to an altered sexual preference.[1] Epi-marks normally protect parents from variation in sex hormone levels during fetal development, but can carry over across generations and subsequently lead to homosexuality in opposite-sex offspring. This demonstrates that gene coding for these epi-marks can spread in the population because they benefit the development and fitness of the parent but only rarely escape erasure, leading to same-sex sexual preference in offspring.[citation needed]


1) William R. Rice, Friberg, Urban and Sergey Gavrilets. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development." The Quarterly Review of Biology 87.4 (2012): n. pag. Print. PMID 23397798 doi:10.1086/668167
2) Rice WR, Friberg U, Gavrilets S. 2013. Homosexuality via canalized sexual development: A testing protocol for a new epigenetic model. BioEssays 35: 343-368
3) Rice W. R., Friberg U., and Gavrilets S. 2016. Sexually antagonistic epigenetic marks that canalize sexually dimorphic development. Molecular Ecology 12: DOI: 10.1111/mec.13490
4) "Ausbildungskonzept "Integrated approaches to teach and study the role of evolution for the emergence of biological complexity"". Archived from the original on 2017-07-01. Retrieved 2016-11-28.
5) "The Epigenome at a Glance." Genetic Science Learning Center. The University of Utah, 2013. Web. 10 Apr. 2013.
6) Richards, Sabrina. "Can Epigenetics Explain Homosexuality?." The Scientist. N.p., 1 Jan. 2013. Web. 13 Apr. 2013.
7) "National Geographic Explains the Biology of Homosexuality." YouTube. YouTube, 04 Feb. 2009. Web. 13 Apr. 2013.
8) Ruthenburg, A., C. Allis, and J. Wysocka. "Methylation of Lysine 4 on Histone H3: Intricacy of Writing and Reading a Single Epigenetic Mark." Molecular Cell 25.1 (2007): 15-30. Print. PMID 17218268 doi:10.1016/j.molcel.2006.12.014
9) Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis
10) "Gene Regulation May Explain How Homosexuality Flourishes." LiveScience.com. N.p., n.d. Web. 12 Apr. 2013.
11) Handunnetthi, Lahiru, Adam Handel, and Sreeram V. Ramagopalan. Contribution of Genetic, Epigenetic and Transcriptomic Differences to Twin Discordance in Multiple Sclerosis. Ebsco Host. Psyc Info, 2010. Web. PMID 20819009 doi:10.1586/ern.10.116
12) Brook, Charles, Gerard S. Conway, and Melissa Hines. "Androgen and Psychosexual Development: Core Gender Identity, Sexual Orientation, and Recalled Childhood Gender Role Behavior in Women and Men with Congenital Adrenal Hyperplasia (CAH)." Journal of Sex Research 41.1 (2004): 75-81. Online PMID 15216426

(Source: https://en.wikipedia.org/wiki/Epigenetic_theories_of_homosexuality August 25th, 2019)

Gender Ideology Harms Children

March 21, 2016 – a temporary statement with references. A full statement will be published in summer 2016.

The American College of Pediatricians urges educators and legislators to reject all policies that condition children to accept as normal a life of chemical and surgical impersonation of the opposite sex. Facts – not ideology – determine reality.

1. Human sexuality is an objective biological binary trait: “XY” and “XX” are genetic markers of health – not genetic markers of a disorder. The norm for human design is to be conceived either male or female. Human sexuality is binary by design with the obvious purpose being the reproduction and flourishing of our species. This principle is self-evident. The exceedingly rare disorders of sex development (DSDs), including but not limited to testicular feminization and congenital adrenal hyperplasia, are all medically identifiable deviations from the sexual binary norm, and are rightly recognized as disorders of human design. Individuals with DSDs do not constitute a third sex.1

2. No one is born with a gender. Everyone is born with a biological sex. Gender (an awareness and sense of oneself as male or female) is a sociological and psychological concept; not an objective biological one. No one is born with an awareness of themselves as male or female; this awareness develops over time and, like all developmental processes, may be derailed by a child’s subjective perceptions, relationships, and adverse experiences from infancy forward. People who identify as “feeling like the opposite sex” or “somewhere in between” do not comprise a third sex. They remain biological men or biological women.2,3,4

3. A person’s belief that he or she is something they are not is, at best, a sign of confused thinking. When an otherwise healthy biological boy believes he is a girl, or an otherwise healthy biological girl believes she is a boy, an objective psychological problem exists that lies in the mind not the body, and it should be treated as such. These children suffer from gender dysphoria. Gender dysphoria (GD), formerly listed as Gender Identity Disorder (GID), is a recognized mental disorder in the most recent edition of the Diagnostic and Statistical Manual of the American Psychiatric Association (DSM-V).5 The psychodynamic and social learning theories of GD/GID have never been disproved.2,4,5

4. Puberty is not a disease and puberty-blocking hormones can be dangerous. Reversible or not, puberty- blocking hormones induce a state of disease – the absence of puberty – and inhibit growth and fertility in a previously biologically healthy child.6

5. According to the DSM-V, as many as 98% of gender confused boys and 88% of gender confused girls eventually accept their biological sex after naturally passing through puberty.5

6. Children who use puberty blockers to impersonate the opposite sex will require cross-sex hormones in late adolescence. Cross-sex hormones (testosterone and estrogen) are associated with dangerous health risks including but not limited to high blood pressure, blood clots, stroke and cancer.7,8,9,10

7. Rates of suicide are twenty times greater among adults who use cross-sex hormones and undergo sex reassignment surgery, even in Sweden which is among the most LGBQT – affirming countries.11 What compassionate and reasonable person would condemn young children to this fate knowing that after puberty as many as 88% of girls and 98% of boys will eventually accept reality and achieve a state of mental and physical health?

8. Conditioning children into believing a lifetime of chemical and surgical impersonation of the opposite sex is normal and healthful is child abuse. Endorsing gender discordance as normal via public education and legal policies will confuse children and parents, leading more children to present to “gender clinics” where they will be given puberty-blocking drugs. This, in turn, virtually ensures that they will “choose” a lifetime of carcinogenic and otherwise toxic cross-sex hormones, and likely consider unnecessary surgical mutilation of their healthy body parts as young adults.

Michelle A. Cretella, M.D.

President of the American College of Pediatricians

Quentin Van Meter, M.D.

Vice President of the American College of Pediatricians

Pediatric Endocrinologist

Paul McHugh, M.D.

University Distinguished Service Professor of Psychiatry at Johns Hopkins Medical School and the former psychiatrist in chief at Johns Hopkins Hospital


1. Consortium on the Management of Disorders of Sex Development, “Clinical Guidelines for the Management of Disorders of Sex Development in Childhood.” Intersex Society of North America, March 25, 2006. Accessed 3/20/16 from http://www.dsdguidelines.org/files/clinical.pdf.

2. Zucker, Kenneth J. and Bradley Susan J. “Gender Identity and Psychosexual Disorders.” FOCUS: The Journal of Lifelong Learning in Psychiatry. Vol. III, No. 4, Fall 2005 (598-617).

3. Whitehead, Neil W. “Is Transsexuality biologically determined?” Triple Helix (UK), Autumn 2000, p6-8. accessed 3/20/16 from http://www.mygenes.co.nz/transsexuality.htm; see also Whitehead, Neil W. “Twin Studies of Transsexuals [Reveals Discordance]” accessed 3/20/16 from http://www.mygenes.co.nz/transs_stats.htm.

4. Jeffreys, Sheila. Gender Hurts: A Feminist Analysis of the Politics of Transgenderism. Routledge, New York, 2014 (pp.1-35).

5. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Arlington, VA, American Psychiatric Association, 2013 (451-459). See page 455 re: rates of persistence of gender dysphoria.

6. Hembree, WC, et al. Endocrine treatment of transsexual persons: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2009;94:3132-3154.

7. Olson-Kennedy, J and Forcier, M. “Overview of the management of gender nonconformity in children and adolescents.” UpToDate November 4, 2015. Accessed 3.20.16 from www.uptodate.com.

8. Moore, E., Wisniewski, & Dobs, A. “Endocrine treatment of transsexual people: A review of treatment regimens, outcomes, and adverse effects.” The Journal of Endocrinology & Metabolism, 2003; 88(9), pp3467-3473.

9. FDA Drug Safety Communication issued for Testosterone products accessed 3.20.16: http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm161874.htm.

10. World Health Organization Classification of Estrogen as a Class I Carcinogen: http://www.who.int/reproductivehealth/topics/ageing/cocs_hrt_statement.pdf.

11. Dhejne, C, et.al. “Long-Term Follow-Up of Transsexual Persons Undergoing Sex Reassignment Surgery: Cohort Study in Sweden.” PLoS ONE, 2011; 6(2). Affiliation: Department of Clinical Neuroscience, Division of Psychiatry, Karolinska Institutet, Stockholm, Sweden. Accessed 3.20.16 from http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0016885.


Is Homosexuality Genetic?
Author / Contributor :: Dr. Neil Whitehead

Twin Studies: Is Homosexuality Genetic?

Written By: Dr. Neil Whitehead ( http://www.mygenes.co.nz/ ) (Posted January 2008)

The answer to all the alleged biological influences is conclusions from - Twin Studies.

In this paper I describe a very simple form, which avoids many complications and gives us the information we need. Usually identical twins are compared with non-identical twins. In the case of SSA this has given very ambiguous results, but we find if we only consider identical twins, the situation becomes much clearer.

We compare whether both identical twins have a given trait. Identical twins have identical genes. And they usually have identical womb environment. And they have virtually identical upbringing. So if they both have the same trait, probably some combination of common genes, prenatal factors and upbringing is responsible. So the critical question is – if one twin has SSA, does the other twin? And in what percentage of cases?

Look carefully at the next figure:

Figure 8. Pairwise concordance among identical twins for 1 Lung Cancer, 2 Criminality, 3 Stroke, 4 Breast Cancer, 5 Same Sex Attraction, 6 Leukemia, 7 Malformation, 8 Alzheimer's, 9 Ulcerative Colitis, 10 Rheumatoid Arthritis, 11 Alcoholism, 12 Schizophrenia, 13 Depression, 14 Suicide attempt, 15 Diabetes type I, 16 Divorce, 17 Crohn's disease, 18 Asthma, 19 Hypertension, 20 Co twin is best friend, 21 Diabetes type II, 22 Autism, 23 Opposite Sex Attraction, 24 Phenylketonuria

The top point, #24 is phenylketonuria, caused by a known gene defect. If one twin has it, the other twin almost always has it. #23 is OSA. The concordance is very high. If one twin is OSA the other is usually OSA as well. However we cannot tell from this whether it is caused by genes, upbringing, or some combination. The concordances decrease as we move to the left, until we reach SSA which has a concordance of 11%. The other points with that kind of value are the cancers, which all oncologists will tell you have a large element of chance involved. SSA has a large element of chance in it. In fact we have to say it has an unusually large element of chance in it compared to most traits. By change we mean non-shared events, which affect one twin and not the other.

This 11% is a terribly important statistic. All the common biological and social influences known and unknown and yet to be discovered, add up to 11% concordance for men and 14% for women twins. All that long list of biological influences previously given in this paper are included, and they only add up to 11-14%.

Four papers agree that SSA pairwise concordance has about this value. One of them, a paper on adolescent twins found an SSA concordance of 7% for men and 5% for women, which is even lower but in the same ballpark. So we have to take it the figure is accurate and not going to change. If one twin has SSA the other usually does not.

There is one complication. People may say to you “I thought the concordance figure was 30%” or they may say “52%”. It is a fact that the early studies had higher figures but are also now universally acknowledged (and by their authors) to be highly biased samples. It is also a fact that they were quoting a concordance called “probandwise concordance” which is more complex than the “pairwise” concordance I quoted to you, significantly higher, and used in later calculations that do not immediately concern us in this paper. The only important conclusion is that whichever form is used, SSA would still be clustered among the traits with a very high chance component. The irony is that far from being a trait with extremely high degree of dictation by genes, it is almost as far from that as it is possible to get. This is another sad example of the public tending to believe the exact opposite of the truth in scientific matters SSA dictated? The exact opposite. I hope that from now on you will not be disturbed into thinking the genes or prenatal conditions are overwhelmingly important, regardless of what new discoveries may emerge.

Four years ago I spoke at the annual NARTH conference, and used the higher probandwise concordance figures. At that stage I was too conservative. I said the genetic effect was small. Now I would say “unusually smallâ€.

The gay activist may say to you – “Oh SSA is still dictated by the genes, but they are not exerting their effects – this is a known genetic phenomenon called poor penetrance”. The answer is that you have to have a known gene or genes producing the trait before you can say that, and in this case there are no genes. You might say to such a person “Please come back when a gene is found!

Now I want to clarify some points because there is significant risk of misunderstanding. I am not saying 11% of all twins have SSA – only about 2-3% do. I am not saying when a twin has SSA that in their case there is genetic influence and in other cases no genetic influences – all of us are subjected to all the genetic and social influences.

Why twins might differ

Now this analysis I am presenting shows that chance – non-shared experience - is an unusually large factor and accounts for differences between identical twins. What would be examples of this?

One twin sees internet SSA porn and the other doesn't
One twin misperceives the father favoring the co-twin
One twin is unlucky in (heterosexual) love and thinks he is gay
One twin is sexually abused and the other is not

Chance events, non-shared circumstances can lead to very different endpoints.

Now a disturbing factor for some at this conference may be to hear that not only are genetics a minor factor but family circumstances are also. While this is generally true for the vast majority, there is a small minority for whom the family circumstances are vitally important. But if one twin rebels against the masculinity expressed by his father or peers, the other usually does not. This is a chance occurrence, and as a generalisation parents are mostly not to blame for the SSA of their children. Accidental misperception of parental motives is much more common.

The Guardian: Male sexual orientation influenced by genes, study shows

FOR IMMEDIATE NOTICE - We want to jump on this new hack article right away because we've been down the Xq28 road before and you know you will be brow beaten with these "facts" ad nauseum. For anyone literate - we've highlighted the laughable holes for you:

"A region of the X chromosome called Xq28 had some impact on men's sexual behaviour – though scientists have no idea which of the many genes in the region are involved, nor how many lie elsewhere in the genome.

Another stretch of DNA on chromosome 8 also played a role in male sexual orientation – though again the precise mechanism is unclear.

Researchers have "speculated" in the past that genes linked to homosexuality in men "may" have survived evolution because they happened to make women who carried them more fertile. This "may" be the case for genes in the Xq28 region, as the X chromosome is passed down to men exclusively from their mothers.

"The work has yet to be published..."

...he found that [only] 33 out of 40 gay brothers inherited similar genetic markers...

The gene or genes in the Xq28 region that influence sexual orientation have a limited and variable impact. Not all of the gay men in Bailey's study inherited the same Xq28 region. -->The genes were neither sufficient, nor necessary, to make any of the men gay.<--

The flawed thinking behind a genetic test for sexual orientation is clear from studies of twins, which show that the identical twin of a gay man, who carries an -->exact<-- replica of his brother's DNA, is more likely to be straight than gay. That means even a perfect genetic test that picked up every gene linked to sexual orientation would still be less effective than flipping a coin.

However, we don't know where these genetic factors are located in the genome.

"We found evidence for two sets [of genes] that affect whether a man is gay or straight. But it is not completely determinative; there are certainly other environmental factors involved." [Women must simply just be of some other species or don't have genes.]

13 February 2014


Born gay or not..... does it matter?

  There is a lot of argument about whether people are born gay or not. The pro-gay crowd wants it to be so, because then they can claim God made them that way, so of course it is OK. The conservative Christians want to say no, you are not born gay, for then they would have to agree it isn't fair of God to expect a gay person to fight his or her feelings.

 I read a comment recently that has made me wonder if it really matters. And if we should even argue against it. If there is a "gay gene" found some day, then Christians are going to have egg on their face, and will have their very foundation of homosexuality being wrong, shaken.

 I personally don't believe people are born gay, but also have learned not to be too dogmatic about that. I do believe people can be born with a predisposition to being gay, and their environment and circumstances can swing them one way or the other.

 But I am going to go with the idea that people can be born gay. The Bible says homosexuality is wrong, as the act and lusting, so therefore, it is unfair of God to let someone be born gay and forbid them to give into their desires. Right? Wrong.

 We are all born sinners, thanks to Adam and Eve. We are all born with the desire to sin, to do wrong, and the same Bible that forbids homosexual behavior, forbids any sinful behavior. A heterosexual man or woman has the desire to have sex, the temptation to lust, and granted, they can marry, but not all of them. I know, and have known, several women who never married. They wanted to, but it never happened. I am sure there have been heterosexual men who wanted to marry, and never did..... and it would have been a sin for them to lust, to have sex with someone they were not married to, as the person attracted to the same gender.

 And there are other sins we are prone to do, that feel natural to us to do, yet we must fight those urges and live for God, not ourselves. Just as the person who may be born gay has to fight his desires to give in and sin, we all have to fight the desire to sin and live for the flesh, instead of for God.

 Is it fair that someone who is attracted to the same gender can never marry, can never know what it is like to be in love and have a relationship that others have? No. It isn't. Some manage to marry a person of the opposite sex and make it work, and many do not. But life isn't fair.

  When I get frustrated about the cross I must bear, and get to thinking that it isn't fair, a couple of people come to my mind. Joni Eareckson Tada, and Nick Vujicic.

  In 1978, at the age of 17, Joni dove into some water and broke her neck, paralyzing her body from the neck down. Since 1978, she has been in a wheel chair, yet God has used her in ways she could never have been used if she were whole. Is it fair? Certainly not. She found a way to paint by holding a paintbrush in her mouth, and has written several books, recorded CDs, and started a program for people to get wheel chairs who cannot afford them. She served God no matter what, and He uses her for good.

 Nick Vujicic was born with no arms or legs, having only a foot. His parents decided when he was very young, that he would live as much as possible as kids with all of their limbs. He surfs, swims, goes all over the world speaking, and got married a little over a year ago and has fathered a child with his wife. Is it fair that he was born the way he was? No way. But what an amazing attitude he has, and God is using him all over the world. If anyone had a right to say it isn't fair, it would be him, but he decided to live life to the fullest and let God use him.

 People are born with all sorts of diseases and deformities. There are people going through their own private hells that we don't know anything about. Is it fair? No it isn't fair, but life isn't fair. When sin entered the world, fairness was tossed out the window.

  So is it fair that men and women have to suffer same-sex attractions, and according to God's Word, never be allowed to give in to those attractions/desires? No. And it isn't easy to ignore what seems to come to naturally.

 But you know what? It wasn't fair that God's Son was nailed to a cross for our sins. He did no wrong, and was totally innocent. Yet He died for our sins. He went through unimaginable pain and horror for us. For the gay person. For the murderer, the child molester, for Joni Eareckson Tada, Nick Vucicic, Adolf Hitler.

 We are all born sinners, with a bent and desire to give into that sin. Gay people are not the only ones who must fight what comes naturally.

 Some day it will be worth it all, when we hear Jesus say "Well done". In the mean time, we must all forsake our sins, take up our cross, die daily to ourselves and our desires, and serve God no matter what. Whether you're gay, or straight.

Mark B.

Excerpt from Freud's study of Leonardo Da Vinci

Homosexual men who have started in our times an energetic action against the legal restrictions of their sexual activity are fond of representing themselves through theoretical spokesmen as evincing a sexual variation, which may be distinguished from the very beginning, as an intermediate stage of sex or as a "third sex". In other words they maintain that they are men who are forced by organic determinants originating in the germ, to find that pleasure in the man which they cannot feel in the woman.

"As much as one would wish to subscribe to their demands out of humane considerations, one must nevertheless exercise reserve regarding their theories, which were formulated without regard for the psychogenesis of homosexuality. Psychoanalysis offers the means to fill this gap and to put to the test the assertions of homosexuals.

"It is true that psychoanalysis fulfilled this task in only a small number of people, but all investigations thus far undertaken brought the same surprising results. In all our male homosexuals there was a very intense erotic attachment to a feminine person, as a rule to the mother, which was manifest in the very first period of childhood and later entirely forgotten by the individual. This attachment was produced or favored by too much love from the mother herself, but was also furthered by the retirement or absence of the father himself during the childhood period…

"It seems almost that the presence of a strong father would assure for the son the proper decision in the selection of his object from the opposite sex.

Why Gays Need to Believe They were Born Gay: A Neurotic Drive for Acceptance
Written By: Don D
(Posted May 2012)

Co-Directors' Introduction: The writer, a married man, who is presently in counseling for same-sex attraction (SSA) issues has frequently expressed frustration about how the gay activist agenda consistently negates his own positive therapeutic experiences and his continuing growth out of homosexuality. His negative experiences with those who support the political gay lobby led him to understand how diversity and tolerance is a one way street for such advocates, only supporting those who want to be gay while attacking both those who want to change and those who wish to assist those who desire change of sexual orientation. His introspection on this question led him to pen the following thesis.
A genetic deterministic argument has been made in the public arena for some very specific reasons that those of us who are same-sex attracted (SSA) need to understand. Acceptance of the genetic deterministic argument is the primary vehicle being used to attack normative religious doctrine in the public policy arena and to create a sea change in attitudes toward gay behaviors.
". . .people who think that gays are born that way are also more likely to support gay rights" Simon LeVay
A similar genetic argument is also used to attack the rights of SSA men who seek help from sympathetic mental health professionals.
"There is this strange connection between whether you think this therapy is useful and whether you are for the civil rights of homosexuals. The gay activists believe that if they could convince everybody that they can never change, then they would be in a better position to argue for gay civil rights...." Dr. Robert Spitzer
If my genetics determines my sexual orientation, then advocates of homosexuality believe it is unjust for them to be denied the same enjoyment and fulfillment of emotional and sexual bonding to a life partner that is enjoyed by heterosexuals; and, religious doctrine to that effect will seem unjust as well. It also means any treatment to overcome homosexual ideation is not only doomed to failure but will likely result in harm (even though numerous studies evidence that no harm exists from reparative therapy.) To understand why this argument is so viscerally important to gay men beyond its persuasive value in the public policy arena, and why understanding the fallacy in it is so important to those of us who define ourselves as dealing with SSA, requires briefly discussing biology and understanding the true causes of SSA. Generally speaking, genetics is never deterministic when it comes to behaviors.
Genetics do not determine behavior in the same way that they determine physical traits, such as eye color. With behavior, the environment itself is substantially involved in genetic transmission, even when the proportion of variation attributable to genetic influence is high.. Genes do not produce behavior; they do not even determine behavior, they only influence the probability that behavior will occur, given a specific environmental influence..[p. 275] Caution is warranted [even in interpreting twin studies that purportedly shows evidence of genetic influences since] the difference between monozygotic and dizygotic concordance overestimates heritability to an indeterminate degree [p. 274]. Journal of Fluency Disorders, 27, 269-288
More than just behaviors, the traits that influence behaviors are also not generally controlled by genes the way that is implied by the over simplifying popular press.
.the interaction of genes and environment is much more complicated than the simple "violence genes" and "intelligence genes" touted in the popular press.. The same data that show the effect of genes, also point to the enormous influence of non-genetic factors [p. 1687]. Mann, C. 1994. Genes and Behavior. Science, 264, 1686-1689
Once I accept the genetic argument, then I internalize a deep sense of rejection. In fact, The true nature of homosexuality is rejection. The child and sometimes the infant at some level perceives rejection by a parent, or later on by peers, or both, or perhaps goes through a trauma such as sexual abuse, then as a result defensively detaches from his own masculine identity. It is, at its core, self rejection of an essential part of myself, my masculinity and my role as a man among men and my ability to identify with other men as like them, in at least the key area of sexual desire. Not always, but usually, the self rejection is much more extensive, and results in my rejection of my own masculinity so deeply that I view manhood as a club I was never invited to join.
The resulting manifestation in the gay community is a neurotic drive for acceptance. A gay pride parade is a cry for acceptance and at the same time an adolescent dare to reject. This is why gay pride parades do not bring out attempts to show everyone just how "normal" gay men are but instead bring out drag queens and men in dog collars and leashes. It is a manifestation of that neurotic drive to demand acceptance by a community of men who at their own core reject themselves and are simultaneously demanding to be rejected because deep down they believe they deserve to be rejected.
That neurotic drive for acceptance is why the gay rights community seeks to fight against the rights of SSA men to get treatment and has campaigned within the APA and through legislation, initially in Europe and South America and now in the USA, to sanction psychologists who treat men with unwanted SSA and therefore seek to change orientation. For the gay-identified personality, my efforts at chastity, or my efforts at change therapy, are too much of a challenge to his neurotic drive for acceptance and thus he seeks to deny me a right of self determination or a right to freedom of religion.
But above all else, here is the really sad thing about the growing acceptance of a genetic determinism of SSA. The vast majority of young men and women who struggle with SSA and grow up in a world where that view dominates will conclude for themselves, as a matter of moral certainty, that prohibitions against homosexual behavior in the Bible must be culturally-based human constructs which have no eternal validity, and no psychological benefits, and will make no attempt at chastity. Those men and women will eventually, or more than likely, leave any religious group that maintains a traditional biblical doctrine on homosexual conduct.
Psalm 1:1 - Blessed is the man that walketh not in the counsel of the ungodly, nor standeth in the way of sinners, nor sitteth in the seat of the scornful.


Jeffrey B. Satinover, M.D. has practiced psychoanalysis for more than nineteen years, and psychiatry for more than ten. He is a former Fellow in Psychiatry and Child Psychiatry at Yale University, a past president of the C.G. Jung Foundation, and a former William James Lecturer in Psychology and Religion at Harvard University. He holds degrees from MIT, the University of Texas, and Harvard University. He is the author of Homosexuality and the Politics of Truth (Baker Books, 1996).

On July 15, 1993, National Public Radio (NPR) made a dramatic announcement on stations across the country: Was a team of scientists at the National Institutes of Health on the trail of a gene that causes homosexuality? Their report would be published the next day in Science, one of the two most prestigious scientific research journals in the world. (1)

The discussion that followed explained for the listening public the implications of these findings for social attitudes toward homosexuality and for public policy concerning it. Science was on the verge of proving what many had long argued: that homosexuality is innate, genetic and therefore unchangeable - a normal and commonplace variant of human nature. In the light of these findings, surely only the bigoted or ignorant could condemn it in any way.

Shortly after the announcement, amidst a well-orchestrated blizzard of press discussions, there ensued the watershed legal battle over "Proposition 2" in Colorado. (This popularly enacted legislation precluded making sexual orientation the basis of "privileged class" minority status, a status conferred previously only on the basis of immutable factors such as race.)

Among the many crucial issues raised by the legislation was the question as to whether homosexuality was indeed normal, innate and unchangeable. One prominent researcher testified to the court, "I am 99.5% certain that homosexuality is genetic." But this personal opinion was widely misunderstood as "homosexuality is 99.5% genetic," implying that research had demonstrated this. Certainly, that was the message promulgated by NPR's report on the recent research, and by all the discussions that followed. In a few weeks, Newsweek would emblazon across its cover the phrase that would stick in the public mind as the final truth about homosexuality: "Gay Gene?"

Of course, just near the end of the NPR discussion, certain necessary caveats were fleetingly added. But only an expert knew what they meant - that the research actually showed nothing whatever in the way of what was being discussed. The vast majority of listeners would think that homosexuality had been all but conclusively proven to be "genetic." But the real question is whether or not there is such a "Gay Gene."

In fact, there is not, and the research being promoted as proving that there is provides no supporting evidence. How can this be? In order to understand what is really going on, one needs to understand some little-know features of the emerging study of behavioral genetics (much subtler than the genetics of simple, "Mendelian" traits such as eye color).

When it comes to questions of the genetics of any behaviors- homosexuality included- all of the following statements are likely to be at least roughly true:

1. Such and such a behavior "is genetic";
2. There are no genes that produce the behavior;
3. The genes associated with the behavior are found on such and such a chromosome;
4. The behavior is significantly heritable;
5. The behavior is not inherited.

The scientific distinctions that make these seeming contradictions perfectly reasonable and consistent seem completely misunderstood by the media who report on them.

For example, in response to the "gay gene" research, the Wall Street Journal headlined their report (which appeared the next day), "Research Points Toward a Gay Gene."(2) A subheading of the Journal article stated, "Normal Variation"-leaving the casual reader with the impression that the research led to this conclusion. It did not, nor could it have. The subhead alluded to nothing more than the chief researcher's personal, unsubstantiated opinion that homosexuality, as he put it, "is a normal variant of human behavior." Even the New York Times, in its more moderate front-page article, "Report Suggests Homosexuality is Linked to Genes," noted that other researchers warned against over-interpreting the work, "or taking it to mean anything as simplistic as that the "gay gene" had been found."

At end of the Wall Street Journal article, at the bottom of the last paragraph on the last page deep within the paper, a prominent geneticist was quoted for his reactions to the research. He observed that "the gene…may be involved in something other than sexual behavior. For example, it may be that the supposed gene is only ´associated' with homosexuality, rather than a 'cause' of it."

This rather cryptic comment would be most difficult to understand without the needed scientific background. Yet it is the most critical distinction in the entire article; indeed, it renders the findings almost entirely worthless. Why bury and fail to explain what it means? Perhaps the motives were innocent, but in fact, the belief that homosexuality is "biological" or "genetic" causes people to develop more positive attitudes toward it. They need not have the foggiest understanding of what "biological" or "genetic" really mean in order change their view:

105 volunteer[s]… were exposed to one of three… [T]he experimental group read a summary… emphasizing a biological component of homosexual orientation… [O]ne control group read a summary… focusing on the absence of hormonal differences between homosexual and heterosexual men. [A]nother control group w[as] not exposed to either article… As predicted, subjects in the experimental group had significantly lower(3) scores [more positive attitudes toward homosexuals] than subjects in the control groups(4).


Analysis indicated that subjects who believed that homosexuals are "born that way" held significantly more positive attitudes toward homosexuals than subjects who believed that homosexuals "choose to be that way" and/or "learn to be that way"(5).

What was actually going in the study the media was trumpeting? Dean Hamer and his colleagues had performed a Kind of behavioral genetics study now becoming widespread -the so-called "linkage study." Researchers identify a behavioral trait that runs in a family and then look to see whether there is a chromosomal variant in the genetic material of that family, and if that variant is more frequent in the family members who have the trait.

To the uninitiated, a positive finding ("correlation" or "association" of a genetic structure with a behavioral trait) is taken to mean that the trait "is genetic" - that is, inherited.

In fact, it means absolutely nothing of the sort, and it should be emphasized that there is virtually no human trait without innumerable such correlations. We will see shortly just how this is can be so. The most important take-home messages will be these:

(1) All the research that has been done on homosexuality has been selectively trumpeted through the press in carefully crafted form in order to shape public opinion -hence public policy- in predictable ways. The research itself means almost nothing.

(2) The research projects that would truly mean something are scarcely being done because they would all explicitly or tacitly lead to but one end highly undesirable to activists: a method or methods for preventing homosexuality or changing it with ever-increasing efficacy; and to one conclusion: homosexuality per se is not inherited.

(3) Most of the research has been hastily and often sloppily done but this point is a distraction. Even were it superb, the findings would still mean almost nothing.

(4) To whatever extent this research has been good enough to generate valid conclusions at all, these conclusions are precisely the opposite of what is claimed in the press.

Before we talk about specifics, here is what serious scientists think about the recent behavior-caused-by-genes research. From Science, 1994:

Time and time again, scientists have claimed that particular genes or chromosomal regions are associated with behavioral traits, only to withdraw their findings when they are not replicated. "Unfortunately" says Yale's (Dr. Joel) Gelernter, "it's hard to come up with many" findings linking specific genes to complex human behaviors that have been replicated. "…All were announced with great fanfare; all were greeted unskeptically in the popular press; all are now in dispute" (6)

A scientist at Washington University School of Medicine calculated what would be required for such replication, He:

…projected that if the trait (in question) was 50% heritable… detecting (just) one of (its) genes would require studying 175 families - that is, almost 2000 people (7). Replicati(on) would require studying 781 families - another 8000… (E)ach additional gene (for a polygenic trait), researches would need… the whole business again. "Suddenly you're talking about tens of thousands of people and years of work and millions of dollars". (8)

Nothing even remotely close to this has been done with respect to homosexuality.
Using arguable-at-best- methods, two American activists recently publish studies showing that if one of a pair of identical twins is homosexual, the odds that the other one is, too, are less than 50% (the study examined a few dozens of pairs). On this basis, they argue that "homosexuality is generic". British researchers generated comparable results in a similar study. Their conclusion? The surprisingly low odds that both twins were homosexual:

… confirmed that genetic factors are insufficient explanation for the development of sexual orientation. (9)

Two Columbia University researches (who have published the most comprehensive research summary on the subject to date) note the unexpectedly:

… large proportion of monozygotic twins who (did not share) homosexuality despite sharing not only their genes but also their prenatal and familial environments. (10) The… (50% odds)… for homosexuality among the identical twins could be entirely accounted for by the increased similarity of their developmental experiences. In our opinion, the major finding of that study is that 48 percent of identical twins who were reared together (and where at least one was homosexual) were discordant for sexual orientation. (11)

Two other genetic researches (one heads one of the largest genetics departments in the country, the other is at Harvard) comment:

… recent studies seeking a genetic basis for homosexuality suggest that.. we may be in for a new molecular phrenology, rather than true scientific progress and insight into behavior.

While the authors interpreted their findings as evidence for genetic basis for homosexuality, we think that the data in fact provide strong evidence for the influence of the environment. (12)

The author of the lead article on genes and behavior in a special issue of Science notes:

... the growing understanding that the interaction of genes and environment is much more complicated than the simple "violence genes" and "intelligence genes" touted in the popular press. Indeed, renewed appreciation of environmental factors is one of the chief effects of the increased belief in genetics' effects on behavior (my emphasis). The same data that show the effects of genes also point to the enormous influence of non-genetic factors. (13)

The director of the Center for Developmental and Health genetics at Pennsylvania State University comments:

Research into heritability is the best demonstration I know of the importance of the environment.

(Note the term "heritability"; we will be returning to it in detail as it lies at the heart of much confusion).
With regard to the work announced by NPR, genetics researchers from Yale, Columbia and Louisiana State Universities noted that:

Much of the discussion of this finding (of a purported gene locus for homosexuality) has focused on its social and political ramifications. (But) inconsistencies… suggest that this finding should be interpreted cautiously…
The results are not consistent with any genetic model… neither of these differences (between homosexuality in maternal versus paternal uncles or cousins) is statistically significant… small sample sizes make these data compatible with a range of… hypotheses.
(T)he… data… present no consistent support for the… results. (14)

By contrast to their public policy statements, the researches responded carefully as follows:

We did not say that (the chromosome segment under study) "underlies" sexuality, only that it contributes to it in some families. Nor have we said that (it) represents a "major" gene, only that its influence is statistically detectable in the population that we studied. (15)
Ignoring possible flaws in the research, have the researches actually pointed to this more modest claim with any degree of certainty? In fact, they have not - as they themselves acknowledge, but in language that will surely evade general understanding - and that will continue to be avoided by the press:

… the question of the appropriate significance level to apply to a non-Mendelian trait such as sexual orientation is problematic. (16)

English translation: "It is possible to know what the findings mean, if anything, since sexual orientation cannot possibly be inherited the way eye-color is". Thus, to their fellow scientists, the researchers properly acknowledge what every serious researcher knows, but the public does not.

Complex behavioral traits are the product of multiple genetic and environmental antecedents, with 'environment' meaning not only the social environment but also such factors as the 'flux of hormones during development, whether you were lying on your right or left side in the womb and a whole parade of other things'… the relationships among genes and environment probably have a somewhat different effect on someone in Salt lake City than if that person were growing up in New York City. (17)

English translation: "You're more likely to become gay growing up in Manhattan than in Utah among Mormons and Christian fundamentalists, even if everything else is the same, including genes."
Unfortunately, anyone who is so disposed can readily offer the public partial truths which are seriously misleading. This is so only in part because of an easily led or poorly educated press. The major reason is really that the ideas being cooked beyond recognition once they leave the labs are inherently complex, even if originally formulated and presented properly. There are no "lite," sound-bite versions of behavioral genetics that are not fundamentally in error in one way or another.
Nonetheless, if one grasps at least some of the basics, in simple form, it will be possible to see exactly why the current research into homosexuality means so little - and will continue to mean little even should the quality of the research methods improve - so long as it remains driven by political, rather than scientific objectives.

There are really two major principles that need to be carefully assimilated in order to see through public relations distortions to the actual meaning of recent research. They are as follows:

1. Heritable does not mean inherited
2. Meaningful genetics research identifies and then focuses on traits that are directly inherited. One prominent genetic researcher (discussing a matter unrelated to homosexuality, but equally frustrated with the bad science reporting) flatly calls the question of heritability "trivial".

Heritable Does Not Mean Inherited

Heritability studies can be done on almost any human trait - physical, behavioral, emotional, etc. - and will show positive results. That is, almost every human characteristic you can think of is in significant measure heritable (thus discussing it is "trivial"). But few human behavioral traits are directly inherited the way simple physiological traits are (e.g. eye color). Inherited means "determined directly by genes", with little or no way of changing the traits by choice, or by preventing it, or by modifying the environment in which the trait has emerged (or is more likely to emerge).
Here is a simple hypothetical example, but it is 100% plausible. It tracks the kinds of studies that have been done with innumerable other traits, including homosexuality. (But only in the area of homosexuality has the meaning of such studies been so badly distorted).
Suppose that for political reasons you want to demonstrate that there is a "basketball gene" that "makes" people become basketball players ("BBPs"). (Please suspend your immediate, current understanding that the idea is absurd). To make your case you would use the same methods as in homosexuality. These methods fall into three categories, and represent important forms of preliminary research when investigating any trait: (1) twin studies; (2) brain dissections; (3) gene "linkage" studies.

Twin Studies
The basic idea in twin studies is to show that the more genetically similar are two people, the more likely it is that they will share the trait you are studying. So, you create a study set of pairs of people, divided into categories according to how genetically similar they are, as follows:

Pair Type Degree of similarity

Identical Twins 100%
Fraternal Twins 50%
Non-twin Siblings 50%
Unrelated people <5%

The most similar are identical twins, the next most similar are fraternal twins (who are on average as different as non-twin brothers or sisters, but no more so), the least similar are unrelated people.
Then you identify those pairs of twins in which at least one is a BBP. It will not be difficult to show that if one such identical twin is a BBP, his brother (or her sister) more frequently will be, too, than would a non-identical twin or a non-twin sibling or a non-sibling. You would create groups of such different kinds of pairs to make the comparison in a large number of cases. (One set of identical twin pairs, one set of non-identical twin pairs, one set of non-twin siblings, and so on.)
From the "concordance rate" in each set (the percentage of pairs in each set in which either both are BBPs or both are not. Pairs in which one was and another was not would be called "discordant for BBP") you would calculate a "heritability" rate. (Perhaps you have an armchair guess as to how many identical twin-pairs either both play or both do not play basketball. Probably a good deal more than half, the concordance rate for homosexuality in such twin-pairs.)
You respond to the reporter from Sports Illustrations that, "Our research demonstrates that BBP is very strongly heritable" and you would be right. But the article that comes out that month reads something slightly different, but completely wrong. "…Recent researchers examined the work and found it substantially accurate and well-performed. They cautioned against arriving at hasty conclusions, however." No one notices the difference.

Brain Dissections
Second, your colleagues perform a series of autopsies on the brains of some dead people who appear to have been BBPs. (Old jerseys, high-top sneakers and Knicks ticket-stubs were found among their possessions, for example). They do the same with a group of dead non-players (no sneakers, jerseys or tickets.) They report that, on average, "certain parts of the brain long thought to be involved with BBP are much larger in the groups of BBPs than in the controls." Certain nationally renowned newspapers in the Northeast pick up on the story and editorialize, "It will be very difficult for anyone to expect poorly educated yokels who believe in Santa Claus, the Tooth-Fairy and God to argue that BBP is not inborn. For not only has it been proven to run in families, even the brains of basketball players are different." (18)
In a pretense of balance, some of these papers interview diehard believers in the old view - yokels who still think that one must decide to play basketball, and play it for a long time, before you really can be considered "a BBP". One of them is quoted as claiming that, "maybe if you do something long enough your brain changes as you get better at it, and that part of the brain gets bigger." (Remarkably enough, this surmise seems obvious to the old-time believer.) The reporter does not merely report the comment, however, he also hints that it is especially idiotic - typical of diehards and yokels - since everyone knows the brain does not change.
Of course, you yourself are well aware that among neuroscientists it is extremely old news that the brain indeed changes, quite dramatically, in just the way the old diehard guessed: those parts responsible for the activity get much bigger over time (and there are definitely parts that are more utilized in BBP). You will not lie about if asked (since you will not be), but neither will you go out of your way to confirm the truth.

Gene "Linkage" Studies
Now for the coup de grace. You find a couple of families of BBPs and compare them to some families of non-BBPs. You have a hunch that of innumerable genes of every imaginable sort likely to be "associated" or "linked" to BBP (you never use the word "causing" because you do not need to - no one knows the difference), there are some genes on, say, the X-Chromosome. After a few false starts, sure enough, you find what you are looking for: among the BBP families one particular chromosomal variant (cluster of genes) is more commonly found (though not always) than among the non-players.
Now, sympathizers at National People's Radio were long ago quietly informed of your research, since they want people to come around to certain beliefs, too. So, as soon as your work hits the press, they are on the air: "Researchers are hot on the trail of the 'Basketball gene!' In an article to be published tomorrow in Sports Science…" Learned-sounding commentators pontificate in soft, accentless, perfectly articulated and faintly condescending tones about the enormous public policy implications of this superb piece of science-in-the-service-of-humankind. Two weeks later, there it is again, at a jaunty angle across the cover of the major national newsweekly: "Basketball Gene."

Now what is wrong with this scenario? It is simple: of course BBP is heritable ("has a non-zero heritability" to use the words of homosexuality researchers). That is because many physiological traits - muscle strength, speed, agility, reflex speed, height, etc. - are themselves directly inherited and they make it more or less likely that one can, and will want to, and will successfully, and will therefore continue to want to, and will in fact continue to, play basketball. In short, because of intermediate inherited traits associated with BBP (none of which are BBP), it shows significant heritability. (The genetic association, of course, is in no way necessary or predetermined, and is highly culturally conditioned: there were no BBPs at all in, say, ancient Greece, yet the same genes were there.)
BBP also shows a strong biological representation in the brain, both at birth (e.g.) nervous system factors contributing to reflex speed) and specially later (e.g. the parts of the cortex that are cultivated and become responsible for movements of basketball, as in the huge increases in finger-related brain tissues among blind people who learn Braille).
And the specific genes that run in families that are responsible for height, athleticism, etc. can surely be found and they will be statistically linked to BBP. And if one identical twin decides to play basketball, the unusually strong emotional bond between such siblings will make it even more likely that his twin will, too. (The fact of their genetic identity, not their specific genes, are here influencing an outcome above and beyond the indirect contributions from any specific genes.)
The basic problem is this: BBP is "influenced" (made more or less an easy and enjoyable thing to do) by the presence or absence of other associated traits. For BBP we can readily guess what they are and so immediately see that the "genetic" component of BBP has nothing to do with the game itself but with these associated (facilitating) traits. What are these traits? Height, athleticism, bone structure, reflexes, muscle refresh rate, and so on. So evident that are the specifics of this association that no serious researcher will waste his time looking into the genetics of BBP proper; he will concentrate on the obvious intermediate traits - height, athleticism, and so on.
The same is true for homosexuality, except (a) the more important, intermediate traits with which it is associated are mostly unknown and unsuspected ones are harder to confirm, and (b) the research agenda is being distorted by the political requirement that no such associated traits be discovered and that homosexuality be falsely presented as directly inherited.

Meaningful Genetics Research Identifies and Focuses on Traits That Are Directly Inherited

Research into more heritable traits is useful only in generating hypotheses about what the directly inherited traits might be. Here is what this means: Let us imagine that it was not immediately evident to us that the heritable aspects of BBP were intermediate traits such as height. A good researcher would not be at all tempted to conclude from the studies we described that BBP itself was inherited. He would conclude however that, indeed, there must be some inherited traits that facilitate BBP, and it would be these as-yet-unknown traits were producing the "non-zero heritability" results. If he could identify the traits correctly, he would find that heritability results, when he redirected his genetics research, would increase dramatically.
In other words, studying the genetics of BBP is really a crude way of unwittingly studying the genetics of height and athleticism, etc. If he selects his population on the basis of the indirect trait (BBP), when it is other traits that are really inherited, the researcher's results will be "fuzzed up" by the inevitable proportion of BBP's who lack these traits, or have them in lesser degree (e.g. a small number of shortish BBPs). But if he correctly identifies the traits in question, his next round of studies will "divide the herd" more efficiently, corralling his subjects not by BBP (or "sexual orientation"), but by height. Of course, there will be more BBPs among the tall subjects than among the short, but that is incidental. He will seek out other tall people who are not BBPs, and in his new study, the heritability factor (height) will be even more concentrated.
How might he guess at what the most important traits are, and then try to confirm his guess, so he could investigate the genetics of these traits? Very simply: he looks, does the best he can to name what he sees, and tries not to run afoul of the currently fashionable taboos enforced by the thought-police! He will probably have no trouble studying height, but he might run into difficulties should he suspect that athleticism (or even height) has a racial association. (More people of Nordic stock, being taller, become basketball players than do people of Appenzeller Swiss stock, being short. Perhaps other such groupings might occur to a researcher.)
In the case of homosexuality, the inherited traits that are more common among homosexuals (and that produce "non-zero" heritability" in studies) might include such qualities as greater than average tendency to anxiety, shyness, sensitivity, intelligence, aesthetic abilities and so on. (Of course, these traits may themselves be further reducible to a variety of mutually influencing, associated genetic and non-genetic factors.) The brain changes that are more prevalent among homosexuals, the tendency of homosexuality to run in families (and to vary with degree of genetic similarity within families) and the presence of associated chromosomal makings are all certainly due to as yet unresearched and therefore not-yet identified intermediate traits. There is no evidence that homosexuality itself is inherited.
Like height and BBP, these traits - intelligence, say, or anxiety - are surely widely distributed in the population at large and densely present therefore in groups that are properly selected to have them. If researchers had divided their populations by shyness or aesthetic sensibility, and ignored the homosexual/non-homosexual division, they might well have found even stronger chromosomal linkages as well as brain changes and twin concordance rates.


Here, then is a final summary, in the form of a dialogue.

Isn't homosexuality heritable?
Yes, significantly

So it is inherited?
No, it is not.

I'm confused. Isn't there is a "genetic component" to homosexuality?
Yes, but "component" is just a loose way of indicating genetic associations and linkages. This will not make sense unless you understand what, and how little, "linkage" and "association" really means.

What about all evidence that shows that homosexuality "is genetic"?
There is not any, and none of the research itself claims there is; only the press and, sadly, certain researchers do - when speaking in sound bites to the public.

But isn't homosexuality "biologically in the brain"?
Of course it is. So is just about everything else. I'll bet people who pray regularly have certain enlarged portions of their brains!
So doesn't that mean that homosexuality is "innate"?
No more than prayer is. The brain changes with use or nonuse as much as muscles do - a good deal more, in fact. We just do not usually see it happening.

But doesn't homosexuality run in families?

So you get it from your parents, right?
You get viruses from your parents, too, and some bad habits. Not everything that is familial is innate or genetic.

But it just seems to make sense. From the people I know there's a type - it's got to be inherited - that runs in families and a lot of these people are gay, right?
That is what associated traits are - but what exactly is the associated trait - or traits - you are detecting? If there is one thing the research confirms, it is that it is not "gayness" itself. That is why these traits are sometimes in evidence at a very early age, long before sexuality is shaped.

So what are these traits?
An important question, indeed. Science is being seriously obstructed in its effort to answer that question. If we were allowed - encouraged - to answer it, we would soon develop better ideas on what homosexuality is and how to change, or better, prevent it. We would know who was at greater risk for becoming homosexual and what environments - family or societal - foster it. As one prominent gay activist researcher implied, all genetic things being equal, it is a whole lot easier to become "gay" in New York than in Utah. So who do you think would benefit from that kind of research?

Well, what traits do you suggest are "associated," as you put it, with homosexuality?
May I speculate, perhaps wildly? That is how scientific hypotheses are first generated. The important thing is not to avoid ideas that prove wrong, just not cling to them if they do.

Okay, go ahead, speculate.
Intelligence, anxiety, sensitivity, aesthetic abilities, taste. You know, all the stereotypes.

But where do these traits come from? Aren't they inherited?
We do not know yet. Some may be. Or rather, we do not know how much is inherited, and which elements are direct and which merely further associated and linked with other yet more fundamental traits. But you are getting the picture. That is how the research ought to proceed. It is not necessarily that the traits that facilitate homosexuality are themselves bad; perhaps many are gifts. Athleticism is a generally good thing, and we think highly of people who satisfy their athletic impulses as, say, outstanding BBPs. Not so the fellow who merely become as thug.


Foot Notes:

1. D. H. Hamer et al, "A linkage Between DNA Makers on the X-chromosome and Male Sexual Orientation," Science (1993), 261, bno. 5119, pp. 321-27

2. "Research points Toward a Gay Gene," Wall Street Journal, 16 July 1993.

3. A lower score on this scale means a less negative attitude toward homosexuality.

4. Piskur and Degelman, "Attitudes Toward Homosexuals," Psychological Reports 71 (1992); my emphasis, pp. 1219-25 (part 2 of 3). See also K.E. Ernulf, "Cross-National Analysis."

5. K.E. Ernulf, S.M. Innala, and F.L. Whitam, "Biological Explanation, Psychological Explanation, and Tolerance of Homosexuals: A Cross-National Analysis of Beliefs and Attitudes, "Psycological Reports 65 (1989), pp. 1003-10 (1 of 3).

6. Mann C. Genes and behavior. Science 264:1687 (1994)

7. None of the studies of the genetics of homosexuality (all of which are initial; none are replicatory) have come even remotely close to studying this many subjects.

8. Mann C. op. cit. p. 1688.

9. King, M and McDonald, E Homosexuals who are twins: a study of 46 probands. British Journal of Psychiatry 160:407-409 (1992)

10. Byne W and Parsons B. Human sexual orientation: the biological theories reappraised. Archives of General Psychiatry. 50, 3:230 (1993).

11. Quoted by Horgan, J., Scientific American: Eugenics Revisited. June 1993, p. 123.

12. Billings, P. and Beckwith, J. Technology Review, July, 1993. p. 60.

13. Mann C op. cit. pp. 1686-1689.

14. Risch N., Squires-Wheeler E., and Bronya J.B.K., "Male Sexual Orientation and GeneticEvidence," Science 262 (1993), pp. 2063-63

15. Hammer DH et al. Response to Risch N et al. ibid p. 2065

16. Hammer DH et al. Response to Risch N et al. loc. cit.

17. Mann C., op. cit. p. 1687

18. Readers may recall Simon LeVay's much touted discovery that the certain parts of the brains of (supposedly) homosexual men were larger than among (supposedly) heterosexual men. But even if the research is valid - its quality has been strongly criticized - the discovery of brain differences per se is on a par with the discovery that athletes have bigger muscles than non-athletes. For though a genetic tendency toward larger muscles may make it easier to - become an athlete, becoming an athlete will certainly give one bigger muscles.
When this particular critique was raised, the press quickly took its accustomed potshot at the usual "poorly educated and easily led" religious groups for the suggestion's politically incorrect implications: "Some religious fundamentalists even suggested that homosexual activity somehow could have caused the structural differences [that LeVay claimed to have discovered]."
But as the editor of Nature - an equally prestigious publication - wrote, commenting on the LeVay research: "Plainly, the natural correlates of genetic determined gender are plastic at a sufficiently early stage... Plastic structures in the hypothalamus allowing the consequences of early sexual arousal to be made permanent might suit [those who claim an environmental origin to homosexuality] well." This editor is not, to anyone's knowledge, a religious fundamentalist.



HEALTH CONCERNS OF HOMOSEXUAL BEHAVIOR - A Voice of the Voiceless Reference. Volume 1. 2/3/2014


Written By Dr. Gerard van den Aardweg

Dr. van den Aardweg explains why he believes the claims for a biological basis for SSA have little merit.

( Permission to reprint this article was graciously given to JONAH from Dr. van den Aardweg and NARTH, the National Association for the Research and Therapy of Homosexuality. This article was originally published in The NARTH Bulletin, Winter 2005, 13,3,19-28.)

In 1898, the Austrian empress Elizabeth was stabbed to death in Genova by 25-year-old Luigi Lucheni. The murderer was proud of his act, which he declared was “revenge for my life.” After turbulent years in prison, Lucheni hanged himself in 1910. A typical representative of the prevailing 19th century thinking on abnormal behavior, professor Mége-vant performed an autopsy, investigating the brain to uncover the anomalies that were supposed to underlie the murderer’s “psychopathic disposition.” However, nothing out of the ordinary could be found; even Lucheni’s brain weight was standard. Disappointed, the professor put the head in a jar with formaldehyde and stored it in the cellar of the Institute for Forensic Medicine. A neuroanatomically normal psychopath, what a scientific riddle!

Yet the explanation of this criminal’s arrogant, merciless, and abnormally hostile personality was close at hand, provided one would pay attention to what he had to say himself about his psychological history. An illegitimate child, abandoned and cruelly abused and exploited by several foster “parents,” he was driven by frustration and embitterment. But psychogenesis had not been discovered by then, so to speak, and psychiatry was dominated by Kraepelin’s postulate: mental aberrations stem from abnormalities in the brain, which moreover are inherited. For criminal behavior, the variant was Lombroso’s theory of the deliquente nato, the born-that-way delinquent.

Perusing the research literature on homosexuality of the last 15-20 years, one recognizes the same 19th century mentality. The nonprofessional reader who is not able to read the rules will get the impression that there is no scientific doubt with respect to homosexuality’s biological causation; at least, that powerful constitutional predispositions have been ascertained. If you are not precisely born a homosexual, you will in any case possess some biological homosexual disposition, which in practice amounts to the same. And if science has not yet unearthed the definitive biological causes, it is in the process of doing so, because the experimental indications are piling up. So science would seem to support the notion of the omosessuale nato. [1]

By and large, this is the message conveyed by the majority of the reports in the professional magazines. If developmental-psychological factors are given some attention they are played down as of secondary importance at most; often no mention is made of them at all. Now what is the truth? First, that not a single genetic, physiological, anatomical, or neuroanatomical correlate of homosexuality has been demonstrated. Secondly, that contrary to the impression they confer, precisely the studies of the last 15-20 years have made the existence of such correlates more unlikely than before. Thirdly, that these realities are either not perceived or purposely kept out of awareness because most academic publications on homosexuality are influenced or determined by the predominant gay ideology.

No Hormonal Correlates

The conclusion arrived at by Perloff in 1965 that no hormonal peculiarities had been demonstrated in homosexuals still holds today. In 1993, Byne and Parsons thus summarized their thorough expert analysis of the investigations on homosexuality and biologic factors, including hormones: “There is no evidence ... to substantiate a biologic theory.” [2] And after 1993? Nothing remotely resembling proof of hormonal influences on homosexuality either. Yet a warmed-up version of the intersex (Zwischenstufen) theory of Magnus Hirschfeld, according to which male homosexuals have a hormone-induced feminized brain and lesbians a masculinized, continues being dished up as if founded in scientific fact. Prenatal androgen deficiency and excess (in homosexual men and women, respectively) are held responsible. [3] This view is however an undifferentiated programmatic sketch more than a testable theory. For what is meant, for instance, by a “feminized” male brain?

Does it mean that in some, as yet postulated, brain structure, the perceptual recognition center of “the feminine,” the “image” of the female Gestalt has been substituted by the Gestalt of “the masculine”? That sounds rather fanciful (and what then caused the picture of the feminine in the homosexual pedophile to be substituted by that of “the boyish”? And so on for the other sexual “orientations”). Or does a “feminized” male brain mean that the boy’s behavior is becoming feminized; or rather, that the boy’s aggression drive is reduced, because lack of daring and of physical fighting spirit is much more tied to homosexuality than “femininity”? [4] In the latter case, the supposed brain anomaly contains nothing that spontaneously generates or inherently predisposes to homosexual desires. Reduced male aggression (and its counterpart, enhanced female aggression/tomboyishness) as a temperamental trait (the current term is “gender nonconformity”) might then be considered at most an “indirectly predisposing,” better still, a “pseudo-predisposing” factor. In fact, it is the environment and the child’s self-view which determine if such temperament plays a role in the genesis of homosexuality. In this variant of the sex-atypical brain theory, the origin of homosexuality itself is not accounted for; in principle it may be easily incorporated in a developmental-psychological view. It certainly does not justify the horrible notion of “gay children.”

There would merely be temperamentally placid boys and “wild” girls, the vast majority of them growing up as normal heterosexuals.

The crucial question however is: What is the evidence for a link between this (or other) behavioral traits and prenatal, or whichever other, hormonal or brain irregularities? The alternative explanation, habit formation and self-view by rearing and other social influences, is certainly not less likely. Mama’s boys and/or boys with “psychologically absent” fathers tend to be over-domesticated, so to speak, and it is precisely these parent-child factors that have incontestably been shown to be associated with male homosexuality. [5]

Fathers’ girls and girls whose personality was not much shaped by their mother, and girls with other defeminizing childhood background factors may adopt more “masculine” or boy-like attitudes and habits. Anyhow, specific parent-child and peer group interactions have been amply demonstrated, while the hormonal-neuronal explanation has precious little to offer but speculations. There are no indications that homosexuals have suffered hormonal deviations before or after birth, their hormonal system is normal and in agreement with their biologic sex.

The evidence proposed by the proponents of the feminized/masculinized brain theory is limited to a few hardly relevant observations: the female lordosis reflex in male rats after testosterone deprivation (which reflex however is not indicative of their sexual drive); the possibly enhanced prevalence of lesbian tendencies in women suffering from congenital adrenal hyperplasia or CAH (who have been exposed to prenatal androgen hormones) [6]; and a few contradictory data regarding finger length ratios.

Regarding CAH, the majority of these women are heterosexual, so that their supposed brain masculinization would affect only a minority. If lesbianism would indeed be relatively frequent among these patients (the data are not conclusive [7] ), it is hard to see why that would argue for a hormonal cause or even predisposition in healthy lesbians who are hormonally normal and whose genitals are not semi-masculinized like in these CAH patients. A psychological explanation of lesbianism in girls with “unfeminine” genitals and the various traumatic experiences associated with it is more realistic than a physiological explanation. For feelings of feminine inferiority are practically inevitable in girls who suffer from such a condition, and that is how a lesbian development often starts.

With respect to men with disturbances leading to prenatal androgen insensitivity or deficiency (and who are therefore believed to possess “feminized” brain centers), no connection with homosexuality has been found. [8] This has been the usual outcome of the older studies on homosexuality in persons who really have some aberration of the sex hormones or sex-chromosomes, too: they do not become psychosexually aberrant. According to some authors their sexuality may be somewhat rudimentary, “infantile,” underdeveloped, though, and this is understandable. [10]

Do homosexuals have a 2D:4D (index finger: ring finger) ratio like the one typical of the opposite sex? It has been declared this “suggests” sex-atypical prenatal hormones and brain formation. But the phenomenon is in all likelihood no more than a peculiar artifact, like others of that kind, [11] so we had better forget about it.

In all, the periodically launched “promising” leads of hormonal correlates of homosexuality have invariably proven dead ends; there is a history of nearly 90 years to illustrate this point. It is at odds with scientific prudence to make the gigantic leap from (otherwise, not sufficiently studied) observations with rats to the complicated level of human sexuality. It is time the criticism of Byne (1995, p. 337) gets through to psychiatrists, psychologists and other professionals who sometimes tend to be overly impressed with reported biologic indications. Byne says there are too many

“...hasty interpretations, based on limited sample sizes, shaky methodologies, and extremely limited knowledge about functions of particular brain structures and even less knowledge about the biological substrates of the mind.”

In other words, there is much amateur speculation instead of serious science. He explains:

“Attempts to prove that gay men have feminized gonatropin responses [12] were made decades after strong evidence suggested that the brain mechanism regulating the response does not differ between men and women” and “It required 25 studies to convince some that testosterone levels in adulthood do not reveal sexual orientation” (p. 336; see also Byne, 1997).

As long as a suspect’s guilt has not been proven, he must be treated as innocent. One may personally believe homosexual persons must have hormonal or neuroanatomical peculiarities, but scientifically there is no reason not to consider them physically normal and healthy (brain evidence: below).

No Genetic Proof

Despite numerous suggestions to the contrary, the last fifteen years of renewed research led even behavioral geneticists in favor of a genetic explanation of homosexuality to the conclusion that genetic factors for homosexual inclinations as such do not exist. This interesting fact hardly gets the attention it deserves. The other remarkable point is that in consequence, current genetic speculations focus on predisposing factors of a non-sexual nature. As a result, it is implicitly admitted that the prime and decisive causes lie in the person’s life history. The indirect evidence for these conclusions has come from twin studies, the direct from the exploration of genetic linkage.

Concordance percentages in volunteer studies vary from 25-66 for monozygotic (MZ) twins, roughly two times the percentages for dizygotics (DZ). [13] This is quite dissimilar from the picture in the case of uncontested genetic factors like the color of the eyes, certain diseases, etc. Apart from the fact that volunteer studies do not adequately represent the total population of homosexuals with twins (see further on), these results are not proof of the genetic determination of homosexuality. First, because only half of the co-twins of the MZ homosexual index persons in these groups were also homosexual. Secondly, because the average concordance of DZ male homosexuals in volunteer studies is 20%, whereas the rate of homosexuality among non-twin brothers of male homosexuals “hovered closely around 9%.” [14] DZ twin brothers of homosexuals are genetically not more similar than other brothers, so the finding that DZ twins of male homosexuals are twice as often homosexual as the average brother of a homosexual man challenges a genetic explanation. Both the higher concordance in MZ than in DZ pairs and the higher incidence in DZ twins as compared with non-twin siblings point to a psychological (environmental) explanation. Very regrettably, the psychological dimension has been virtually neglected in all of these studies, except for an occasional observation like the footnote by Bailey and Pillard (1995, note 34):

We found in both our male and female studies that discordant MZ twins also reported quite different childhood experiences. ... the homosexual twins reported more sex-atypical behavior....

(“Sex-atypical behavior” is the concept of gender nonconformity we dealt with above).

Why did an observation like that did not lead to collecting detailed developmental-psychological data of these subjects of identical genetic make-up regarding their relationships with parents and peers and self-image in relation to their co-twin? Anyhow, the observation of Bailey and Pillard is satisfactorily explained by the psychology of twins. Their self-view is shaped by intense comparison with their co-twin (and by their being compared to each other by their environment); either they feel “identical” (want to be and act like their alter ego) or they overemphasize their differences, e.g., with respect to their virility or femininity. [15] Thirdly, 11% of adoptive brothers of homosexual males are reported to be homosexual, too. [16] This finding, which neither genetic nor perinatal hormones can account for, casts more than a little doubt on the genetic explanation of the homosexuality of the biological sons, thus on the whole genetic hypothesis.

However, concordance rates in volunteer samples appear to be inflated, since homosexuality-concordant twins, especially MZ twins, are as a rule overrepresented. [17] Therefore, samples from twin registers are considered more representative. [18] Bailey et al. (2000) found 3 out of 27 MZ male homosexuals from the Australian twin register to be concordant (11%), versus 0 out of 16 same-sex dizygotics (0%) and 2 of 19 opposite-sex dizygotics (12%). Of 22 female MZ twins, 3 (14%) were concordant, versus 0 of 16 same-sex dizygotics (0%) and 2 of 19 opposite-sex dizygotics (12%). This was not “statistically significant support for the importance of genetic factors,” which the reader who inspects the simple numbers given above may readily see. Significantly, though, it has subsequently been attempted to squeeze as much “heredity” as possible out of these obvious data by applying more “flexible” (and thus more debatable) criteria for “homosexuality” and using a “hereditability” formula.

And, lo!, the magic formula turns the defeat for the genetic explanation into a victory so that henceforth what was evidently “no support for genetic factors” can be sold as modest “support” (Kirk et al., 2000)! Such handling of the raw numbers borders on what the French call “statistical massage”; it is at any rate no test of the power of a genetic versus a non-genetic model. [19] The same is true of the interpretation in a similar study that the “[homo] sexual orientation was substantially influenced by genetic factors.” [20]

In this case too, the simple numbers tell the tale better than sophisticated calculations based on a speculative model [21]: Two of 10 MZ homosexual men had a homosexual twin brother (20%) vs. 4 of a combined group of 28 male DZ twin pairs and pairs of non-twin brothers one of whom was a homosexual (14%). Four of 9 female MZ pairs were concordant (44%) vs. 8 of a combined group of 28 female DZ twins plus non-twin sisters one of whom was a lesbian (29%). This indicates a slight preponderance of MZ concordance, not significant statistically though. In a non-random sample of never-married twins from the Minnesota Twin Registry, which seems to contain the majority of the twins of this State, Hershberger (1997) found hereditability coefficients that were mildly consistent with genetic influences for lesbians, not for male homosexuals. [22]

In sum, MZ concordance becomes lower the more representative the samples; at the same time, the difference between MZ and DZ concordances becomes less convincing. [23] The more important conclusion, however, is that the genetic hypothesis has become increasingly less plausible and seems engaged in a rearguard action. For no theorists of genetic influences can be found any more who believe in the existence of a “gay gene” proper. The view of the role of genes underwent a silent, but very significant change: no longer the prime determinants, they now function at most as predisposing factors. In short, the decisive cause(s) of homosexuality are not hereditary. Even Hamer, the man who in 1993 caused the media stir with his “near-discovery” of the gay gene [24] admits:

We do not expect to find (in the future) a gene that is the same in every gay man ... just one that is correlated to sexual orientation. [25]

Unclearly as it is worded, he seems to hint at predisposing factors. Bailey theorizes in the same direction after finding that childhood gender nonconformity was (to a degree) compatible with a genetic statistical model while homosexual feelings were not. [26] But the case for the genetic origin of gender nonconformity is far from strong either. Wasn’t it Bailey himself who previously had noticed that it was this very item of gender nonconformity which distinguished the homosexual from the heterosexual twin in MZ pairs discordant for homosexuality? [27]

Dramatically decreasing genetic evidence from modern twin research was on the one side, while on the other, the search for a genetic linkage came to a dead end. The well-known 1993 finding of Hamer, et al., did indeed not demonstrate the existence of a single gene, because it was not shown that the highly selective group of homosexual men showing a moderate correlation between DNA markers and a region of the X chromosome shared a particular molecular sequence. [28] The supposed genetic factor thus might have been any physical or temperamental resemblance with the mother (from whom the X chromosome is inherited). The whole thing was, after all, a storm in a tea cup. Subsequent analysis and research vindicated the verdict by the famous French authority in the field, Jerome Lejeune, that the methodological defects of the investigation were so serious that “were it not for the fact that this study is about homosexuality, it would probably never have been accepted for publication.” [29]

A first replication by the same team with a small group reported a barely significant confirmation for homosexual men, not for lesbians [30]; the calculations of the team were, however, rejected by the statistician experts. [31] And an independent Canadian team failed to uncover a link between male homosexuality and the X chromosome in a larger sample. [32] So much for the direct exploration of the genes. Circumstantial evidence is sometimes deduced from familial and pedigree findings. It has long been known that homosexuality occurs relatively more frequently in certain families and pedigrees, but genetic explanations are implausible in view of the erratic way it is distributed within these families and pedigrees: “We never found a single family in which homosexuality was distributed in the obvious pattern that Mendel observed.” [33]

And this statement by Hamer is even an understatement. On the aforementioned higher correlation in lesbian propensities between lesbians and their mothers than between them and their sisters, [34] he comments: “The rate was a whopping 33 percent, meaning that the daughter of a lesbian had a one-in-three chance of also being a lesbian. Genetically speaking, this result was impossible.” [35] Psychologically not so, however. [36] Many specific personality-shaping habits are transmitted from one generation to the next by learning. This may explain varied familial phenomena a genetic hypothesis cannot. It is therefore arbitrary to present a possibly somewhat elevated occurrence of male homosexuality among maternal relatives as evidence for genetic influences, as has been done in a recent publication [37] (Fortunately the authors admit that it is “still possible” to attribute their data to “culturally, rather than genetically, inherited traits”). [38]

In an attempt to present the long known [39] and recently well-replicated [40] phenomenon that homosexual men (not women) have relatively more older brothers than heterosexual men as an indication of the biological cause of male homosexuality, a far-fetched theory has been invented. Mothers of male homosexuals might progressively produce an “antibody” to male fetuses every time they are pregnant with a boy, which in turn would eventually feminize the developing brain of the younger male embryos (The theory has only relevance for 15% of the male homosexuals, viz., those with more older brothers). [41] Physiological anti-boy mechanisms have never been demonstrated, however, and the fully speculative status of the feminized male brain has already been described. Why not try a psychological explanation? Already in 1937 psychiatry professor Schultz pointed to the impact of the position of the “nice little brother” (liebe Brüderchen) among his older brothers on his psychosexual development. [42]

No Neuroanatomical Correlates

Like professor Mégevant a century ago, present-time brain researchers have never really been awarded in their quest for unambiguous brain anomalies in homosexuals. E.g., an initial report of larger inter-hemispheric fiber bundles in homosexual men could not be replicated. [43] Nor was there a convincing reason to explain LeVay’s 1991 over-publicized observation of a smaller hypothalamic nucleus (INAH3) in some homosexual men who had died of AIDS in comparison with heterosexual intravenous drug users as evidence of a feminized brain center. Differences between the groups other than the homosexuality variable might have caused the effect: procedures of tissue preparation, length of the disease period, previous occurrence of other venereal diseases, or medication. A replication by Byne et al. (2001), hailed by some as “proof” of a “homosexual brain center” [44] has in fact made that explanation even more unlikely. In a small group of homosexual men who had died of AIDS they found a trend for the ratio of INAH3-volume to brain weight to be smaller than that ratio for deceased heterosexual men who were drug users. The trend was not significant statistically, hence strictly speaking, the difference is not uncontestable. Byne suspects that since the brain weights of the heterosexual men with AIDS were much lower than both those of the HIV-negative heterosexual men and the homosexuals with AIDS, the trend,

“... may reflect the superior health care received by the homosexual male group compared to the heterosexual male group with AIDS, all of whom were intravenous drug users.” [45]

Nor does he exclude that histological preparation caused the relative shrinkage of INAH3 in the homosexuals:

“Since some New York hospitals have a preponderance of HIV+ patients who are gay men, while others have a preponderance of HIV+ patients who are drug users, the homosexual and heterosexual patients tended to come from different institutions, and therefore, there were likely variations in autopsy and fixation procedures that were confounded with sexual orientation.”

For these reasons, he believes his second finding is the more reliable and important one: the nuclei of the homosexuals contained as many neurons as those of the heterosexual men. That is, 60% more neurons than the female nucleus. This is the more interesting because INAH3 seems the only brain-anatomical structure which is sexually dimorphic. [46] In sum: no evidence for the “wrongly put on nerves” (like the strings of a guitar) the poet Dante ascribed to homosexuals! [47]


The main conclusion is obvious if we keep our eyes on the interesting factual observations in the reports of the last few decades and let our sight not be obscured by the biology-biased interpretations they are wrapped in. No bodily correlates of homosexuality have been demonstrated. Like with the monster of Loch Ness, there are periodic claims that a biologic factor has been spotted, but upon closer inspection, the claims evaporate. [48] This renders any discussion of whether a determinate correlate would be a cause, an effect, or an insignificant byproduct of another homosexuality-connected variable superfluous.

But there is more. Whereas constitutional theories seem increasingly speculative, they are only the psychological correlates of homosexuality that are well-established. The highest correlations have systematically been found for what is currently designated as childhood and adolescent gender nonconformity: lack of integration in the boyhood/girlhood world and feelings of not belonging to the same-sex world. [49]

This syndrome has been established in clinical as well as nonclinical samples, in various countries and over several generations. Significantly, it is also recognized by authors who prefer to believe in biological theories (Hamer, LeVay, Bailey). The second-highest correlations exist with the finding of defective relations with the same-sex parent; the third-highest with maternal dominance/overprotection for the homosexual man, and with varied father factors for the lesbian. [50] Empirically, then, a psychological explanation is the most realistic.

Furthermore, belief in a causal contribution of some (mostly unspecified) biologic variable, which is shared by many professionals who view homosexuality basically as a psychological phenomenon, is purely hypothetical. I think Schultz-Hencke, one of the coryphées of German psychiatry, was right when he wrote as far back as 1932: Homosexuality and every correlate of it is “psychologically explicable, without leaving a remainder.” [51] Even the unboyishness of many prehomosexual boys may rather be seen as an effect of intra-family factors, habit formation, and self-concept than as temperamental. [52] And certainly is all talk of “gay children” irresponsible, not only morally, but also scientifically. There is nothing intrinsically “gay” in either the biological or the psychological nature of children, nothing that spontaneously would push them to homoerotic feelings. The theoretical improbability of the existence of physiological correlates specific for homosexuality may appear more clearly if homosexual and heterosexual pedophilia, transvestism, exhibitionism etc. are taken into account (curiously, this is almost never done). For either specific hormonal, hormonal-brain or other factors are postulated for each of them, or they are regarded as “environmentally” caused. The first option is wild, the second challenges the biologic co-causation of homosexuality, because on what grounds should homosexuality be the exception, since the desires of pedophiles, etc. have the same characteristics as those of homosexuals (exclusiveness, obsessiveness)?

Proven Psychological Variables Ignored

Methodologically, it is a pity that most of the reviewed studies did not include the psychological variables of proven validity as to their relation with homosexuality. The more so since their results are mostly used as arguments for a (biologic) theory. But what is the value of a theory based on research which left out some of the most important variables? Notably the various collections of MZ and DZ twins might have yielded rich data had thorough psychological examinations been conducted of the childhood/ adolescence background, parental and peer factors, self-view, and neurotic emotionality. [53] That is equally true of studies on familial or pedigree clustering and the more-brothers phenomenon in a subgroup of male homosexuals. This missed opportunity points to either ignorance of the psychology of homosexuality or unwillingness to give it the credit it deserves (or both).

Gay Activists Dominate Research

Whence this 19th century step-motherly treatment of psychology by our present-day professors Mégevant? It is because with few exceptions they are gay persons wedded to the gay ideology. They are the Weinbergs, LeVays, Hamers, Baileys, Hershbergers etc., who openly admitted that biological roots of homosexuality favor social acceptance of the gay agenda (and right they are). It is in their interest to be single-mindedly biology-biased. And since the gay ideology has become the party line in the official establishment of the human sciences, inclusive of most professional journals, all findings “support” homosexuality’s biologic origin and mental normality or at least “suggest” it. Free research and free thinking is taboo as soon as it seems to threaten the gay cause. The ideologically distorted science thus produced and sponsored profoundly misleads the public. On a deeper level, it is often motivated not by thirst for the truth, but by the wish to rationalize or justify the normality sought by so many persons who are committed to a sexually abnormal lifestyle.

End Notes

1. This misrepresentation of the present state of research is imitated by not a few authors who apparently accept it without critical examination. A painful example is the contention of Serra (2004) that there would be “a coherent complex of observations indicating with sufficient strength that ... a (causal) biological component may not be excluded and which even suggest that this has an appreciable weight” (p. 232). That boils down to suggesting the existence of the omosessuale nato, though Serra’s formulation is vague. I mention this example because Father Serra is a retired professor of genetics of the Gregoriana University in Rome and a honorary member of the Papal Academy for Life. His misleading article in the Jesuit periodical La Civiltà Cattolica will probably make some impression in certain Catholic circles.

2. P. 228. Unlike the authors who blithely dream up physiological “explanations” without solid expertise in this area, Byne is an authority in the field of psychiatric neuroanatomy, Parsons in psychiatric genetics (both at the New York institute of Psychiatry).

3. E.g., Mustanski et al., 2002; Hershberger & Segal, 2004. They quote Meyer-Bahlburg (2001) although this author gives no evidence on hormonal or brain peculiarities of homosexuals, only on the psychosexual development of women with a chromosomal disturbance (classic CAH). According to some (not all) studies they manifest more lesbian inclinations than other women; yet their “prenatal hormonal milieu does not dictate a bisexual or lesbian outcome” and “few consider themselves lesbians” (p. 163).

4. Research data: van den Aardweg, 1986, chpt. 15; Freund & Blanchard, 1987; Hockenberry & Billingham, 1987.

5. As for the habit-formation explanation of boyish aggressiveness and daring or the lack of it, a comparison of the behavior of boys from families of working men with boys from academic families is instructive. Boys from the latter families are generally “softer,” more “feminine” if we prefer this psychological term, less physically aggressive. Also, compare boys from slums with boys from middle-class families.

6. Meyer-Bahlburg, 2001. Byne & Parsons (1993) make it clear how unconvincing the masculinized-brain hypothesis is to account for this otherwise not conclusively demonstrated phenomenon (p. 232).

7. See note 2, above.

8. Byne & Parsons, 1993, p. 232.

9. E.g., the older study of Raboch & Nedoma, 1958.

10. Züblin, 1957. Interestingly, Züblin remarked that the weak sexuality of these physically abnormal men seems strongly determined by their need to “behave like other men.” Meyer-Bahlburg (2001) points to the rudimentary sexual drive of women with CAH.

11. Mustanski et al., 2002.

12. Gonadotropins: hormones working on the sexual glands. Feminized gonadotropin responses: responses comparable to those of the female physiological cycle.

13. Of 56 American male MZ pairs, 59 (29%) were concordant, against 12 (22%) of 54 DZ pairs (Bailey & Pillard, 1991); of 20 British male and female MZ pairs, 5 (25%) were concordant, against 3 (12%) of 25 DZ pairs. The difference was not significant (King & McDonald, 1992). Of 38 American male MZ pairs, 25 (66%) were concordant, against 7 (30%) of 23 DZ pairs (Whitam et al., 1993). Of 71 American female MZ pairs, 34 (48%) were concordant, against 6 (16%) of 37 DZ pairs (Bailey et al., 1993).

14. Bailey & Pillard, 1995

15. I know a few such cases. The homosexual twin of these MZ pairs had viewed himself (and was seen by his parents) as the weaker of the two or was mother’s boy (the other one, father’s boy). Farber (1981) described two MZ sisters reared apart, one of whom a lesbian, the other heterosexual. In contrast with her co-twin, the lesbian had a conflict-ridden relation with her foster mother and a strong attachment to her foster-father, whom she imitated. Psychology give the clues!

16. Bailey & Pillard, 1995, note 30. Homosexuality seems to be relatively frequent in adoptive children in general, which has to do with many of those children’s liability to feeling not belonging (less valuable) in comparison with their biological siblings.

17. The phenomenon of “concordance-dependent ascertainment bias,” which was responsible for the suspect 100% MZ concordance (against 11.5% DZ concordance; or, under a broader definition of homosexuality, 42.3% DZ concordance) in the male group of Kallmann (1952). The figure of Kallmann raises some questions, by the way. A favorite disciple of psychiatrist Ernst Rüdin, the highest Nazi authority on the medical aspects of “racial hygiene” and a zealous advocate of forced sterilization of the mentally disturbed and “psychopaths,” Kallmann, like Rüdin, saw twin research as a means to improve the diagnosis of family members of “racially inferior” persons. He called for the sterilization of schizophrenics and many of their seemingly healthy family members who allegedly carried the postulated sick recessive gene, estimating that this made necessary the sterilization of about 5% of the population (!). Probably not by coincidence, he found extremely high concordance rates for MZ schizophrenics. What did he originally, before his flight to the U.S., have in mind for homosexuals? (Müller-Hill, 1984; Blondet, 1995).

18. It is not clear, though, how representative because the volunteer effect cannot be ruled out. Only about half of the twins invited for the study eventually participated. In addition, the register itself is a volunteer register which may contain no more than 10-20% of the Australian MZ and DZ twins (Kirk et al., 2000, note 39).

19. Hereditability formulas are statistics to estimate the part of score variance that might fit a proposed heredity model. Besides being based on assumptions which are susceptible of debate, hereditability coefficients are not measurements of genetic influence, merely quantifications of the degree obtained observations are compatible with a postulated genetic model. It does not really enhance the plausibility of heritability coefficients for personality traits that according to their reckonings viewpoints on the death penalty, abortion on demand, and even a virtue like “humility” are “50%” genetically determined (Excellent analyses: Whitehead & Whitehead, 1999). *Another source of confusion flows from the use of proband-wise concordance percentages in stead of the usual pair-wise percentages. The proband formula overestimates “real” concordance, yielding genetically-biased results. Proband-wise formula: 2(++): [2(++)+-] x 100%; pair-wise formula: (++) : N x 100%.

20. Kendler et al., 2000, p. 1843. The sample came from a U.S. national survey, but is not a representative of homosexuals with twins, nor can the volunteer factor be excluded.

21. The authors use the proband-wise concordance formula, overestimating MZ twin resemblance; in this text, pair-wise percentages are given.

22. With reference to this “moderate consistency” with a genetic model, see the contradictory finding of Pattatucci and Hamer (1995) that the highest correlation concerning lesbian interests was not between the lesbians and her sisters, but between the lesbians and their mothers. See also the failure of Hu et al. (1995) to find markers for a gene for lesbianism.

23. We cannot rule out the hypothesis that MZ concordance for homosexuality (and for other features) in former days was indeed higher than at present. It may be that the MZ children of former generations were more than at present reared and viewed as being identical, whereas MZ children of recent generations are more treated as distinctive individuals, their differences being emphasized in stead of their similarities. Examination of the relative proportions of MZ and DZ twins in non-Western cultures might help clarifying this issue.

24. Hamer et al.,1993.

25. Hamer & Copeland, 1994, p. 198.

26. Bailey et al., 2000.

27. Bailey & Pillard, 1995, footnote 34.

28. Byne, 1994.

29. Lejeune wrote this to me (1993) in response to my question about his opinion on Hamer’s article in Science. Lejeune was a great and erudite scientist, the discoverer of the gene causing Down syndrome.

30. Hu et al., 1995.

31. Risch et al., 1993.

32. Rice et al., 1999.

33. Hamer & Copeland, 1994, note 47.

34. Pattatucci & Hamer, 1995.

35. Hamer & Copeland, 1994, p. 191.

36. The finding must be repeated before it can be generalized. It is certainly relevant in connection with the debate on parenting and adoption by lesbian couples.

37. Camperio-Ciani et al., 2004. This is a rather shoddy study. “Measurement” of the homosexual inclinations of the relatives consisted in the opinion of the interviewed homosexuals themselves (The tendency of self-defensive homosexuals to project homosexuality in others is a well-known phenomenon). Besides, the informants were volunteers, so that the results may be an artifact. Otherwise, the authors emphasize that only 20% of the variance of pedigree sexual orientation could be accounted for by the genetic hypothesis.

38. Ibidem, p. 2220. “Culturally inherited” sounds strange. Why not: “Transferred by habits of rearing and education”? For example, male-female role imbalances which clearly stem from habit can be observed in certain families; maternal overprotection can sometimes be traced back for several generations, not to speak of personality shaping world views or beliefs.

39. E.g., the study of Lang, 1936.

40. Bogaert, 2003. Statistically, the probability that a boy in certain families with more brothers becomes a homosexual increases 38% with each older brother. In view of the increasing rarity of families with a series of brothers, this familial factor will have affected few future homosexuals in Western society.

41. Bogaert, 2003. Bogaert’s 15% nicely accords with that of Lang, 1936, who estimated 10-20%.

42. Homosexual men with more brothers not seldom felt inferior to them, were more overprotected, treated in a softer way.

43. Lasco et al., 2002.

44. In his book, Bailey (2003) misunderstood a communication of Byne to him as a confirmation of LeVay’s finding. He euphorically writes he would like to invest big money in Byne’s research (if he had it, of course), probably in the hope that this scientist will come up with the ardently desired biological proof. The scientific quality of Byne’s publications indicates that funding him is not a bad idea, indeed, but: will the outcome make Bailey cheerful?

45. Letter of July 20, 2005, to this author. The next quote is from this letter, too.

46. Byne et al., 2001, p. 90.

47. Inferno, XV, verse 114: li mal protesi nervi.

48. One of the recent one-day butterflies: the Swedish discovery of feminized body odor preferences of homosexual men. Evidence for a genetic cause of homosexuality, or for the sense of humor of the authors?

49. A survey of the studies until the eighties: van den Aardweg, 1986, Table 13.1; for later studies: e.g., Bem, 1996.

50. van den Aardweg, 1986, Table 15.1 and 27.5; Fisher & Greenberg, 1996, p. 137.

51. “restlos psychologisch erklärbar” (p. 300).

52. The analysis of the evidence concerning the specific “femininity” or nonaggressiveness in prehomosexual boys and “masculine” tendencies in some prelesbian girls is a chapter in itself. Here I can merely state my conclusion.

53. Earlier in the text I recalled Bailey’s observation that homosexuality-discordant MZ male twins differed in boyhood gender nonconformity.


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Interesting new scientific claim: "Born gay" does not necessarily mean there is a "gay gene"...


Two quotes from the American Psychiatric Association (taken from here: http://www.psychiatry.org/mental-health/people/lgbt-sexual-orientation. April 1st, 2013):

"In 1973 the American Psychiatric Association’s Board of Trustees removed homosexuality from its official diagnostic manual, The Diagnostic and Statistical Manual of Mental Disorders, Second Edition (DSM II). The action was taken following a review of the scientific literature and consultation with experts in the field. The experts found that homosexuality does not meet the criteria to be considered a mental illness."

"No one knows what causes heterosexuality, homosexuality, or bisexuality."

Let me get this straight: In 1973 they removed homesexuality from their diagnostic manual, after a "review" of "scientific" literature and consultation with "experts". It does not fit the criteria of a mental illness. To this day, however, they say that no one knows what causes homosexuality. In other words: Those "experts" have no idea what they are talking about, but it sure is no mental illness. And the "scientific" literature supports that view. I wonder what defines "scientific" then. I am just a simple dude from the country, but doesn't "scientific" refer to that what can be measured or watched or proven in some sort of way?

Could it be that even today they don't have the guts to say that it was not science, but political pressure that made them take it off the manual list?


A FASCINATING OBSERVATION -- Assume a 'gay' gene were found. Now assume that an unknown percentage of gay self-identified participants -- did not have the gene on testing. Imagine the explosive chaos within the gay community to discovering their friends and partners were not "true" gays. The mind boggles at the internal war that would ensue and the pressure from within and without on those proving not to have the gene but are adamantly gay self-identified. The campaign to find this gene suddenly becomes an unwitting walk to the gallows for LBGT'ers.


‘We don’t need psychotherapists to explain away our sins and tell us we’re sick. We need priests to remind us of our sinfulness and show us the way to our Redeemer’.
Venerable Archbishop Fulton Sheen