http://apologeticspress.org/APContent.aspx?category=11&article=1388
"This is the Way God Made Me"--A Scientific Examination of Homosexuality and the "Gay Gene"
The trumpets were left at home and the parades were canceled. The press
releases and campaign signs were quietly forgotten. The news was big,
but it did not contain what some had hoped for. On April 14, 2003, the
International Human Genome Consortium announced the successful
completion of the Human Genome Project—two years ahead of schedule. The
press report read: “
The human genome is complete and the Human Genome Project is over”
(see “Human Genome Report...,” 2003, emp. added). Most of the major
science journals reported on the progress in the field of genetics, but
also speculated on how the information would now be used. The one piece
of information that never materialized from the Human Genome Project was
the identification of the so-called “gay gene.”
Homosexuality has been practiced for thousands of years. Simply put,
homosexuality is defined as sexual relations between like genders (i.e.,
two males or two females). It was Sigmund Freud who first postulated
that parental relationships with a child ultimately determine the
youngster’s sexual orientation. But this “nurturing” aspect has
effectively given way to the “nature” side of the equation. Can some
behaviors (e.g., alcoholism, homosexuality, schizophrenia)
be explained by genetics?
Are these and other behaviors influenced by nature or by nurture? Are
they inborn or learned? Some individuals believed that the answer would
be found hiding amidst the chromosomes analyzed in the Human Genome
Project.
The human X and Y chromosomes (the two “sex” chromosomes) have been
completely sequenced. Thanks to work carried out by labs all across the
globe, we know that the X chromosome contains 153 million base pairs,
and harbors a total of 1168 genes (see NCBI,
2004). The National Center for Biotechnology Information reports that
the Y chromosome—which is much smaller—contains “only” 50 million base
pairs, and is estimated to contain a mere 251 genes. Educational
institutions such as Baylor University, the Max Planck Institute, the
Sanger Institute, Washington University in St. Louis, and others have
spent countless hours and millions of research dollars analyzing these
unique chromosomes. As the data began to pour in, they allowed
scientists to construct gene maps—using actual sequences from the Human
Genome Project. And yet,
neither the map for the X nor the Y chromosome contains any “gay gene.”
What is the truth regarding homosexuality? Too often, speculation,
emotions, and politics play a major role in its assessment. The
following is a scientific investigation of human homosexuality.
BEHAVIORAL GENETICS AND CIVIL RIGHTS
In an effort to affect public policy and gain acceptance, the assertion
often is made that homosexuals deserve equal rights just as other
minority groups—and should not be punished for, or forbidden from,
expressing their homosexuality. The fight for the acceptance of
homosexuality often is compared to “civil rights” movements of racial
minorities. Due to America’s failure to settle fully the civil rights
issue (i.e., full and equal citizenship of racial minorities), social
liberals, feminists, and homosexual activists were provided with the
perfect “coat tail” to ride to advance their agenda. Using this
camouflage of innate civil liberties, homosexual activists were able to
divert attention away from the
behavior, and focus it on the “
rights.”
The argument goes like this: “Just as a person cannot help being black,
female, or Asian, I cannot help being homosexual. We were all born this
way, and as such we should be treated equally.” However, this argument
fails to comprehend the true “civil rights” movements. The law already
protects the civil rights of
everyone—black, white, male, female, homosexual, or heterosexual. Homosexuals enjoy the same civil rights everyone else does.
The contention arises when specific laws deprive all citizens of certain behaviors (e.g., sodomy, etc.).
We should keep in mind that these laws are the same for all members of
society. Because of certain deprivations, homosexuals feel as though
“equal” rights have been taken away (i.e., marriage, tax breaks, etc.).
Skin color and other genetic traits can be traced through inheritance
patterns and simple Mendelian genetics. Homosexuals are identified not
by a trait or a gene, but rather by their actions. Without the action,
they would be indistinguishable from all other people. It is only when
they alter their behavior that they become a group that is recognized as
being different. If we were to assume momentarily that homosexuality
was genetic, then the most one could conclude is that those individuals
were not morally responsible for being homosexual. However, that does
not mean that they are not morally responsible for
homosexual actions! Merely having the gene would not
force
one to carry out the behavior. For instance, if scientists were able to
document that a “rape gene” existed, we certainly would not blame an
individual for possessing this gene, but neither would we allow him to
act upon that rape disposition. Neil Risch and his coworkers admitted:
There is little disagreement that male homosexual orientation is not a Mendelian trait. In fact, a priori,
one would expect the role of a major gene in male homosexual
orientation to be limited because of the strong selective pressures
against such a gene. It is unlikely that a major gene underlying such a
common trait could persist over time without an extraordinary
counterbalancing mechanism (1993, 262:2064).
Evan S. Balaban, a neurobiologist at the Neurosciences Institute in San Diego, noted that
the search for the biological underpinnings of complex human traits has
a sorry history of late. In recent years, researchers and the media
have proclaimed the “discovery” of genes linked to alcoholism and mental
illness as well as to homosexuality. None of the claims...has been
confirmed (as quoted in Horgan, 1995).
Charles Mann agreed, stating: “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 were not
replicated” (1994, 264:1687). It appears that the gay gene will be added
to this category of unreplicated claims.
The real issue here is homosexual
actions that society has
deemed immoral and, in many instances, illegal. Since no study has
firmly established an underlying genetic cause for homosexuality,
arguments suggesting “equal rights” are both baseless and illogical.
REAL STATISTICS
Anyone who has tuned into prime-time television within the past few
years has observed an increasing trend of shows featuring characters who
are homosexual—and proud of it. It seems as though modern sitcoms
require “token” homosexuals in order to be politically correct. The
perception is that these individuals share the same apartment buildings,
offices, clubs, etc., with heterosexual people, and that we need to
realize just how prevalent homosexuality is. So, exactly what fraction
of the population do homosexuals actually represent?
The famous Kinsey Institute report often is cited as evidence that 10% of the population is homosexual. In his book,
Is It a Choice?: Answers to 300 of the Most Frequently Asked Questions About Gays and Lesbians,
Eric Marcus used the Kinsey studies to demonstrate that one in ten
people is homosexual (1993). In truth, Kinsey never reported figures
that high. The Kinsey Report clearly stated that: “Only about
4 percent
of the men [evaluated] were exclusively homosexual throughout their
entire lives.... Only 2 or 3 percent of these women were exclusively
homosexual their entire lives” (see Reinisch and Beasley, 1990, p. 140).
However, there is good reason to believe that the real percentage is
not even this high.
While no one has carried out a door-to-door census, we do have a fairly
accurate estimate. Interestingly, these statistics came to light in an
amicus curiae
(“friend of the court”) brief filed with the U.S. Supreme Court on
March 26, 2003, in the Lawrence vs. Texas case (commonly known as the
Texas sodomy case). On page 16 of this legal brief, footnote 42 revealed
that 31
homosexual and pro-homosexual groups admitted the following:
The most widely accepted study of sexual practices in the United States is the National Health and Social Life Survey (NHSLS). The NHSLS
found that 2.8% of the male, and 1.4% of the female population identify
themselves as gay, lesbian, or bisexual (Laumann, et al., 1994).
The study also found that only 0.9% of men and 0.4% of women reported
having only same-sex partners since age 18—a figure that would represent
a total of only 1.4 million Americans as homosexual (based on the last
census report, showing roughly 292 million people living in America).
The resulting accurate figures demonstrate that significantly less than
one percent of the American population claims to be homosexual. The NHSLS
results are similar to a survey conducted by the Minnesota Adolescent
Health Survey (1986) of public school students. The survey showed that
only 0.6% of the boys and 0.2% of the girls identified themselves as
“mostly or 100% homosexual.”
The 2000 census sheds even more light on the subject. The overall statistics from the 2000 Census Bureau revealed:
-
The total population of the U.S. is 285,230,516.
-
The total number of households in the U.S. is 106,741,426.
-
The total number of unmarried same-sex households is 601,209.
Thus, out of a population of 106,741,426 households, homosexuals represent 0.42% of those households.
That is less than one half of one percent!
But since most people are not mathematicians, we would like to make
this point in a way that most individuals will be able to better
comprehend. If we were to start a new television sitcom, and wanted to
accurately portray homosexual ratios in society, we would need
199 heterosexual actors before we finally introduced
one homosexual actor.
And yet modern television casts of three or four often include one or
more homosexual actor(s). The statistics from the 2000 census are not
figures grabbed from the air and placed on a political sign or Web site
to promote a particular agenda. These were census data that were
carefully collected from the
entire United States population, contrary to the limited scope of studies designed to show a genetic cause for homosexuality.
IS HOMOSEXUALITY GENETIC?
It is one of the most explosive topics in society today. The social and
political ramifications affect the very roots of this country. But is
the country being told the truth concerning homosexuality? Is there
really a genetic basis for homosexuality?
Former democratic presidential candidate and Vermont Governor Howard
Dean signed a bill legalizing civil unions for homosexuals in Vermont.
In defending his actions, he commented: “The overwhelming evidence is
that there is a very significant, substantial genetic component to it.
From a religious point of view, if God had thought homosexuality is a
sin, he would not have created gay people” (as quoted in VandeHei,
2004). Dean is not alone in such thinking.
Most
people are familiar with the idea that research has been performed that
allegedly supports the existence of a gay gene. However, that idea has
been a long time in the making. Almost fifty years ago, the landmark
Kinsey report was produced using the sexual histories of thousands of
Americans. While that report consisted of a diverse sample, it was not a
representative sample of the general population (Kinsey, et al., 1948,
1953). In 1994, Richard Friedman and Jennifer Downey published a review
on homosexuality in
The New England Journal of Medicine. In reviewing Kinsey’s work, they noted:
Kinsey reported that 8 percent of men and 4 percent of women were
exclusively homosexual for a period of at least three years during
adulthood. Four percent of men and 2 percent of women were exclusively
homosexual after adolescence (1994, 331:923).
With this “statistical information” in hand, some sought to change the
way homosexuality was viewed by both the public and the medical
community. Prior to 1973, homosexuality appeared in the
Diagnostic and Statistical Manual of Mental Disorders (DSM)
,
the official reference book used by the American Psychiatric
Association for diagnosing mental disorders in America and throughout
much of the rest of the world. Homosexuality was considered a sickness
that doctors routinely treated. In 1973, however, it was removed as a
sexual disorder, based on the claim that it did not fulfill the
“distress and social disability” criteria that were used to define a
disorder. Today, there is no mention of homosexuality in the DSM-IV
(aside from a section describing gender identity disorder), indicating
that individuals with this condition are not suitable candidates for
therapy (see American Psychiatric Association, 2000).
Physicians treating patients for homosexuality (to bring about a change
in sexual orientation) frequently are reported to ethics committees in
an attempt to have them cease. Robert Spitzer lamented:
Several authors have argued that clinicians who attempt to help their
clients change their homosexual orientation are violating professional
ethical codes by providing a “treatment” that is ineffective, often
harmful, and reinforces in their clients the false belief that
homosexuality is a disorder and needs treatment (2003, 32:403).
Thus, the stage was set for the appearance of a “gay gene.”
SIMON LEVAY—BRAIN DIFFERENCES
The first “significant” published study that indicated a possible
biological role for homosexuality came from Simon LeVay, who was then at
the Salk Institute for Biological Studies in San Diego, California. In
1991, Dr. LeVay reported subtle differences between the brains of
homosexual and heterosexual men (1991). LeVay measured a particular
region of the brain (the interstitial nuclei of the anterior
hypothalamus—INAH) in postmortem tissue of three
distinct groups: (1) women; (2) men who were presumed to be
heterosexual; (3) and homosexual men.
LeVay’s Reported Findings
LeVay reported that clusters of these neurons (INAH)
in homosexual men were the same size as clusters in women, both of
which were significantly smaller than clusters in heterosexual men.
LeVay reported that the nuclei in INAH 3 were
“more than twice as large in the heterosexual men as in the women. It
was also, however, more than twice as large in the heterosexual men as
in the homosexual men” (1991, 253:1034). This difference was interpreted
as strong evidence of a biological link to homosexuality. LeVay’s
assumption was that homosexual urges can be biologically based—so long
as cluster size is accepted as being genetically determined.
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Diagram showing INAH area. LifeART images copyright © 2004 Lippincott Williams & Wilkins. All rights reserved. Used by permission.
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Problems with LeVay’s Study
When looking at the methodology of the LeVay study, one of the key
problems is that the study has never been reproduced. As William Byne
noted, LeVay’s work
has not been replicated, and human neuroanatomical studies of this kind
have a very poor track record for reproducibility. Indeed, procedures similar to those LeVay used to identify nuclei have previously led researchers astray (1994, 270[5]:53, emp. added).
Additionally, of nineteen homosexual subjects used in the study, all
had died of complications of acquired immunodeficiency syndrome (AIDS). AIDS
has been shown to decrease testosterone levels, so it should be
expected that those who suffered from that condition would have smaller INAH. Byne continued his comments on LeVay’s work.
His inclusion of a few brains from heterosexual men with AIDS did not adequately address the fact that at the time of death, virtually all men with AIDS
have decreased testosterone levels as the result of the disease itself
or the side effects of particular treatments. To date, LeVay has
examined the brain of only one gay man who did not die of AIDS (270:53).
Furthermore, in a scientific environment where controls and standards
are a necessity, LeVay did not possess a complete medical history of the
individuals included in his study. He therefore was forced to
assume the sexual orientation of the non-AIDS
victims as being heterosexual, when some may not have been. In
addition, bear in mind that he had no evidence regarding the sexual
orientation of the women whose brains he examined. LeVay has admitted:
It’s important to stress what I didn’t find. I did not prove that
homosexuality is genetic, or find a genetic cause for being gay. I
didn’t show that gay men are born that way, the most common mistake
people make in interpreting my work. Nor did I locate a gay center in
the brain (as quoted in Byrd, et al., 2001, emp. added).
Many have argued that what LeVay discovered in the brains of those he examined was only a
result of prior behavior, not the
cause
of it. Mark Breedlove, a researcher at the University of California at
Berkeley, has demonstrated that sexual behavior has an effect on the
brain. In referring to his own research, Breedlove commented: “These
findings give us proof for what we theoretically know to be the
case—that sexual experience can alter the structure of the brain, just
as genes can alter it.... [I]t is possible that differences in sexual
behavior cause (rather than are caused by) differences in the brain” (as
quoted in Byrd, et al., parenthetical item in orig.). Considering this
type of research, it makes sense that a homosexual lifestyle (and/or the
AIDS condition) could alter the size of the nuclei LeVay was measuring.
What exactly did LeVay find? In actuality, not much. He did observe
slight differences between the groups—if you accept the method he used
for measuring the size of the neuron clusters (and some researchers do
not). When each individual was considered by himself, there was not a
significant difference; only when the individuals involved in the study
were considered in groups of homosexuals vs. heterosexuals did
differences result. Hubbard and Wald commented on this lack of
difference:
Though, on average, the size of the hypothalamic nucleus LeVay
considered significant was indeed smaller in the men he identified as
homosexual, his published data show that the range of sizes of the
individual samples was virtually the same as for the heterosexual men.
That is, the area was larger in some of the homosexuals than in many of
the heterosexual men, and smaller in some of the heterosexual men than
in many of the homosexuals. This means that, though the groups showed
some difference as groups, there was no way to tell anything about an individual’s sexual orientation by looking at his hypothalamus (1997, pp. 95-96, emp. added).
Being homosexual himself, it is no surprise that LeVay observed:
“...[P]eople who think that gays and lesbians are born that way are more
likely to support gay rights.” In a
Newsweek article, LeVay was
quoted as saying, “I felt if I didn’t find any [difference in the
hypothalamuses], I would give up a scientific career altogether” (as
quoted in Gelman, et al., 1992, p. 49). Given how (poorly) twisted
LeVay’s data are, and his own personal bias, his abandonment of science
may have ultimately been of greater service.
Brain Plasticity—A Fact Acknowledged by All Neuroscientists
Today, scientists are keenly aware of the fact that the brain is not as
“hard-wired” or permanently fixed as once thought—an important factor
that LeVay failed to acknowledge. One of the properties of plastic is
flexibility—many containers are made out of plastic so that they will
not shatter when dropped. In a similar manner, the brain was once
considered to be rigid, like Ball
®
jars used for canning—but we now know the brain is “plastic” and
flexible, and able to reorganize itself. Research has shown that the
brain is able to remodel its connections and grow larger, according to
the specific areas that are most frequently utilized. Given that we know
today that the brain exhibits plasticity, one must ask if the act of
living a homosexual lifestyle itself might be responsible for the
difference LeVay noted? Commenting on brain plasticity, Shepherd noted:
The inability to generate new neurons might imply that the adult
nervous system is a static, “hard-wired” machine. This is far from the
truth. Although new neurons cannot be generated, each neuron retains the
ability to form new processes and new synaptic connections (1994).
Interestingly, since Shepherd’s textbook was published, additional
research has even documented the ability of neurons to be generated
within certain areas of the brain. This information must be considered
when examining comparative anatomical experiments such as LeVay’s. These
cortical rearrangements that occur are not as simple as unplugging a
lamp and plugging it into another socket. The changes observed by
researchers indicate that if the brain were represented by a home
electrical system, then many of the wires within the walls would be
pulled out, rewired to different connections in different rooms, new
outlets would appear, and some would even carry different voltages. Due
to the colossal connectivity that takes place within the brain, any
“rewiring” is, by its very nature, going to have an effect on several
areas—such as INAH3. Scientists understand these things, yet LeVay’s work is still mentioned as alleged support for the so-called gay gene.
BAILEY AND PILLARD—
THE FAMOUS “TWINS” STUDY
One of the most frequently cited studies used in promoting the genetics
of sexual orientation is a 1952 study by Kallmann. In this famous work,
he reported a concordance rate (or genetic association) of 100% for
sexual orientation among monozygotic (identical) twins (1952, 115:283).
This result, if true, would prove nearly insurmountable for those people
who doubt the biological causation of homosexuality. However, Kallmann
subsequently conjectured that this perfect concordance was an artifact,
possibly due to the fact that his sample was drawn largely from mentally
ill and institutionalized men (see Rainer, et al., 1960, 22:259). But
Kallmann’s research opened the door to twin studies in regard to sexual
orientation.
Michael Bailey and Richard Pillard, researchers at Northwestern
University and the Boston University School of Medicine, carried out a
similar experiment, examining 56 pairs of identical twins, 54 pairs of
fraternal twins, 142 non-twin brothers of twins, and 57 pairs of
adoptive brothers (1991, 48:1089-1096). Bailey and Pillard were looking
to see if homosexuality was passed on through familial lines, or if one
could point to environmental factors as the cause. Their hypothesis: if
homosexuality is an inherited trait, then more twin brothers would be
expected to have the same orientation than non-twin or non-biological
brothers.
Their Reported Findings
-
52% of identical (monozygotic) twins of homosexual men were homosexual
-
22% of fraternal (dizygotic) twins were likewise homosexual
-
11% of adoptive brothers of homosexual men were homosexual
-
9.2% of non-twin biological siblings reported homosexual orientations
(Bailey and Pillard, 1991, “A Genetic Study of Male Sexual Orientation”)
-
48% of identical twins of homosexual women were likewise homosexual
-
16% of fraternal (dizygotic) twins were likewise homosexual
-
6% of adoptive sisters of homosexual women were likewise homosexual
(Bailey and Benishay, 1993, “Familial Aggregation of Female Sexual
Orientation”)
Problems with Bailey and Pillard’s Study
While the authors acknowledged some of the flaws with their research, they still were quoted in
Science News
as saying: “Our research shows that male sexual orientation is
substantially genetic” (as quoted in Bower, 1992, 141:6). However, the
most glaring observation is that clearly not 100% of the identical twins
“inherited” homosexuality.
If there was, in fact, a “gay gene,” then all of the identical twins should have reported a homosexual orientation. And yet, in nearly half of the twins studied, one brother was
not homosexual. In a technical-comment letter in
Science,
Neil Risch and colleagues pointed out: “The biological brothers and
adoptive brothers showed approximately the same rates. This latter
observation suggests that there is no genetic component, but rather an
environmental component shared in families” (1993, 262:2063). In fact,
more
adoptive brothers shared homosexuality than non-twin
biological brothers. If there was a genetic factor, this result would be counter to the expected trend. Byne and Parsons noted:
However, the concordance rate for homosexuality in nontwin biologic
brothers was only 9.2—significantly lower than that required by simple
genetic hypothesis, which, on the basis of shared genetic material,
would predict similar concordance rates for DZ
[dizygotic] twins and nontwin biologic brothers. Furthermore, the fact
that the concordance rates were similar for nontwin biologic brothers
(9.2%) and genetically unrelated adoptive brothers (11.0%) is at odds
with a simple genetic hypothesis, which would predict a higher
concordance rate for biological siblings (1993, 50:229).
A more recently published twin study failed to find similar concordance
rates. King and McDonald studied 46 homosexual men and women who were
twins. The concordance rates that they reported were 10%, or 25% with
monozygotic twins—depending on whether or not the bisexuals were
included along with the homosexuals. The rates for dizygotic twins were
8% or 12%, again, depending on whether bisexuals were included (King and
McDonald, 1992). Byne and Parsons commented: “These rates are
significantly lower than those reported by Bailey and Pillard; in
comparison of the MZ [monozygotic] concordance
rate, including bisexuals (25%), with the comparable figure from Bailey
and Pillard (52%)” (p. 230). They went on to observe: “Furthermore, if
the concordance rate is similar for MZ and DZ twins,
the importance of genetic factors would be considerably less than that suggested by Bailey and Pillard” (p. 230, emp. added).
Another factor that may have had a drastic affect on the results of
this study (and other similar studies) centers on methodology. Bailey
and Pillard did not study a
random sample of homosexuals.
Instead, the subjects were recruited through advertisements placed in
homosexual publications. This method can be deemed questionable because
it is highly dependent on the readership of those publications and on
the motives of those who respond. Thus, it may lead to skewed
results—for example, inflated rates of concordance in identical twins
owing to preferential participation (see Baron, 1993). Hubbard and Wald
observed:
The fact that fraternal twins of gay men were roughly twice as likely
to be gay as other biological brothers shows that environmental factors
are involved, since fraternal twins are no more similar biologically
than are other biological brothers. If being a fraternal twin exerts an
environmental influence, it does not seem surprising that this should be
even truer for identical twins, who the world thinks of as “the same”
and treats accordingly, and who often share those feelings of sameness
(1997, p. 97).
In summarizing their findings, Byne and Parsons stated: “Critical
review shows the evidence favoring a biologic theory to be lacking”
(50:228). Commenting on Bailey and Pillard’s report, researchers
Billings and Beckwith wrote:
While the authors interpreted their findings as evidence for a genetic
basis for homosexuality, we think that the data in fact provide strong
evidence for the influence of the environment (1993, p. 60).
When evaluated scientifically, twin studies fail to provide any valid support for the longed-for “gay gene.”
DEAN HAMER—THE GAY GENE
ON THE X CHROMOSOME
Two years after Simon LeVay’s report, a group led by Dean H. Hamer of
the National Cancer Institute allegedly linked male homosexuality to a
gene on the X chromosome. His team investigated 114 families of
homosexual men. Hamer and his colleagues collected family history
information from 76 gay male individuals and 40 gay brother pairs as
they searched for incidences of homosexuality among relatives of gay
men.
In many families, gay men had gay relatives through maternal lines.
Thus, they concluded that a gene for homosexuality might be found on the
X chromosome, which is passed from the mother alone. They then used DNA linkage analysis in an effort to find a correlation between inheritance and homosexual orientation.
Their Reported Findings
Because many of the families with a prevalence of homosexual relatives had a common set of DNA
markers on the X chromosome, Hamer’s group assumed a genetic etiology.
Of the 40 pairs of homosexual brothers he analyzed, Hamer found that 33
exhibited a matching DNA region called q28—a gene
located at the tip of the long arm of the X chromosome. In summarizing
their findings, Hamer and colleagues noted: “Our experiments suggest
that a locus (or loci) related to sexual orientation lies within
approximately 4 million base pairs of DNA on the
tip of the long arm of the X chromosome” (1993, 261:326, parenthetical
item in orig.). This discovery prompted Hamer and his colleagues to
speculate:
The linkage to markers on Xq28, the subtelomeric region of the long arm
of the sex chromosome, had a multipoint lod score of 4.0, indicating
a statistical confidence level of more than 99 percent that at least
one subtype of male sexual orientation is genetically influenced (261:321, emp. added).
It is important to note that Hamer did not claim to have found a “gay
gene,” or even the set of genes, that might contribute to a propensity
for homosexuality. According to
Chicago Tribune staff writer, John Crewdson, what Hamer claimed to have found was “statistical evidence that such genes exist” (1995).
Problems with Hamer’s Study
One of the most significant problems with Hamer’s approach is that he
and his colleagues did not feel that it was necessary to check whether
any of the heterosexual men in these families shared the marker in
question! Would it not be useful to know whether or not this “gay gene”
is found in heterosexuals? Even if only a few of them possess the gene,
it calls into question what the gene or the self-identification
signifies. Additionally, Hamer never explained why the other seven pairs
of brothers
did not display the same genetic marker. If this is
“the gene” for homosexuality, then one must assume all homosexual
individuals would possess that particular marker—and yet that was not
the case in Hamer’s study.
In a letter to
Science, Anne Fausto-Sterling and Evan Balaban pointed out some of the additional problems with Hamer’s study. They noted:
Despite our praise for aspects of Hamer, et al.’s work, we feel
it is also important to recognize some of its weaknesses. The most
obvious of these is the lack of an adequate control group. Their study
demonstrates cosegregation of a trait (which Hamer, et al. have
labeled “homosexuality”) with X chromosome markers and the trait’s
concordance in homosexual brothers. This cosegregation is potentially
meaningful if the mother is heterozygous for the trait. In this case,
segregating chromosomes without the markers should show up in
nonhomosexual brothers, but Hamer, et al. present no data to that effect (1993, 261:1257, emp. added).
Fausto-Sterling and Balaban continued:
This sensitivity to assumptions about background levels makes Hamer, et al.’s
data less robust than the summary in their abstract indicates....
Finally we wish to emphasize a point with which we are sure Hamer, et al. would agree: correlation does not necessarily indicate causation (261:1257).
In other words, Hamer’s methodology leaves something to be desired. One
also should keep in mind that Hamer’s sampling was not random, and, as a
result, his data may not reflect the real population.
George Rice and his colleagues from Canada looked intently at the gene
Xq28. They then observed: “Allele and halotype sharing for these markers
was not increased over expectation.
These results do not support an X-linked gene underlying male homosexuality” (1999, 284:665, emp. added). Rice, et al., included 182 families in their study. They noted:
It is unclear why our results are so discrepant from Hamer’s original
study. Because our study was larger than that of Hamer et al., we
certainly had adequate power to detect a genetic effect as large as was
reported in that study. Nonetheless, our data do not support the
presence of a gene of large effect influencing sexual orientation at
position Xq28 (284:667).
That is a tactful way of saying that any claims of having found a “gay
gene” were overblown, if not outright false, and that Hamer’s results
are dubious at best. Commenting on the study of Rice and his colleagues,
Ingrid Wickelgren remarked: “...the Ontario team found that gay
brothers were no more likely to share the Xq28 markers than would be
expected by chance.... Ebers interprets all these results to mean that
the X linkage is
all but dead” (1999, 284:571, emp. added).
In June of 1998, University of Chicago psychiatrist Alan Sanders
reported at the meeting of the American Psychiatric Association that he,
too, had been unable to verify Hamer’s results. Looking for an increase
in Xq28 linkage, Sanders’ team studied 54 pairs of gay brothers. As
Wickelgren indicated, Sanders’ team had found “only a weak hint—that
wasn’t statistically significant—of an Xq28 linkage among 54 gay brother
pairs” (284:571). Commenting on the validity of Hamer’s study,
Wickelgren quoted George Rice: “Taken together, Rice says,
the results ‘suggest that if there is a linkage it’s so weak it’s not important’” (1999, emp. added). Two independent labs failed to reproduce anything even remotely resembling Hamer’s results.
CHANGEABILITY OF HOMOSEXUALS—
EVIDENCE AGAINST GENETICS
An individual born with diabetes has no hope of changing that
condition. Likewise, a child born with Down’s syndrome will carry that
chromosomal abnormality throughout his or her life. These individuals
are a product of the genes they inherited from their parents.
Homosexuality appears to be vastly different. Many people have been able
to successfully change their sexual orientation. [Truth be told, some
individuals experiment with a variety of sexual
partners—male/female—often, going back and forth. One might inquire if
the bisexuality denotes the existence of a “bisexual gene?”] Ironically,
however, the removal of homosexuality as a designation from the
Diagnostic and Statistical Manual of Psychiatric Disorders by the American Psychiatric Association has kept many physicians from attempting to provide reparative therapy to homosexuals.
Robert Spitzer conducted a study on 200 self-selected individuals (143
males, 57 females) in an effort to see if participants could change
their sexual orientation from homosexual to heterosexual (2003,
32:403-417). He reported some minimal change from homosexual to
heterosexual orientation that lasted at least five years (p. 403).
Spitzer observed:
The majority of participants gave reports of change from a
predominantly or exclusively homosexual orientation before therapy to a
predominantly or exclusively heterosexual orientation in the past year
(p. 403).
In summarizing his findings, Spitzer declared: “Thus, there is evidence
that change in sexual orientation following some form of reparative
therapy does occur in some gay men and lesbians.” He thus concluded:
“This study provides evidence that some gay men and lesbians are able to
also change the core features of sexual orientation” (p. 415).
Six years earlier, the National Association for Research and Therapy of Homosexuality (NARTH) released the results of a two-year study stating:
Before treatment, 68 percent of the respondents perceived themselves as
exclusively or almost entirely homosexual, with another 22 percent
stating that they were more homosexual than heterosexual. After
treatment, only 13 percent perceived themselves as exclusively or almost
entirely homosexual, while 33 percent described themselves as either
exclusively or almost entirely heterosexual (see Nicolosi, 2000,
86:1071).
The study also reported:
Although 83 percent of respondents indicated that they entered therapy
primarily because of homosexuality, 99 percent of those who participated
in the survey said they now believe treatment to change homosexuality
can be effective and valuable (p. 1071).
These data are consistent with the ongoing research project of Rob
Goetze, who has identified 84 articles or books that contain some
relevance to the possibility of sexual orientation change (2004). Of the
data reported, 31 of the 84 studies showed a quantitative outcome of
individuals able to change sexual orientation. These are not studies
that merely speculate on the ability to change; they actually have the
numbers to back it up! All of these data come on the heels of warnings
from the Surgeon General, The American Academy of Pediatrics, and all of
the major mental health associations, which have issued position
statements warning of possible harm from such therapy, and have asserted
that there is no evidence that such therapy can change a person’s
sexual orientation. For instance, the 1998 American Psychiatric
Association Position Statement on Psychiatric Treatment and Sexual
Orientation noted:
...there is no published scientific evidence supporting the efficacy of
reparative therapy as a treatment to change one’s sexual
orientation.... The potential risks of reparative therapy are great,
including depression, anxiety, and self-destructive behavior (see
American Psychiatric Association, 1999, p. 1131).
Thus, physicians are caught in a quandary of a double standard. On the
one hand, they are told that it is “unethical” for a clinician to
provide reparative therapy because homosexuality is not a diagnosable
disorder, and thus one should not seek to change. Yet, they contend that
not enough studies have been conducted to determine the effectiveness
of reparative therapy. The message is loud and clear: “Do not do this
because it is unethical to ask a homosexual person to change. However,
truth be told, we have not collected enough data to know if a person can
safely change his or her sexual orientation.”
In situations where sexual orientation is being measured, studies face
serious methodological problems (i.e., follow-up assessment, possible
bias, no detailed sexual history, random sampling, etc.). But even given
these serious shortcomings from behavioral studies such as these, there
are sufficient data to indicate that an individual can change his or
her sexual orientation from homosexual to heterosexual—something that
would be an impossibility if homosexuality were caused by genetics.
CONCLUSION
Consider the obvious problem of survival for individuals who allegedly possess a gay gene:
individuals who have partners of the same sex are biologically unable to reproduce
(without resorting to artificial means). Therefore, if an alleged “gay
gene” did exist, the homosexual population eventually would disappear
altogether. We now know that it is not scientifically accurate to refer
to a “gay gene” as the causative agent in homosexuality. The available
evidence clearly establishes that no such gene has been identified.
Additionally, evidence exists which documents that homosexuals can
change their sexual orientation. Future decisions regarding policies
about, and/or treatment of, homosexuals should reflect this knowledge.
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