XENOESTROGENS AND INTERSEXUALITY

Xenoestrogens, also called endocrine disruptors, have been demonstrated in multiple studies to be the cause of genital underdevelopment in males, as explained in my book The Complete Guide to Penis Enlargement 2018.

This poses a serious question: if xenoestrogens influence the development of male sexual organs, could they also be influencing that of other organs like the brain?

And if the answer is yes, could they be the cause of the increase in the last 50–60 years in the confusion in gender identity and same-sex attraction in both sexes?

To be able to answer this question, let’s first see how gender identity is obtained in a human being, starting from its life as a fetus.

During the intrauterine period, the fetal brain develops in the male direction through the direct action of testosterone on the developing nerve cells or in the female direction in the absence of this hormone surge. In human neonates, the testosterone level is tenfold higher in males than in females at 34–41 weeks of gestation (Zegher et al. 1992).

In this way, our gender identity (the conviction of belonging to the male or female gender) and sexual orientation are programmed into our brain structures when we are still in the womb.

However, since sexual differentiation of the genitals takes place in the first two months of pregnancy and sexual differentiation of the brain starts in the second half of pregnancy, these two processes can be influenced independently, which may result in transsexuality.

Figure 1: The external genital structures in males and females as they differentiate during fetal development, and also the typical appearance at birth (Tye 2013).

This also means that in the event of ambiguous sex at birth (intersex *1 ), the degree of masculinization of the genitals may not reflect the degree of masculinization of the brain (Swaab et al. 2010).

It is androgen hormones that switch the growth of a fetus from female (we all start as non-gender specific or females in the fetus) to male, allowing the male chromosome Y component to fully express.

Any alteration of the action of androgen would inhibit this differentiation.

Swaab in his study claimed that the most critical phase for sexual differentiation is the prenatal phase, in fact observations in male subjects with cloacal exstrophy (a severe birth defect wherein much of the abdominal organs, the bladder and intestines, are exposed. It often causes the splitting of both male and female genitalia -specifically, the penis and clitoris respectively - and the anus is occasionally sealed), who were sex-reassigned to females at birth and later declared themselves male, indicated that it is the prenatal testosterone surge that is most important for the development of gender identity in the brain (Dick F. Swaab et al. 2004), however, another study, performed in 1998 by Cooke et al., however, claims that brain differentiation is influenced up until adulthood and not only during the “prenatal testosterone surge”:

Usually, the androgen must act early in life, often during the fetal period to masculinize the nervous system and behavior. However, there are a few examples of androgen, in adulthood, masculinizing both the structure of the nervous system and behavior. In the modal pattern, androgens are required both during development and adulthood to fully masculinize brain structure and behavior Because you've cited this above (and to keep things simple), I will move the detailed reference to the reference list at the end.

So, what would happen to the brain structure of these individuals if androgens in these periods of adulthood were blocked by chemicals found in the environment like xenoestrogens?

Brain differentiation between sexes

Several studies examined various areas of the hypothalamus—a section of the brain involved in gender and sex—to see if any sex differences were present. One of these, a 1995 article by Hofman et al. published in Nature and entitled “A Sex Difference in the Human Brain and Its Relation to Transsexuality,” showed that male-to-female transsexuals have a number of neurons matching what would be found in the female brain in a region of the hypothalamus known as the bed nucleus of the stria terminalis (BSTc), supporting the idea that this brain region is responsible for gender identity in humans.

The study concludes (emphasis mine):

"Transsexuals have the strong feeling, often from childhood onwards, of having been born the wrong sex. The possible psychogenic or biological aetiology of transsexuality has been the subject of debate for many years. Here we show that the volume of the central subdivision of the bed nucleus of the stria terminals (BSTc), a brain area that is essential for sexual behaviour, is larger in men than in women. A female-sized BSTc was found in male-to-female transsexuals. The size of the BSTc was not influenced by sex hormones in adulthood and was independent of sexual orientation. Our study is the first to show a female brain structure in genetically male transsexuals and supports the hypothesis that gender identity develops as a result of an interaction between the developing brain and sex hormones".

Another study, performed in 2008 by Garcia-Falgueras and Swaab, confirms that sex reversal in homosexuals or transsexuals is at least partly a marker of an early atypical sexual differentiation of the brain. It is interesting to note that this study advances the hypothesis that social behavior could also influence sexual differentiation:

If sexual differentiation of the brain indeed takes place postnatally, not only chemical and hormonal factors may influence this process but also social factors. A prominent theory on the development of sexual orientation is that it develops as a result of an interaction between the developing brain and sex hormones.

The Xenoestrogen (EDCs) Link

So, what happens if xenoestrogens, or EDCs (Endocrine-Disrupting Chemicals), happen to block the androgens that are supposed to sexually differentiate the male brain in the pre and postnatal periods like they do with the genitals? Fetuses are the most sensitive and likely exposed to EDCs, and the male reproductive system is most vulnerable to estrogenic agents during the critical periods of cell differentiation and organ development in the fetus. Studies have shown that this brain differentiation primarily takes place in the period "that spans" from conception to four years old.

If, therefore, mothers are exposed to these substances, fetuses will most likely develop alteration in their sexuality.

The effects, of course, are dose dependent.

If androgens (testosterone and/or DHT) are blocked, suppressed, or antagonized during these delicate periods of the fetus's life by xenoestrogens (we have seen that this happens a lot in studies with pesticides – see the DHT section of my book) and/or even through adulthood, the brain's transition from having no gender to male cannot take place, or at least not fully (gene expression inhibition), since the Y gene component of the XY chromosome will not be expressed due to a lack of androgens (see XY 46 disorders of sex-differentiation DSDs).

If xenoestrogens bind to brain cells' androgen receptors or inhibit androgens somehow, there is a high chance that the “boy” will be a hermaphrodite *2 both in his body and in his brain, or that he will develop homosexual behavior since his male brain genes won’t express, while his feminine part (present in all men) will overexpress due to the estrogenization effects of xenoestrogens.

Currently, it is not known which xenoestrogen have more affinity for the brain body's androgen receptors.

In the case of homosexuals, it is possible that exposure could have been to those xenoestrogens that affect only brain receptors, and only in the second period of conception (when the brain forms), while, in transsexuals and hermaphrodites, the exposure occurred during both halves of pregnancy.

Xenoestrogens (EDCs) and the male confusion about their sexuality

Exposure of pregnant mothers to xenoestrogens, I speculate, is almost assuredly the reason why so many young males today are confused about their sexuality or why they claim to be a combination of sexes (non-binary or genderqueer).

Countries like Brazil and the Dominican Republic, for example, have the highest concentration of transsexuals and hermaphrodites (see also guevedoces *3 ) in the world, and they also happen to be the countries where pesticides like DDT have been used the most (and are still used).

DDT was heavily used in the 50s and 60s in Brazil to successfully eliminate the Zika virus (malaria). The techniques used would be almost non-feasible today—very aggressive and heavy use of DDT, even spraying in homes—as the general public would now not be amenable to accepting them (Brown 2016).

The transsexual generation we are seeing is the result of the heavy spraying of DDT in those years, DDT can remain in the waters and environment for a very long time, even years, and much is still present in the environment even today. A study by João Paulo M. Torres et al. published in the Journal of the Brazilian Chemical Society (2009) confirmed this, saying:

"The organochlorine insecticide DDT was extensively used in Brazil since 1945, both for agricultural purposes and for vector control measures. In 1986 its uses were forbidden in agriculture and in 1997 it was also phased-out in vector controls programs. However, the presence of DDT in urban and forested soils, breast milk and aquatic biota is still common, especially at the Amazon region. The results gathered since the middle of the 90s indicate that environmental contamination with this pesticide is still relatively high."

Due to the high fish consumption by traditional riverside populations, human breast milk may represent an important source of DDT exposure to newborns. New results on DDT and PCBs in red dolphin (Inia geoffrensis), an endemic aquatic mammal of the Amazon region, is also reported.

Many African countries using these powerful pesticides for agricultural purposes or for controlling viruses are also now experiencing a higher number of transsexuals and hermaphrodites in their populations, and they are being subject to terrible violence and discrimination by the local governments due to poor knowledge of what it is to be intersex.

Figure 2: South African athlete Caster Semenya has always identified as female. After winning the women’s 800 and 1500 meters at the African Junior Championships in 2009, her sex was called into question. News that the International Association of Athletics Federations had asked her to undergo a gender test broke three hours before the final of the 800 meters at the 2009 World Championships, which Semenya won. According to press reports, the tests showed that she had internal testes instead of ovaries, and no womb. The IAAF decided that she could continue to compete as a female because her condition did not give her an unfair competitive advantage.

In America, the estimate of the transgender population has doubled in recent years to 1.4 million adults (Hoffman 2016). America still uses potent endocrine disruptors like BPA (in plastic bottles and some DDT derivatives). But these are not the only endocrine disruptors known to cause these problems; some medications have also been identified as causing transgenderism.

Proof that medication can cause alteration of sexual differentiation

Even though studies have not confirmed a correlation yet, Swaab in his study in 2010 calls for the possible effects on sexual differentiation of the brain by endocrine disrupters in the environment and in medicines given to the pregnant mother should be investigated.

Consider that epileptic women who were given phenobarbital or diphantoine (an estrogen-like substance) during pregnancy also had an increased risk of giving birth to a transsexual child. Both these substances change the metabolism of the sex hormones and can act on the sexual differentiation of the child’s brain.

In a group of 243 women who had been exposed to such substances during pregnancy, Dessens et al. (1999) found three transsexual children and a few others with less radical gender problems; This is a relatively high rate for such a rare condition.

In the book "Sex Differences in the Human Brain, their Underpinnings and Implications" researchers state that transsexuality occurs in 35.5% of children exposed to DES (diethylstilbestrol) and a problem with gender in 14%. This is alarming, but must, of course, be confirmed in a formal study. In the same book the authors claim that there are no indications that postnatal social factors could be responsible for the occurrence of transsexuality. Only in 23% of cases does a childhood gender problem lead to transsexuality in adulthood. With regard to sexual orientation, the most likely outcome of childhood gender identity disorder is homosexuality or bisexuality.

Calculating the potential risk of exposure

These hormone-disrupting chemicals are now widespread in the environment and food chain. Sources include pesticides, pharmaceuticals, industrial chemicals, plastics, dry-cleaning, personal care products, detergents, etc.

It is interesting to note that Harry Benjamin, a New York endocrinologist and sexologist who wrote the first modern work on transsexualism, The Transsexual Phenomenon in 1966, found that 40% of his male-to-female and 45% of his female-to-male patients had some degree of hypogonadism (reduced size of testicles/ovaries).

Despite the 1972 ban on DDT in the US, the chemical and its metabolites keep showing up in pregnant women.

A 2000 study performed by Foster W et al. published in the Journal of Clinical Endocrinology and Metabolism measured the levels of several pesticides in amniotic fluid during the second trimester. The authors found that approximately one out of three human fetuses in Los Angeles is exposed to a DDT breakdown product at “physiologically relevant levels.”

They also added: “Although we did not test for adverse health effects in this phase of the study, the concentrations of contaminants measured are sufficient to be cause for alarm.”

However, DDT is hardly the only endocrine disruptor in existence.

Our Stolen Future’s website (www.ourstolenfuture.org) lists 85 chemicals that are known to be endocrine disruptors or classes of chemicals such as PCBs and dioxins, which have many variants.

Phthalates are often used in plastic food packaging to soften them (think margarine container) and bisphenol-A is used to line metal cans to eliminate the metallic taste and is commonly found in resins, plastics, and dental sealants.

Mercury is one of the most widespread EDCs, being present in dental amalgam and childhood vaccines, and lead is commonly found in Seattle water, reportedly due to the corrosion of lead in home plumbing because of the corrosive chemicals used for disinfecting the water. (Seattle.gov) (At least 33 US cities used water testing 'cheats' over lead concerns - The Guardian)

So, if you were wondering if your small penis was only genetic, if your attraction for men was something you were born with, or if your desire to be a woman is natural, you might now have an answer: xenoestrogens. Your genetic expression might have been altered by the effects of these chemicals, and you should therefore not condemn yourself for what you feel.

EDCs Can Masculinize Females

One of most striking characteristics of these chemicals is that some feminize males, while others masculinize females.

A study performed in 1995 by Meyer-Bahlburg et al. found diethylstilbestrol (DES) to be able to cause homosexuality and bisexuality in women. Human exposure to DES occurred through diverse sources such as dietary ingestion from supplemented cattle feed and medical treatment for certain conditions, including breast and prostate cancers. From about 1940 to 1971, DES was given to pregnant women in the mistaken belief it would reduce the risk of pregnancy complications and losses.

The study states (emphasis mine):

"In psychobiological research on sexual orientation, the prenatal hormone theory has a central position. This article examines the hypothesis that prenatal estrogens contribute to the development of human sexual orientation.

Several groups of women with a history of prenatal exposure to diethylstilbestrol (DES), a nonsteroidal synthetic estrogen, were compared with several samples of control women in the context of a comprehensive study of the psychiatric and psychologic effects of prenatal DES. Various aspects of sexual orientation were assessed by systematic interview. Consistently across samples, more DES-exposed women than controls were rated as bisexual or homosexual (scores 2–6 on Kinsey-format scales ranging from 0 to 6).

The data are compatible with the hypothesis that prenatal estrogens may play a role in the development of human sexual orientation."

Parks et al. (2001) found similar masculinization effects in mosquitofish:

"Female mosquitofish (Gambusia affinis holbrooki) downstream from Kraft paper mills in Florida display masculinization of the anal fin, an androgen-dependent trait. … Eighty percent of the female mosquitofish from the Fenholloway River were partially masculinized while another 10% were completely masculinized, based upon the numbers of segments in the longest anal fin ray (18.0 +/- 0.4 vs. 28.1 +/- 0.9 [p < 0.001]) in the Econfina River vs. the Fenholloway River, respectively). … PME induced androgen-dependent gene expression in CV-1 cells.... In summary, water collected downstream of the Kraft mill on the Fenholloway River contains unidentified androgenic substances whose presence is associated with masculinization of female mosquitofish."

If these substances affect female brains, this would also explain why many women have become more masculine and aggressive in the last 50–60 years—a change that some think is due to the feminist movement and women's emancipation. We find that this is the case of the synthetic estrogen diethylstilbestrol (DES), which is classified as an ECD.

Even Animals Are Victims of Xenoestrogens

Studies on wildlife have clearly demonstrated that alligators, fish, aquatic invertebrates, amphibians, and many others are also victims of xenoestrogens (Matthiessen and Sumpter 1998; Jobling et al. 2006; Liney et al. 2005).

The most striking example found in these studies is the one following the accidental spill of high amounts of dichlorodiphenyltrichloroethane (DDT) and dicofol from a chemical company into Lake Apopka in Florida in the 1980s. It has been noted that male alligators living in the lake had smaller phalluses, reduced serum testosterone levels, and abnormal gonadal structures concurrently with high serum DDT levels (Semenza et al. 1997).

Some consequences of chemical contamination have been rivers that only produce female fish, turtle and bird populations that have developed weird reproductive problems, and frog populations that have feminized around the world, causing them to diminish or vanish.

Male gulls in the Great Lakes region of the US have been found to have “female (ovarian) type structures” due to high levels of DDT and DDE in the eggs.

Male Florida panthers have been found to have undescended testicles and a number of reproductive problems, and both males and females have been found to contain high levels of several endocrine-disrupting chemicals. (Mansfield G. 2002)

In Northwest America, a study was published in Environmental Health Perspectives that showed that 84% of genetically male Chinook salmon appeared to be female in the Columbia River. Regarding the cause, lead author James J. Nagler of the University of Idaho reports that pesticides and other chemicals that are estrogenic have been detected in the river and may play a role in this observed sex-reversal. (J. Nagler 2001)

In the laboratory, similar results are found when animals are exposed to hormone-disrupting chemicals.

In her book Our Stolen Future, author Theo Colborn relates the story of two Syracuse University researchers who, in 1950, injected roosters with DDT for two to three months. They found that the roosters’ testicles only reached 18% of the size of the controls, and the typical male secondary sex characteristics were significantly suppressed.

In 1994, the Journal of Wildlife Diseases reported the first case of a hermaphroditic beluga whale (De Guise et al. 1994).

These are all clear demonstration that Xenoestrogen can be dangerous not only for humans but also for animals. The negative consequence for animal are clearly alteration of their natural rhythm of reproduction which may eventually also affect their food chains.

For a more comprehensive overview, I suggest you read the book The Dirty Dozen: Toxic Chemicals and the Earth's Future by Bruce Elliott Johansen.

Conclusions

To learn how to avoid xenoestrogen exposure, and to protect your sexuality and that of your children from these environmental disruptors, shielding them from the hardship, challenges, discrimination, and surgical sexual reassignment that they may face in life, I recommend reading my books The Complete Guide to Penis Enlargement and Nutrition for Penis Enlargement.

*1To be intersex, study author Justine van Rooyen of the Aids Foundation of South Africa explained, was to be born with “atypical” or ambiguous genitalia or reproductive organs. An example is a person born with a vagina but who also has undescended testes. Female pseudohermaphrodites have ovaries and exhibit an XX chromosomal pattern, but the external genitalia look masculinized. The most common cause is congenital adrenal hyperplasia (CAH), a condition in which the adrenal glands of the fetus produce relatively large amounts of androgens (male sex hormones). Male pseudohermaphrodites have testes and an XY chromosomal pattern but are born with feminine-looking genitals. There are two main causes: testicular feminization syndrome, or androgen insensitivity syndrome, and 5-alpha-reductase deficiency (which may be both caused by Xenoestrogen exposure). In the latter case, the body develops along more masculine lines at puberty; the testes often descend into the assumed-labia, and the penis/clitoris grows to look and act more like a penis. Women with complete androgen insensitivity syndrome are technically ‘male’ pseudohermaphrodites because they have internal testes rather than ovaries. However, this label seems inappropriate because these women often have primary and secondary sexual characteristics typical of other women and feel they have normal (external) female bodies.

*2 The term "pseudohermaphroditism" was first used in 1876, long before the discovery of X and Y chromosomes, and the term "intersexuality" was introduced in 1923. However, most intersex or hermaphrodite people think of themselves as being either boys/men or girls/women. A multidisciplinary meeting of medical and nonmedical experts in Chicago in 2005 (the Chicago Consensus) proposed that congenital conditions associated with atypical development of chromosomal, gonadal, or anatomical sex should be called disorders of sex differentiation (DSDs), and that terms such as intersex, hermaphroditism, and pseudohermaphroditism should be dropped (Kim and Kim 2012). In the new terminology, male and female pseudohermaphroditism are known as 46,XY DSD and 46,XX DSD respectively. However, since "disorder" implies that any differences of this kind are pathological, this term has also been challenged, and terms like "intersex conditions" are still in use. *3 Guevedoces are some males born looking like girls and only grow penises at puberty, So the boys, despite having an XY chromosome, appear female when they are born. At puberty, like other boys, they get a second surge of testosterone. This time the body does respond and they sprout muscles, testes and a penis. The discovery was made in a small community in the Dominican Republic, This observation, made in 1974, was picked up by Roy Vagelos, head of research at the multinational pharmaceutical giant, Merck. He thought this was extremely interesting and set in progress research which led to the development of what has become a best-selling drug, finasteride, which blocks the action of 5-alpha-reductase, mimicking the lack of dihydro-testosterone seen in the Guevedoces.

References:

Brown L. 2016 May 4. Dr. Fauci: Brazil eliminated Zika-carrying mosquitos historically—using DDT. CNSNews.com. http://www.cnsnews.com/news/article/lauretta-brown/dr-fauci-zika-spreading-mosquito-was-eliminated-brazil-60s-heavy-use-ddt.

Cooke B, Hegstrom C, et al. 1998. Sexual differentiation of the vertebrate brain: principles and mechanisms. Front Neuroendocrinol. 19(4):323–62.

De Guise S, Lagacé A, Béland P. 1994. True hermaphroditism in a St. Lawrence beluga whale (Delphinapterus leucas). Journal of Wildlife Diseases. 3(2): 287–290.

Foster W Chan S, Platt L, Hughes C. Detection of endocrine disrupting chemicals in samples of second trimester human amniotic fluid. J Clin Endocrinol Metab. 2000 Aug;85(8):2954-7.

Garcia-Falgueras A, Swaab D. 2008. A sex difference in the hypothalamic uncinate nucleus: relationship to gender identity. Brain. 131(Pt. 12):3132–46. doi: 10.1093/brain/awn276.

Hoffman J. 2016 June 30. Estimates of U.S. transgender population doubles to 1.4 million adults. New York Times. https://www.nytimes.com/2016/07/01/health/transgender-population.html.

J J Nagler, J Bouma, G H Thorgaard, and D. Dauble High incidence of a male-specific genetic marker in phenotypic female chinook salmon from the Columbia River. Environ Health Perspect. 2001 Jan; 109(1): 67–69.

Jobling S, Williams R, et al All authors should be listed in complete reference. . 2006. Predicted exposures to steroid estrogens in U.K. rivers correlate with widespread sexual disruption in wild fish populations. Environ Health Perspect. 114(Suppl 1): 32–39. doi:10.1289/ehp.8050.

Kim K, Kim J. 2012. Disorders of Sex Development. Korean Journal of Urology. 53(1):1–8

Liney K, Jobling S, et al. 2005. Assessing the sensitivity of different life stages for sexual disruption in roach (Rutilus rutilus) exposed to effluents from wastewater treatment works. Environ Health Perspect. 113(10): 1299–1307. doi: 10.1289/ehp.7921

Mansfield KG1, Land ED. Cryptorchidism in Florida panthers: prevalence, features, and influence of genetic restoration. J Wildl Dis. 2002 Oct;38(4):693-8.

Matthiessen P, Sumpter JP. 1998. Effects of estrogenic substances in the aquatic environment. EXS. 86:319–35.

Meyer-Bahlburg H, et al. 1995. Prenatal estrogens and the development of homosexual orientation. Developmental Psychology. 31(1):12–21.

Parks L, Lambright C. 2001 Masculinization of female mosquitofish in Kraft mill effluent-contaminated Fenholloway River water is associated with androgen receptor agonist activity. Toxicol Sci. 62(2): 257–267.

Semenza J, Paige E, et al. 1997. Reproductive toxins and alligator abnormalities at Lake Apopka, Florida. Environ Heda/ Poep. 105:1030–1032. Torres J, Lailson-Brito et al. 2009. Persistent Toxic Substances in the Brazilian Amazon: Contamination of Man and the Environment. J. Braz. Chem. Soc. 20(6): 1175–1179. Tye M. 2013. Sexuality and Our Diversity: Integrating Culture with the Biopsychosocial. Vol. 1.0. Section 4.2. catalog.flatworldknowledge.com. Zhou J, Hofman M, Gooren L, Swaab D. 1995. A sex difference in the human brain and its relation to transsexuality. Nature. 378:68–70.