Gay Marriage and Diet

Jacob Schor ND, FABNO

September 13, 2015


We attended a wedding last June in Boulder, a wedding of two women who have been together for nearly 30 years and who have raised two extraordinary children together.  We have known them almost that long. One is a dear colleague and her spouse helped deliver my daughter two dozen years ago.


Rather than contemplating what seems to be the tectonic shift in attitudes regarding gay marriage over recent years during the service, I found myself dwelling on the implications  of  a conversation I overheard while eating lunch up at Mary Jane last spring. [4]    Three college students were discussing their various ‘hook ups’ over the past semester with more detail and detachment than I was accustomed to.  Granted that lifelong monogamy is quite rare among mammals [5], it is still a social construct that most people in our culture aspire to, even if not always successfully.  Nothing in this overheard discussion  gave any hint that interest in an even temporarily monogamous relationship provided any allure for these young people.  This struck me as a far greater shift in social structure in contrast to the religious service that bound these two lovely women in what all present hoped would be a lifelong social contract.


In contrast to these young people, the deep love and conviction we witnessed during the Boulder ceremony celebrated in the Episcopalian church renewed my faith in the value of marriage as a valuable force in both society and in particular individual emotional development. 


It’s one thing for gay marriage to feel acceptable in Boulder, after all lots of things are acceptable in Boulder, but this wedding occurred about the same time that Ireland, by popular referendum, voted to legalize gay marriage. 


How did things change so suddenly?


Attitudes have shifted in part because more people know friends, family members and work colleagues who are gay.  Is this just because people are no longer hiding their sexual orientations or it because there are a higher percentage of homosexuals in our population? [6]    

That is, has homosexuality become more common over recent years than it was in the past? 


Wikipedia has a page that nicely sums up current estimates of gay and lesbian populations in the United States, including state-by-state statistics, (California wins with 4% and North Dakota is last with a gay and lesbian population of only 1.7%.). [7]   There is little accurate data on changing frequency or incidence over time. The Wikipedia site lists data from only as far back as 1990.


Thus we cannot answer the most basic question, “Are there more gay people now than there used to be?”


It is interesting to note that Americans far overestimate how many gay and lesbian people there are.  “U.S. adults, on average, estimate that 25% of Americans are gay or lesbian. More specifically, over half of Americans (52%) estimate that at least one in five Americans are gay or lesbian, including 35% who estimate that more than one in four are. Thirty percent put the figure at less than 15%.” [8]   The actual number is probably closer to 3.5%. [9] 


Has frequency of homosexuality changed with environmental factors such as population density, stress, standard of living or maternal or infant exposure to hormonal mimetics during gestation?  Could the Bisphenol-A in our food packaging distort sexual programming?  Or as some of my recent correspondents appear to believe, preservatives in our food supply? There are lots of basic questions that we can’t begin to answer.


There is decent evidence that sexual orientation may be due to both genetic inheritance and some evidence that it is also related to epigenetic changes.  It is well established that identical twins are more likely to share similar sexual orientations (that is they will either both be straight or not) while fraternal twins may do not, suggesting that there is a genetic factor.


The argument for epigenetic influences comes from women with congenital adrenal hyperplasia (CAH).   In these women, the adrenal glands are unable to make the hormones cortisol and aldosterone, because the women can’t make 21-hydroxylase,  the enzyme necessary to make these hormones.  Their bodies instead produce excess androgen, a type of male sex hormone. This causes male characteristics to appear early in the case of males with this disease or inappropriately in the case of women.


These women are exposed to high levels of testosterone in utero.   They also have much higher rates of non-heterosexual orientation compared to non-CAH women. In simpler words, they are more likely to be lesbian.  Studies using animals suggest that such long-term effects of hormonal exposures such as these CAH women undergo in-utero are mediated by epigenetic mechanisms. [10,11]     


From this we might extrapolate that other environmental impacts capable of causing epigenetic changes might be changing sexual orientations.   These are tricky questions to ponder, both due to lack of information but also because people are touchy on this subject. 


In a series of papers starting in 2006, William Rice et al have advanced this theory for the epigenetic causes of homosexuality [12]  identifying particular epigenetic changes in embryonic stem cells that may boost sensitivity to testosterone in male (XY) fetuses and lower it in female (XX) fetuses. [13]  Their theory suggests that there is a subset of fetuses where these markers vary and lead to “…to mosaicism for sexual development in opposite-sex offspring--the homosexual phenotype being one such outcome.” [14]   It probably helps that Rice is a marine biologist and so has the excuse that he’s not talking about people.


This is a troubling theory because epigenetic changes are often considered to be environmental and not totally out of our control.  There are nutritional strategies that affect these epigenetic changes.  There are also chemicals polluting our environment that may also affect changes.  Thus it is not a stretch to imagine homosexuality being categorized as the result of a vitamin deficiency or the result of eating non-organic food.  We humans are often quick to jump to conclusions.


There’s an interesting paper, “The epigenetic diet’ suggesting how  diet might be used to impact cancer risk, a paper that could theoretically touch on this discussion.


“ A number of bioactive dietary components are of particular interest in the field of epigenetics. Many of these compounds display anticancer properties and may play a role in cancer prevention. Numerous studies suggest that a number of nutritional compounds have epigenetic targets in cancer cells. Importantly, emerging evidence strongly suggests that consumption of dietary agents can alter normal epigenetic states as well as reverse abnormal gene activation or silencing. Epigenetic modifications induced by bioactive dietary compounds are thought to be beneficial. Substantial evidence is mounting proclaiming that commonly consumed bioactive dietary factors act to modify the epigenome and may be incorporated into an ‘epigenetic diet’.” [15] 


Could homosexuality be a matter of diet?  That would be a stretch.  Still it is a question that’slikely never been asked.

There are a good number of foods are associated thought to have epigenetic impacts.  Sulforaphane and other chemicals found in curciferous vegetables, for example, certainly have what is considered a beneficial epigenetic impact offering protection against breast and prostate cancer. [16] 


It's not just cabbage; lots of things affect epigentics. Problems ranging from autism to heart disease and cancer are being laid at the door of folate metabolism and it’s role in methylation and epigenetic changes to cellular DNA. [17] Folate deficiency is a major factor in epigenetic changes and the current fad of taking high dose methyl hydroxy folate to ‘fix methylation defects’ may lead to some interesting changes in a generation or so.  At this point there is no direct published evidence that I’ve found that connects folate with homosexuality.


Thinking about cancer for a moment, as that’s really all that we are interested in, we know that about half of all tumor suppressor genes are inactivated through epigenetic changes during cancer development (tumorigenesis) and we are quite aware of at least some of the dietary agents that affect epigenetic processes


Dietary polyphenols such as those found in green tea, resveratrol, an curcumin inhibit DNA methyltransfereases and act as histone modifiers and this is one possible explantion for their anti-cancer action.  The isoflavones such as genistein found in soy and other beans have anticancer action that also likely involves DNA methylation and epigenetic changes. The isothiocyanates, in particular sulforaphane, derived from curciferous vegetables also affect the epigenome by acting as histone deacetylase inhibitors.  We could go on listing quite a few foods.  The curious thing here is that the foods that we think improve our health and protect us against cancer, may impact the same biochemistry that Rice et al think is associated with homosexuality.


Will consuming these ‘cancer fighting foods’ increase homosexuality or decrease it?  Now that’s a thought that will no doubt provoke a few email responses to this newsletter. The honest answer is that we have no idea. They certainly may protect against cancer.










4.  [Mary Jane, for those of you not from Colorado, is our local ski area about an hour west of the city, a bit north  Berthoud Pass and is not named for the common practice of using marijuana by native Colorado skiers.  Rather Mary Jane was apparently the proprietor of a railway brothel in former years]


5.  Of the roughly 5,000 species of mammals, only 3 to 5 % are known to form lifelong pair bonds.


6.  I realize that someone will write to correct my old fashioned terminology, that I should not be using homosexual or gay interchangeably.  My apologies. I’m old fashioned.








10.  Arch Meyer-Bahlburg HF1, Dolezal C, Baker SW, New MI. Sexual orientation in women with classical or non-classical congenital adrenal hyperplasia as a function of degree of prenatal androgen excess. Sex Behav. 2008 Feb;37(1):85-99.


11.  Adv Genet. 2014;86:167-84. doi: 10.1016/B978-0-12-800222-3.00008-5.

The biological basis of human sexual orientation: is there a role for epigenetics?

Ngun TC1, Vilain E1.


12.  Gavrilets S1, Rice WR. Genetic models of homosexuality: generating testable predictions. Proc Biol Sci. 2006 Dec 22;273(1605):3031-8.


13.  Rice WR1, Friberg U, Gavrilets S. Homosexuality as a consequence of epigenetically canalized sexual development. Q Rev Biol. 2012 Dec;87(4):343-68.


14.  Rice WR1, Friberg U, Gavrilets S. Homosexuality via canalized sexual development: a testing protocol for a new epigenetic model. Bioessays. 2013 Sep;35(9):764-70. doi: 10.1002/bies.201300033. Epub 2013 Jul 19.

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15.  Tabitha M Hardy and Trygve O Tollefsbol. Epigenetic diet: impact on the epigenome and cancer. Epigenomics. 2011 Aug 1; 3(4): 503–518.

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16. Regulation by Sulforaphane: Opportunities for Breast and Prostate Cancer Chemoprevention. Curr Pharmacol Rep. 2015 Apr 1;1(2):102-111.


17.  DeVilbiss EA1, Gardner RM2, Newschaffer CJ1, Lee BK1. Maternal folate status as a risk factor for autism spectrum disorders: a review of existing evidence. Br J Nutr. 2015 Aug 5:1-10. [Epub ahead of print]