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New Theory: Homosexuality Is a Mistake of Nature

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New Theory: Homosexuality Is a Mistake of Nature

James R. Aist

Introduction

Homosexuality is believed to be caused by some combination of biological and environmental factors. Several biological theories have been offered, the most feasible being the genetic, the hormonal and the epigenetic theories. In 2012, a new theory was introduced that combines aspects of the genetic theory with the hormonal theory. This is the epigenetic theory. Epigenetics is a relatively new and vigorously investigated field of biological science that deals with the regulation of gene expression (production of proteins) in cells. The components of chromosomes that regulate genes are called “epi-marks.” These include such things as methylated DNA and variously modified histone proteins, but do not include changes in the DNA sequences themselves that code for specific proteins.

The Theory

Rice et al. (2012) published a review article presenting a speculative and hypothetical model (theory) to explain the development of homosexuality in both male and female homosexuals. Their goal was to develop a model that would explain why 1) molecular studies have failed to conclusively identify “gay genes” and 2) concordance for homosexuality between identical twins is low (click HERE). The theory draws on research supporting the hormonal theory as well as known properties and functions of epi-marks. The model would explain homosexuality on the basis of epi-mark-controlled prenatal testosterone (a sex hormone) levels, to the virtual exclusion of a role for either a strictly genetic influence or post-natal environmental influences.

Normally, epi-marks regulating sexual orientation are “erased” after they have produced the intended sexual development (i.e., heterosexual males and females). But, occasionally, a mistake is made, and the epi-mark is not erased but is, instead, passed on to the next generation. According to the model, when this mistake is made, epi-mark regulated testosterone overexposure in a female fetus would result in a masculinized female who will prefer females (a lesbian), whereas epi-mark regulated testosterone underexposure in a male fetus would result in a feminized male who will prefer males (a gay). The low concordance in twin studies would be explained not by a low-level genetic influence, as is usually assumed, but by the occasional passing of testosterone-enhancing epi-marks from father to daughter (creating a lesbian) and of testosterone-limiting epi-marks from mother to son (creating a gay man).

It is interesting to note that this model posits homosexuality as an aberrant accident of nature, in which normal prenatal development of a fetus produces the intended effect (heterosexuality), and abnormal prenatal development produces an unintended effect (homosexuality) by mistake. Abnormal prenatal development results when a mistake is made and an epi-mark in a parent is not erased, but is, instead, passed on to the offspring, where its effect (homosexuality) is seen in the subsequent generation. Thus, according to this theory, homosexuality is a mistake of nature, and it is not biologically normal, as gay activists want us to believe.

Although this model is highly speculative and presently has very little, if any, direct experimental support, it does have merit as a scientific hypothesis, because 1) it would explain both male and female homosexuality, 2) it could explain the low concordance for homosexuality found in twin studies, 3) it seems to provide a feasible explanation for the long-term survival of a reproductively deleterious trait in the human population, and 4) it is, at least to some extent, testable. Only further research will determine whether or not this theory will join the many previous theories purporting to represent an almost exclusive influence on the development of homosexuality, all of which have failed.

Caveat

Twin studies have shown that the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epigenetics, hormones, etc.) on the development of homosexuality in adults is only weak to weakly moderate (click HERE). Thus, post-natal influences (e.g., cultural, social and experiential factors) are far more influential than is epigenetics in the development of homosexuality (click HERE).

Reference Cited:

Rice, G., et al. 2012. Homosexuality as a Consequence of Epigenetically Canalized Sexual Development. Quarterly Review of Biology 87:343-368.

(For more articles on HOMOSEXUALITY, click HERE)

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What Twin Studies Tell Us about Homosexuality: Nature vs. Nurture

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What Twin Studies Tell Us about Homosexuality: Nature vs. Nurture

James R. Aist

(Note: Numbers in parentheses refer to specific, numbered references listed at the end of the article.)

Introduction

I presented a much broader treatment of possible causes of homosexuality elsewhere (click HERE). Most of the more recent research on possible biological origins of homosexuality has focused on the degree to which genes, along with other prenatal factors such as hormones and epi-genetics, may influence the development of homosexuality. In this regard, the most conclusive and telling results have come from studies of “identical” twins (who both have virtually the exact same complement of genes). Although it is commonly assumed that identical-twin studies reveal the influence of genes per se on a trait or behavior, the results of such studies have the unique advantage of reflecting, in fact, the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epi-genetics, hormones, etc.) on the development of homosexuality in adults (1). This is because identical twins not only share the same complement of genes, but they also share the same pre-natal environment (their mother’s womb), where biological factors are postulated to operate.

Twin Studies: Overview

The design of research studies using identical twins has improved greatly since the mid-1990s, with the advent of large, twin registries which can afford much larger data bases and less biased sampling procedures. The former approach of recruiting identical twins via advertisements in gay and lesbian publications is now known to have a very strong “volunteer effect” that produced the appearance of relatively large genetic effects (1). Nevertheless, even with the use of large twin registries, the number of identical twin pairs found with homosexuality is often very small in individual studies, resulting in a standard deviation that is greater than the calculated genetic effect, meaning that the results are not statistically different from zero. In other words, the genetic influence or contribution in several of these studies may actually be zero, making definitive conclusions impossible. Whitehead and Whitehead (1) have presented and discussed, in some detail, these and other problems inherent in twin studies of homosexuality and have presented reasons to expect that the genetic influence on, or contribution to, homosexuality will eventually be agreed to be in the 10%-15% range (i.e., weak). One reason for this (anticipated) lower actual genetic influence is that epi-genetic effects operating through identical twins sharing one placenta probably represent about 15% of the total influence that has been attributed to genetics in published twin studies (2). Another reason has to do with the apparently predominant influence of post-natal environmental factors on the development of homosexuality (10). Schumm (9) found that children with homosexual parents are 12-15 times more likely than children of heterosexual parents to be homosexual as adults. This is the strongest environmental influence ever reported for the development of homosexuality, and it involves very close family members, the parent-child relationship. In a family environment, identical twins share a common bond and common experiences more so than do other siblings, including non-identical twins; siblings can’t be any “closer” than that. The results of a study by King and McDonald (8) illustrate how such a close, family relationship could inflate the calculated genetic influence on homosexuality in identical twin studies. They studied 46 twin pairs having homosexuality present in one or both of the twins in each pair and found that 54% of the twin pairs had discussed their sexual orientation with each other, 89% had “shared knowledge” of each other’s sexual orientation, and 30% of these twin pairs had actually had sex with each other. Because identical twins identify so closely with each other, and post-natal experiences  – especially close family relationships – strongly affect the development of homosexuality, it seems plausible, if not likely, that a homosexual member of a twin pair would influence the other member of that pair to embrace and explore homosexuality also, thus inflating the apparent genetic influence reported in identical twin studies. That is to say, a significant portion of what may appear, in identical twin studies, to be a genetic influence on the development of homosexuality may turn out to be, instead, a post-natal, environmental influence involving shared knowledge of sexual orientation and shared sexual experiences within identical twin pairs.

Twin Concordance Studies

The “pair-wise concordance” answers the simple question, “Where one twin of an identical pair is homosexual, what percentage of co-twins is also homosexual”. The mathematical formula for pair-wise concordance of identical twins is C/C+D, where C is the number of concordant (similar) twin pairs and D is the number of discordant (dissimilar) twin pairs found in the study. For example, if C=1 and D=9, then the pair-wise concordance would be 1/1+9=1/10 or 10%. This result would indicate that for every twin pair with both members being homosexual, there are 9 twin pairs with only one homosexual member.

Using data provided in several reports of large, twin registry studies in different countries, I performed a meta-analysis and calculated the range of pair-wise concordance to be 9.9% to 31.6%, with the average being 13.0% for males, 13.3% for females, and 13.2% when the raw data for males and females were combined. These pair-wise concordance values indicate that for every twin pair with both members being homosexual, there are 7 twin pairs with only one homosexual member. Now, compare this result to the range of theoretically possible outcomes where no twin pairs would both be homosexual (= 0%) and where all twin pairs would both be homosexual (= 100%) and you can see, intuitively, that a pair-wise concordance of only 13.2% would indicate a real, but relatively minor, contribution of genetics to homosexuality. This minor role is similar to the estimated level of genetic contribution to virtually any kind of human behavior (3) and is known to be non-determinative and, in many cases, treatable by therapy and/or counseling. For instance, the best example to date of a genetically related behavior (mono-amine oxidase deficiency leading to aggressive behavior) has shown itself remarkably responsive to counseling (3). Therefore, on the basis of pair-wise concordance in identical twins, it seems appropriate to conclude that there is, at the most, only a minor genetic contribution to the development of homosexuality, and that this relatively minor influence can be overcome (i.e., nullified) through behavioral therapy (1), which we know to be a fact (4, 5).

The other measure of concordance in twin studies is “proband-wise” concordance. This estimate of concordance is necessary in order to use both identical and fraternal twins in a study to disentangle the relative contributions to homosexuality of genetic and non-genetic (environmental) factors. The formula used is 2C/2C+D, which, compared to the formula for pair-wise concordance, gives much more weight to the individual twins (probands). The effect is to greatly increase, relative to pair-wise concordance values, the apparent genetic contribution to homosexuality in identical twin studies. To illustrate this point, if we use the example given above where the pair-wise concordance calculates to be 1/10 = 10.0%, the proband-wise concordance calculates to be 2/11 = 18.2%. Although it is less intuitive, proband-wise concordance is generally believed to give a better overall estimate of “genetic influence” than does pair-wise concordance.

Classical Twin Studies

While pair-wise concordance gives an intuitive indication of the genetic influence on homosexuality as expressed in identical twins, it does not provide information on what factors may provide the remaining, non-genetic influence. To answer this question, researchers are using other measures, broader-ranging questionnaires and more sophisticated statistical procedures to evaluate such things as heritability, additive genetic effects and postnatal environmental influences. In order to be able to put the results of classical twin studies into perspective, it is important to keep in mind that, by convention in the twin study literature in general, a genetic contribution of around 25% is considered weak, of around 50% is considered moderate and of 75% or more is considered strong (6).

In a meta-analysis, Whitehead (6), using the results from seven of the recent twin registry studies that were designed to reveal contributions of both genetic and non-genetic factors to homosexuality, found that the mean contribution of genetics to male homosexuality was around 22%, and to female homosexuality, around 33%. Because of the relatively large standard deviations in the data, these two values were not statistically different from each other.  Thus, the mean genetic contribution to male homosexuality in these studies is weak and to female homosexuality is weakly moderate. Such levels of genetic contribution indicate a real but weak-to-weakly moderate and indeterminate role of genetics in the development of homosexuality. For comparison, other traits that have around 50% (moderate and indeterminate) genetic contribution in twin studies include such things as divorce and alcoholism, while puberty has a 90% (strong and determinate) genetic contribution (1). Furthermore, the non-shared, post-natal environmental contribution to homosexuality is moderate to strong, around 64%-78%, has a relatively small standard deviation and is consistently around the same percentage (6), indicating that homosexuality is influenced primarily by post-natal environmental factors and experiences that are not directly related to prenatal, biological contributions of any kind or combination.

The recent study by Zietsch, et al. (7) can be used to illustrate representative research results obtained with large samples from twin registries. They used a very large sample (9,884) of twins from the Australian Twin Registry, one of the largest samples to date for twin studies of homosexuality. In this sample, there were 1,840 identical twin pairs (1,133 female and 707 male). Their calculated value of only 24% for the proband-wise concordance for homosexuality indicates a weak genetic influence. Moreover, their calculated figure of 31% for heritability of homosexuality also indicates a weak genetic component. This leaves around 68% of the variance represented by post-natal, “shared environment” and “residual” environmental influences combined.

Summary

In view of the fact that twin studies have shown that the combined influence of all possible, pre-natal, biological factors (e.g., genetics, epi-genetics, hormones, etc.) on the development of homosexuality in adults is only weak-to-moderate, it is important to understand that all of the biological theories combined can address only this weak-to- weakly moderate amount of influence, while ignoring the far more important post-natal influences (e.g., culture, parental divorce, and having a homosexual parent). Furthermore, twin studies clearly support the inference, based on results obtained through therapy and counseling (4, 5), that post-natal, environmental influences have a far greater role in the development of homosexuality than do pre-natal, biological influences. Thus, where the development of homosexuality is concerned, twin studies have demonstrated that nurture is far more important than nature.

(For more articles on HOMOSEXUALITY, click HERE)

References Cited:

1. Whitehead, N. and B. Whitehead. 2016. Chapter 10. Twin studies: The strongest evidence.(click HERE)

2. Whitehead, N. and B. Whitehead. 2016. Chapter 1. Can genes create sexual preferences? (click HERE)

3. Whitehead, N. and B. Whitehead. 2016. Summary. (click HERE)

4. Whitehead, N. and B. Whitehead. 2016. Chapter 12. Can sexual orientation change? (click HERE)

5. Aist, J. 2012. Homosexuality: Good News! (click HERE)

6. Whitehead, N.E. 2011. Neither Genes nor Choice: Same-sex Attraction is Mostly a Unique Reaction to Environmental Factors. Journal of Human Sexuality 3:81-114. (click HERE)

7. Zietsch, B., et al. 2012. Do Shared Etiological Factors Contribute to the Relationship between Sexual Orientation and Depression? Psychological Medicine 42:521-532.

8. King, M., and E. McDonald. 1992. Homosexuals who are Twins. British Journal of Psychiatry 160: 407-409.

9. Schumm, W. 2010. Children of Homosexuals More Apt to be homosexuals? A Reply to Morrison and to Cameron Based on an Examination of Multiple Sources of Data. Journal of Biosocial Science 42:721-742.

10. Aist, J. 2012. Are Homosexual People Really Born Gay? (click HERE)