Endocrine Disrupting Chemicals and Transsexualism

Christine Johnson - 2001


Summary

One proposed etiology of transsexualism often reported in the literature suggests the presence of hormonal imbalances which occur during the course of fetal development. This paper puts forth the hypothesis that maternal exposure to a wide variety of endocrine disrupting chemicals ubiquitous in the environment produces disruptions to the fetal/neonatal endocrine system which can produce numerous developmental anomalies, including varying degrees of gender dysphoria. Communication between the central nervous system and cells of the body are, in part, controlled by hormones which act as chemical messengers to direct the activity of cells. Endocrine disrupting chemicals behave much like natural hormones, but unlike naturally produced hormones, the signals they represent are uncorrelated with the signals sent by the endocrine glands. These interfering signals result in erroneous decisions at the cellular level because the cell's receptors accept both endocrine disruptors and natural hormones as valid signals, albeit with different strength. Many of these chemicals are persistent and are not efficiently excreted via the body’s detoxification pathways, but are passed to the fetus during pregnancy and nursing.

The current paradigm for the worldwide use of chemicals is not based upon the precautionary principle, resulting in profound difficulties for scientists examining causal connections between the presence of a specific chemical its effects. Synergistic combinations of the 100,000 chemicals manufactured by man can multiply the effects of a single hormone disruptor by up to 1,600 times. Inadequate (essentially nonexistent) testing of the hormone disrupting nature of chemicals and novel materials has resulted in the situation where they are ubiquitous in many common products and in the environment, being distributed via air, land, and water. Many household products including most pesticides and some plastics contain endocrine disrupting chemicals, placing almost everyone at risk. Residues in water and on plants are ingested by animals and are concentrated as one goes higher up the food chain. Animals at the top of the food chain have the highest concentrations of these chemicals due to the bioaccumulative nature of many persistent hormone disrupting chemicals. Various studies indicate that everyone in the world is carrying a number of man-made chemicals in their body and that the level of these chemicals in humans is near, or at the level required to result in sexual developmental anomalies which are seen in wildlife populations.

Because of the rapid growth of scientific research, practitioners in one field are often not aware of the significance of developments in a seemingly unrelated field. In the study of gender identity, although many practitioners are acquainted with the results of studies in brain dimorphism, they are naturally less familiar with the results of toxicology. However, in the field of toxicology, developments in the last decade have highlighted the reproductive, behavioral, and anatomical effects of endocrine disruptors on animals exposed to these chemicals. Effects due to endocrine disrupting chemicals are observed at concentrations as low as parts per trillion for animals in the laboratory, indicating that the fetal endocrine system is more sensitive to disruption than any other known body system. These results of toxicology are significantly related to the field of gender identity and indicate a possible causal connection between exposure to these chemicals and anomalies in the expression of gender identity and other disorders such as reproductive failure.
 
 


 

The Wingspread Statement

In 1991, after years of reviewing research that examined a variety of problems with the wildlife of the Great Lakes region of the United States, Theo Colborn and a team of scientists pieced together troubling data from several fields of science which indicated that man-made chemicals introduced into the environment are having a variety of effects on animals and humans which were summarized in a set of statements which is now known as the Wingspread Statement. The full statement was included in the book "Our Stolen Future (1)," by Colborn, Dumanoski, and Myers, which discussed some of the consequences of endocrine disrupting chemicals upon wildlife and humans.

Regarding their conclusions, the following statements reflect those items that the participants of the Wingspread conference, a multidisciplinary team of scientists, could state with scientific certainty:

"We are certain of the following:

o        1) A large number of man-made chemicals that have been released into the environment, as well as a few natural ones, have the potential to disrupt the endocrine system of animals, including humans. Among those are the persistent, bioaccumulative, organohalogen compounds that include some pesticides (fungicides, herbicides, and some insecticides) and industrial chemicals, and other synthetic products, and some metals.

o        2) Many wildlife populations are already affected by these compounds. The impacts include thyroid dysfunction in birds and fish; decreased fertility in birds, fish, shellfish, and mammals; decreased hatching success in birds, fish, and turtles; metabolic abnormalities in birds, fish, and mammals; behavioral abnormalities in birds; demasculinization and feminization of male fish, birds, and mammals; defeminization and masculinization of female fish and birds; and compromised immune systems in birds and mammals.

o        3) The pattern of effects vary among species and among compounds. Four general points can nonetheless be made: (1) the chemical of concern may have entirely different effects on the embryo, fetus, or perinatal organism than on the adult; (2) the effects are most often manifested in the offspring, not in the exposed parent; (3) the timing of the exposure is crucial in determining its character and future potential; and (4) although critical exposure occurs during embryonic development, obvious manifestations may not occur until maturity.

o        4) Laboratory studies corroborate the abnormal sexual development observed in the field and provide biological mechanisms to explain the observations in wildlife.

o        5) Humans have been affected by compounds of this nature, too. The effect of DES (diethylstilbestrol), a synthetic therapeutic agent, like many of the compounds mentioned above, are estrogenic. Daughters born to mothers who took DES now suffer increased rates of vaginal clear cell adenocarcinoma, various genital tract abnormalities, abnormal pregnancies, and some changes in immune responses. Both sons and daughters exposed in utero experience congenital abnormalities of their reproductive system and reduced fertility. The effects seen in in utero DES-exposed humans parallel those found in contaminated wildlife and laboratory animals, suggesting that humans may be at risk for the same environmental hazards as animals."

They also state: "Chemicals known to disrupt the endocrine system include: DDT and its degradation products, DEHP (di(2-ethylhexyl)phthalate), dicofol, HCB (hexachlorobenzene), kelthane, kepone, lindane, and other hexachlorocyclohexane congeners, methoxyclor, octachlorostyrene, synthetic pyrethroids, triazine herbicides, EBDC fungicides, certain PCB congeners, 2,3,7,8-TCDD and other dioxins, 2,3,7,8-TCDF and other furans, cadmium, lead, mercury, tributyltin, and other organo-tin compounds, alkyl phenols (non-biodegradable detergents and anti-oxidants present in modified polystyrene and PVCs), styrene dimers and trimers, soy products, and laboratory animal and pet food products."

A more complete listing of Endocrine Disrupting Chemicals can be found at http://www.ourstolenfuture.org.


 

Anyone who has attempted to understand the various proposed etiologies of transsexualism must find this statement striking. In 1966, Harry Benjamin himself suggested a possible hormonal mechanism of action in his book "The Transsexual Phenomenon."(2) Many other gender researchers have also suggested a hormonal role, but to date, a possible relationship between endocrine disrupting chemicals and gender dysphoria has not yet been examined.

Hormone disruptors appear to interfere with sexual development by affecting normal communications between the hypothalamus, pituitary, and gonadal glands. Chemicals which modulate (up or down) the reception or secretion of hormones in any of these glands change the concentrations of hormones which have been programmed by genetics. That is, there is a "correct," or genetically programmed value of specific hormones produced by the fetus during development. Endocrine disruptors in the fetus change this "correct" value to some value which is not programmed by genetics, thereby upsetting the proper hormone levels. "Correct" in this context refers to the proper implementation of the instructions of the genes, not a reference to any particular quality of the genome.

Regarding the possible links between endocrine disruption and genital abnormalities, Benjamin made several observations which are relevant. He noted that "It may or may not have an endocrine significance that among my 152 male[-to-female] transsexuals, nearly 40 percent were found to have more or less distinct signs of a degree of sexual underdevelopment (hypogonadism)…"

Given the known feminizing effects of endocrine disrupting chemicals, as indicated in the Wingspread Statement, Benjamin’s observation is predictable. In adult males, it is well established that administration of estrogens will reduce the production of testosterone and cause a reduction in the size of the testes. This is precisely what happens when male-to-female transsexuals start estrogen therapy. A 25% reduction in the volume of the testes after one year on estrogen therapy for male-to-female transsexuals has been reported in the literature.(3) Endocrine disruptors which are estrogenic behave in a similar fashion, with the only difference being their effectiveness relative to the respective sex hormones.

Benjamin also related the following regarding the effects of maternal hormone medications during pregnancy, saying: "In recent years, evidence has accumulated that hormone medication during pregnancy can have serious consequences for the newborn. If the mother was given testosterone or progesterone for any length of time during her pregnancy (usually to prevent abortion), genital deformities of the newborn may have resulted if the genetic sex of the baby was female. Pseudohermaphroditism was the consequence."

Here he explicitly mentions the relationship between exogenous hormones (hormones from an external source) and genital abnormalities of the fetus. At the time his book was published, however, researchers were testing transsexuals for abnormalities in natural hormone levels, unaware that many commonly used chemicals and materials have properties which are estrogenic, anti-estrogenic, androgenic, and anti-androgenic. These chemicals can also affect enzymes which amplify the effect of hormones.

Benjamin then asks a similar question about the converse case: "What if the fetus is a male? It is normally under the influence of the mother’s female hormone (her estrogen) for nine months. Could that, under certain circumstances, interfere with the development so that the maleness of the newborn is repressed and a too feminine or underdeveloped infant is born? … Could that explain why there are so many more male transsexuals, transvestites, and homosexuals than female?"

Regarding the first part of this question, Colborn reports: "A new study from researchers at Tulane University and the University of Florida provides added evidence that some natural and synthetic estrogens differ in another extremely critical respect – their ability to circumvent the body’s natural defense system. In a pregnant woman, the binding action between special blood proteins and estrogens ties up most of the hormone circulating and thus acts to protect fetuses from excessive estrogen exposure in the womb. … some researchers have suspected that humans acquired some defense against plant estrogens through their long evolutionary experience with such substances in food. At the same time, studies on DES showed that these protective proteins do not bind with this synthetic estrogen, raising fears that the body might be defenseless against other man-made estrogenic compounds as well."

As for the disparity between the number of male-to-female compared to female-to-male transsexuals, it seems clear that many chemicals which are ubiquitous around the world, such as DDT, have estrogenic potential, whereas there are fewer chemicals which have androgenic potential. This disparity has been seen in wildlife as well. Scientific American recently reported on a study published in Environmental Health Perspectives, which showed that 84% of genetically male Chinook salmon appeared to be female in the Columbia river in the Northwest US, but they do not report sex reversed female salmon. (4)

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. Obviously, the particular endocrine disruptors in the water, on food, or in the air are related to the sources and the modes of distribution, and vary significantly depending upon where and when you look. In some cases, a single chemical will be primarily to blame, in others, multiple chemicals will be involved, so different outcomes will derive from the particulars of the exposure(s). This implies that the rates and distribution of transsexualism (and every other disorder which is due to endocrine disruption) will be highly variable and difficult to predict. Nevertheless, the balance of the scientific evidence suggests that there are a large number of estrogenic chemicals and a lesser number of androgenic ones.

A number of wildlife studies have been performed which examined feminization and masculinization of various species due to chemical exposures.(5) In the UK, alkylphenols and phthalates have been identified as the prime suspects for feminized fish in some areas. These chemicals are persistent breakdown products of alkylphenol ethoxylates, chemicals used in industrial detergents and as inert ingredients in pesticides. In Florida, an extensive spill of DDT and dicofol in Lake Apopka resulted in male alligators with abnormally small penises, abnormalities of the testes, and altered levels of sex hormones. 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 are found to contain high levels of several endocrine disrupting chemicals. Since there are only about 50 Florida Panthers remaining in the wild, this impact from endocrine disrupting chemicals will likely result in the extinction of this species.

In the laboratory, similar results are found when animals are exposed to hormone disrupting chemicals. Colborn relates one study on male mice born from mothers exposed to diethylstilbestrol (DES), a synthetic hormone, performed at the National Institute of Environmental Health Sciences by John McLachlan. This study showed that "These males had a variety of genital defects, including undescended testicles, stunted testicles, and cysts in the epididymis, a portion of the reproductive tract adjacent to the testicles where the sperm mature."

Other laboratory animal experiments have been performed examining the effects of TCDD, which is considered the most potent of the dioxin congeners. These studies report: "Pregnant rats exposed to a single dose of TCDD of 1ug/kg body weight give birth to males with low sperm count and testosterone levels, delayed testicular descent, and altered sexual behavior."(5)

A study on dioxin reported: "At concentrations that have no effect on testosterone levels, dioxin permanently alters the distribution of androgen receptors and delays cellular differentiation in the prostate of male rats." It is difficult to imagine that this is insignificant from a developmental standpoint. Alteration of the numbers of receptors will directly affect the dynamic behavior and may alter the homeostatic set-point of various components of the endocrine system. (5)

In November 1999, the Center for Health, Environment, and Justice published a document entitled "America’s Choice - Children’s Health or Corporate Profit," which included a section which examined scientific findings of animal experiments examining exposure to dioxins. They stated that:

"Although the mechanism by which dioxin produces its reproductive toxicity in males is unknown, many of dioxin’s effects on males appear to occur because it decreases testosterone production or because it disrupts the feedback communication mechanism [within the] … hypothalamic-pituitary-gonadal (HPG) axis. Normally, when testosterone levels are low, the pituitary gland secretes leutenizing hormone (LH), which sends signals to the testes to produce more testosterone. The testosterone surges in fetal and early life help set in place, or "imprint" this feedback system in the HPG axis. … Dioxin’s effect on testosterone may alter sexual differentiation of the brain during these early developmental stages when male hormones imprint the brain for male-mating behavior, male-type response in the hypothalamus, and male-type biochemical response to hormones such as LH." (leutenizing hormone) (5)

Gender researchers will likely notice the mention of a biological imprinting mechanism which would be consistent with one theory of transsexualism which suggests a similar imprinting effect.


 

Brain Dimorphism

Brain dimorphism is defined as a structural or other observable difference between the brains of males and females. In a 1995 article entitled "A Sex Difference in the Human Brain and its Relation to Transsexuality" published in Nature, J.-N. Zhou, et al. demonstrated an observable difference in certain structures in the hypothalamus of transsexuals males compared to males, females, and homosexual males. (6) They report:

"The possible psychogenic or biological etiology 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 terminalis (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."

D.F. Swaab, one of the authors of the study, commented in the January 1996 issue of Discover magazine that this research "shows that transsexuals are right. Their sex was judged in the wrong way at the moment of birth because people look only to the sex organs and not to the brain." (7)

The authors of this study reiterate a common theme in the study of transsexualism: that brain changes can arise due to an alteration in sex hormone levels - precisely the consequence of exposure to endocrine disrupting chemicals.


 

Rates of Transsexualism

Early attempts to determine the rate of transsexualism were crude approximations which counted only those individuals seeking gender reassignment. Rates were highly variable, but as one author noted: "… the number of applicants for gender reassignment depends largely on social acceptance, legal rights, and the availability of treatment."

In the Netherlands, an attempt to quantify changes in the rate was performed by Eklund, et al. (8) They noted that there was a general increase in the rate of transsexualism over the period from 1980 to 1986. They gave the following data: "Prevalence of male-to-female transsexualism was 1:45,000 in 1980, 1:26,000 in 1983, and 1:18,000 in 1986. Prevalence rates for female-to-male transsexuals showed a similar increase from 1:200,000 in 1980, 1:100,000 in 1983, and 1:54,000 in 1986."

They assert that since the age distribution of those seeking treatment was basically constant, increases in the rate of transsexualism reflected increased numbers of patients seeking treatment. They claim this is due to the increasing benevolence of society toward transsexuals. This may be possible in the Netherlands, a more liberal society with socialized medicine that covers transsexuals. But increasing rates could also be reflective of general increases in the quantities and numbers of endocrine disruptors which are present in the environment. As of early 2001, the prevalence in the Netherlands was estimated at 1:11,900 for male-to-female and 1:30,400 for female-to-male.(9) Clearly the trend is upwards.

Endocrine Disruptors: Distribution, Synergism, Persistence, and Bioaccumulation
Endocrine disruptors have increasingly become ubiquitous in our environment. In the US, the FDA Total Diet Survey reveals disturbing levels of many different chemicals in common foods. In an article discussing the body burden of environmental toxins and their effects, Walter Crinnion reported in Alternative Medicine Review (10) that:

"While the Total Diet Survey looks for the presence of many different chemicals, their findings of chlorinated pesticides are alarming. DDE (upon degradation, DDT becomes DDE or DDD) was found in 100% of samples of raisins, spinach (fresh and frozen), chili con carne (beef and bean), and beef. 93% of American processed cheese, hamburger, hot dogs, bologna, collards, chicken, turkey, and ice cream sandwiches contained DDE. DDE was also found in 87% of lamb chops, salami, canned spinach, meatloaf and butter, and in 81% of samples of cheddar cheese, pork sausage, hamburger, white sauce, and creamed spinach. Of all the items sampled, 42 had DDE in 63% or more of the samples."

As for the reason why these pesticides are present in so many foods, Crinnion suggests that "Since DDT and DDE have been banned for use in this country since 1972, it is likely that contamination is from produce imported from other countries where these chemicals are still used."

The results of the Total Diet Survey are significant because it appears that animals and humans are exquisitely sensitive to endocrine disruption. For many carcinogens, an effect is seen with concentrations in the parts per million to parts per billion range. For endocrine disruptors, an effect is seen in concentrations as low as parts per trillion for the developing fetus.

The EPA’s Human Adipose Tissue project is an effort to quantify the man-made chemicals present in tissue specimens of the US population. Since 1982 the EPA has been studying tissue samples from cadavers and elective surgeries from all over the country, looking for the presence of 54 environmental chemical toxins. Crinnion reports:

"Their results were astounding. Five of these chemicals – OCDD (a dioxin) and four solvents: styrene, 4-dichlorobenzene, xylene, and ethylphenol – were found in 100% of the samples. The quantitative ranges of these five compounds were also alarming. OCDD levels ranged from 19-3,700ng per gram of fat, styrene 8-350ng/g, 1,4-dichlorobenzene 12-500ng/g, xylene 18-1,400ng/g and ethylphenol 0.4-400ng/g. These alone would give each person a total toxic burden ranging from 57.4-6,350ng of toxins per gram of fat."

(1 ng/g = 1 part per billion)10

He also reports that "Another nine chemicals were found in 91-98 percent of all samples, including such toxins as benzene, toluene, chlorobenzene, ethylbenzene, one furan, three dioxins, and DDE… PCB’s were found in 83% of all samples, and beta-BHC in 87 percent, yielding a total of 20 toxic compounds found in 76 percent or more samples." One point is evident, as soon as we start looking for chemicals and actually quantifying exposures, it becomes abundantly clear that everyone is affected and it is merely a matter of dose and timing that determines what happens to whom.

Multiple chemical exposures in humans are today the rule, and an important idea in the study of the effects of multiple chemicals upon animals and humans is that of synergism. Synergism occurs when the effect or response of a combined exposure of two or more chemicals is greater than additive. An example would be exposure to both mercury and lead, both known endocrine disruptors. Laboratory experiments on animals and observations in humans show a greater effect than would be predicted based upon the effects of mercury added to the effects of lead, if each was administered separately. (11)

The same results are seen with respect to other endocrine disrupting chemicals. In some cases, certain combinations can multiply the effects of a single endocrine disruptor by up to 1,600 times.10 This makes it difficult, if not impossible, to use a test for a specific chemical as a diagnostic tool for likely endocrine disruption effects. Given that approximately 100,000 man-made chemicals are currently in production, it is inconceivable that every possible combination can be examined in a laboratory setting or in human studies. Additionally, the vast majority of man-made chemicals cannot be detected in humans at this time and only a small number have been evaluated from the standpoint of endocrine disruption.

Persistence is related to excretion and/or breakdown of endocrine disrupting chemicals inside the body or breakdown in the environment. Many of the chemicals which have been found to be endocrine disruptors circulate in the bloodstream or get sequestered in tissue, escaping breakdown or excretion. In the environment, some resist breakdown essentially indefinitely. Due to this resistance to breakdown and excretion, endocrine disruptors can permanently alter hormone concentrations.

Bioaccumulation is due to the inability of the body to excrete certain chemicals. If the body is unable to excrete chemicals which alter the endocrine system, an accumulation will occur. Increased concentrations of endocrine disrupting chemicals can either increase or decrease the effects, since the dose-response curve has the shape of an inverted U. That is, at low concentrations, the effects will increase as the concentration is increased, but at higher doses, an increase in concentration results in a decrease in the effect. This compounds the difficulty of determining a threshold for effects to occur, since classical toxicology presumes that an increase in concentration will result in an increase in the effect. (12)

It has been observed that there are two fairly efficient mechanisms for the excretion of many endocrine disrupting chemicals. The first mechanism is transfer of endocrine disruptors from the mother to the fetus during pregnancy. The second mechanism is via the breast milk of the mother. Both account for a significant fraction of the lifetime accumulation of the mother which is then passed to the fetus during pregnancy and breast feeding. This means that each subsequent generation will begin life with that much higher of a concentration of these chemicals. Given that the manufacture of these chemicals has not yet ceased and that significant amounts already manufactured have not yet reached the environment (PCB’s in power line transformers, for instance), it is predictable that these concentrations will continually increase until corrective measures are taken to eliminate them from the environment.

Colborn discusses this situation: "Humans also carry PCB’s and other persistent chemicals in their body fat, and they pass this chemical legacy on to their babies. Virtually anyone willing to put up the $2000 for the tests will find at least 250 chemical contaminants in his or her body fat, regardless of whether he or she lives in Gary, Indiana, or on a remote island in the South Pacific. You cannot escape them."

It can be predicted that as these concentrations increase in each subsequent generation, reproductive failures and anomalies such as transsexualism will increase in frequency for many generations. It is conceivable that at some point in the future, reproductive failures will be the norm, as seen in many animal populations such as the Florida Panther and other species at the top of the food chain. However, we may be closer to that point than previously thought; a recent National Research Council report found that 50% of all pregnancies in the US result in prenatal or postnatal mortality, birth defects, or other chronic conditions. (13) These statistics do not include transsexualism or any form of gender dysphoria as a birth defect, primarily because these are delayed manifestations of signaling errors that are not anatomically obvious.

Another significant observation related to reproductive effects made by Benjamin was that the number of his patients who were "only" children was higher than that of the general population. He reported that 17.6% of male-to-female and 25% of female-to-male transsexuals under his care were "only" children, compared to 10% in the general population. This raises questions about the hormonal status of mothers who were not able to have more than one child. If they had high levels of endocrine disrupting chemicals in their system, it would be expected that there would be a higher rate of reproductive problems, and that "only" children would occur with a higher frequency. This result has been observed of mothers who took DES during pregnancy, which resulted in a higher incidence of failed pregnancies compared to women who did not take the drug.


 

Issues related to the treatment of Transsexualism

As is noted on the website http://www.ourstolenfuture.org, "Human epidemiology is biased toward false negatives in the search for health effects of endocrine disruption. It will be exceedingly difficult, if not impossible, to establish scientific certainty of causation of many heath problems in humans, even though based on laboratory data it is likely that endocrine disruption is involved in a range of human diseases. Because the animal data demonstrate plausible, serious risk to human health, this bias toward false negatives (a statistical term that means finding no association when in fact there is one) requires the application of the precautionary principle, using animal data as the guide."

Regarding animal data, one experiment performed in 1950 by two Syracuse University researchers showed the following important result, which has parallels to transsexualism that are difficult to ignore. Colborn relates the experiment:

"The Syracuse team decided to explore the effects of long-term poisoning from DDT by injecting the pesticide into forty young roosters for a period of two to three months. As they watched what happened to the white leghorns, they must have puzzled about this most peculiar poison. The daily doses of DDT didn’t kill the roosters or even make them sick. But it certainly did make them weird. The treated birds didn’t look like roosters at all; they looked like hens.

As young cockerels mature, tall red combs blossom on their heads and luxurious cherry-colored skin folds called wattles burgeon at their necks – hallmarks of rooster masculinity. The birds dosed with DDT, however, failed to develop in the expected way. Even as adults, their combs remained pale and stunted, measuring just one-third the size displayed by untreated roosters raised in the zoology lab for the purpose of comparison. When the researchers examined the birds’ testicles, the findings were even more startling. The sex organs had grown to only 18 percent of normal size. From all appearances, the birds had suffered chemical castration."

This finding has profound significance because it shows a direct and incontrovertible causal connection between an endocrine disruptor and altered sexual development. From the time of Benjamin’s "The Transsexual Phenomenon" until now, gender researchers have never examined the potential impact from endocrine disruptors upon the sexual development of humans. This is true despite the fact that this data was published in 1950, with results that are clearly related to issues such as transsexualism and other anomalies in sexual development. In the last decade, there has been a steady stream of scientific studies with one consistent finding – endocrine disrupting chemicals are capable of altering normal sexual development.

In a 1997 Greenpeace article on endocrine disruptors, the authors state: "A trivial amount of government resources is devoted to monitoring environmental chemicals and health effects. The public is unaware of this and believes that they are adequately protected. The message that endocrine disruptors are present in the environment and have the potential to affect many people over a lifespan has not effectively reached the general public, the scientific community, regulators or policy makers. Although this message is difficult to reduce to simple statements without over- or underestimating the problem, the potential risks to human health are so widespread and far-reaching that any policy based on continued ignorance of the facts would be unconscionable." (14)

One of the most ominous signs reported by Colborn is that "A number of pediatricians from various parts of the United States have expressed their concern about an increasing frequency of genital abnormalities in children such as undescended testicles, extremely small penises, and hypospadias, a defect in which the urethra that carries the urine does not extend to the end of the penis, but it is virtually impossible to document these anecdotal reports. Unfortunately, the problems caused by endocrine disruption may have to reach crisis proportion before we have a clear sign that something serious is happening."

This is indeed unfortunate, because it is an indication that we will need to reach the edge of the abyss before we can definitively prove that the cause of a great many problems are the result of numerous chemicals in the environment. By then, it may not be possible to reverse the damage done. One thing is clear: if current trends continue, there are going to be a whole lot more transsexuals in this country and around the world with every successive generation.

This raises the obvious question: Is it ethical for gender therapists to consider transsexualism and other sexual developmental anomalies as "mental disorders" given the preponderance of evidence indicating a causal connection between endocrine disrupting chemicals and altered sexual development? Are the fish, birds, and mammals in the wild also suffering from "mental disorders," or is there a better explanation for the observed anatomical and behavioral changes that are vividly demonstrated when laboratory animals are exposed to these chemicals? This paper has asserted that there is a better explanation, one that fits many of the observations of Benjamin and others, and that this new paradigm offers humanity an insight into the future. It amounts to a preview of what is to come if we continue to pollute our environment, ourselves, and our children with endocrine disrupting chemicals.


 

References


 


 

  1) Colborn T., Dumanoski D., Myers J.P. Our Stolen Future, Dutton (1996)

See also http://www.ourstolenfuture.org/

  2) Benjamin, H. The Transsexual Phenomenon, Julian Press (1966)

http://www.symposion.com/ijt/books/index.htm#Harry Benjamin

  3) Meyer W.J., Webb A., Stuart CA., Finkelstein J.W., Lawrence B, Walker P.A.

Physical and hormonal evaluation of transsexual patients during hormonal therapy.

Arch of Sex Behav (1986) 9:21-26.

  4) Wong K. Sex-Changed Salmon, Scientific American, December 2000

http://www.sciam.com/news/121900/3.html

  5) Center for Health, Environment and Justice, "America’s Choice – Children’s Health orCorporate Profit, The American People’s Dioxin Report, Technical SupportDocument," November 1999. Falls Church, VA

http://www.chej.org/report.html

  6) Zhou J.-N, Hofman M.A., Gooren L.J., Swaab D.F. (1997) A Sex Difference in theHuman brain and its Relation to Transsexuality. IJT 1,1,

http://www.symposion.com/ijt/ijtc0106.htm

  7) Glausiusz J, Transsexual Brains. Discover Magazine, p83, January 1996.
 

  8) Eklund PLE, Gooren LJG, Bezemer PD. Prevalence of transsexualism in theNetherlands. Br J Psychiatry (1988) 152:638-640.
 

  9) The Standards of Care for Gender Identity Disorders -- Sixth Version, Harry BenjaminInternational Gender Dysphoria Association, 2001

http://www.symposion.com/ijt/soc_2001/soc_02.htm

  10) Crinnion WJ, Environmental Medicine, Part 1: The Human Burden of EnvironmentalToxins and Their Common Health Effects, Altern Med Rev 2000;5(1)

http://www.thorne.com/altmedrev/fulltext/med5-1.html

  11) Allsopp M, Stringer R, Johnston P. Unseen Poisons – Levels of Organochlorine Chemicals in Human Tissues, Greenpeace Research Laboratories, Dept. Biological Sciences, University of Exeter, UK. June 1998.

http://www.greenpeace.org/~toxics/

  12) Ziff S, Ziff MF, Infertility and Birth Defects: Is Mercury From Silver Dental Amalgam Fillings An Unsuspected Cause?, p.15, Bioprobe, Orlando, FL, 1987.

Available at http://www.bioprobe.com

  13) National Academy of Sciences, National Research Council, Committee on Developmental Toxicology, Scientific Frontiers in Developmental Toxicology and Risk Assessment, June 1, 2000, 313 pages.

http://www.nap.edu/books/0309070864/html/

  14) Allsopp M, Santillo D, Johnston P. Poisoning the Future: Impacts of Endocrine Disrupting Chemicals on Wildlife and Human Health, Greenpeace Research Laboratories, Dept. Biological Sciences, University of Exeter,UK. Oct 1997.

http://www.greenpeace.org/~toxics/



Last modified: 11/30/09