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Polycystic Ovary Syndrome

Part 1: A Body State of Evolution In Reverse

Majid Ali, M.D.

Polycystic ovary syndrome (PCOS) is a disorder of young women and comprises high blood insulin and testosterone levels, inability to have babies, weight gain, and facial hair. The syndrome is spreading like an epidemic.

In 1968, as a pathology resident I began to diagnose polycystic ovary syndrome (PCOS) in biopsy and surgical specimens. Our whole department saw ten to twelve cases in a hospital that delivered more than 2,000 babies. A 2010 report cited an incidence of PCOS of up to 20 percent among U.S. women between 20 and 45 years of age. Why?

Chemical Chicken Coming Home to Roost

PCOS, of course, is not a new problem. What is new is its epidemic spread. The rate of increases in its incidence in every region of the world correlates well with the use of two types of synthetic chemicals: synthetic hormones and industrial pollutants with hormone-like effects (xenoestrogens and xenoandrogens). The greater the mounts of these chemicals in water, food, and air, the higher the incidence of PCOS. Simply stated, the epidemic of PCOS is caused by the chemical chicken coming home to roost. What might be the underlying mechanisms of disruption of hormonal pathways which set the stage for PCOS? A study of evolution provides the answer.

PCOS: Evolution in Reverse

Nature evoloved two separate genders among humans, slowly over hundreds of millions of years. In a thought experiment, suppose we abolish the evolutionary influences which were responsible for creating women and men. What can we expect? How will the genes responsible for keeping women "women-like" and men "men-like" respond to such a change? We can reasonably expect to see a weakening of these genetic pathways. With time, there will be a loss of gender differentiation, such that women and men become "gender-skewed"—females would become "male-like" and males would become "female-like,"so to speak. If some consistent patterns of such gender-skewing caused by specific environmental or genetic factors could be recognized, can a unifying model of "gender devolution"—evolution in reverse, so to speak—be proposed to explain a vast array of seemingly disparate observations concerning gender differentiation?

With incremental load of xenoestrogens and xenoandrogens, little girls will be expected to have precocious development of primary and secondary sexual characteristics, such as the premature appearance of pubic hair, breast enlargement, and menarche. In older girls, one would expect phenotypic changes to include hirsutism, male-pattern baldness, alopecia, acne, anovulation, oligomenorrhea, and amenorrhea. Other expected changes in this context would be higher incidence of premenstrual syndrome, endometriosis, and the Stein-Leventhal syndrome (polycystic ovary syndrome, PCOS). In older women, we may anticipate rising incidences of cancers of the breast, ovary, and other related organs. Now, let us consider the published data on these subjects.

The age of menarche (onset of menstruationaturation) has been dropping in European countries. The downward trend has essentially leveled off in recent years. The European trend contrasts sharply with that seen in the U.S, with the onset of puberty (as determined by age at breast development) occuring much earlier than it did 20 years ago.27-30 For example, in a study of 17,077 American girls, at age seven, 27.2% of African American and 6.7% of white girls showed such secondary development; at age eight, the corresponding numbers were 48.3% and 14.7%.27 Amazingly, at age three, 3% of African-American girls and 1% of white girls showed precocious development with breast enlargement and/or appearance of pubic hair. These data concerning precocious pubertal development in U.S. girls contrasts sharply with that concerning Danish girls. From an epidemiologic study based on national registries, only 0.2% of all Danish girls had some form of precocious pubertal development.30

In 2007, Time magazine reported that 3 million U.S. citizens were gender- variant—children and adults who do not identify with their biological sex. The gender-variant adolescent were two-to-three times as likely to attempt suicide as children without gender identity issues. In February of that year, Boston's Children's Hospital opened the first U.S. clinic for gender-variant children. The treatment plan includes injections of a puberty-delaying hormone to regulate gonadotrophin-releasing hormone (GnRH)—a treatment that carries increased risk of infertility when injection therapy is discontinued and puberty allowed to occur. Not unexpectedly, the Boston hospital showed no interest in crucial subjects of liver and bowel detox procedures and the special nutrient requirements of children.

Diagnostic Criteria for Polycystic Ovary Syndrome

In 1968, when I began my work as a pathologist, the diagnostic criteria for the diagnosis of PCOS included: (1) bilateral symmetrical enlargement of the ovaries; (2) ovarian stromal cortical hyperplasia; (3) multiple cysts formed by arrested Graafian follicles; and (4) absence of microscopic evidence of ovulation failure. By these diagnostic criteria, PCOS was a distinctly uncommon disorder, seen less often than once monthly. Currently reported incidences of PCOS are sharply higher. Estimates of the prevalence of polycystic ovary syndrome (PCOS) in the general population have ranged from 2–20%.31-34 According to a December 2005 report of the CDC's National Survey on Family Growth (NSFG), U.S. women under 25 years of age comprised the fastest-growing segment with impaired fecundity, as defined by the capacity to conceive and carry a child to term. The report identified obesity as an important characteristic of such women. Based on the 2005 NSFG report, approximately 12% of American couples experienced impaired fecundity in 2002, a 20% increase from the 6.1 million couples who reported an inability to have children in 1995. I return to the crucial subject of PCOS to illustrate core aspects of the gender devolution model, as well as to show the folly of using drugs to treat the disorder, as regrettably recommended by The New England Journal of Medicine.25

The incidence of endometriosis is rising in most regions of the world. One line of evidence for this trend is drawn from prospective studies on asymptomatic women undergoing tubal sterilization, who have markedly higher than expected frequency of endometriosis lesions.35,36 Consider the following text from the website of Endometriosis Association (http://www. endo-online.org/):

Endometriosis affects all races, personalities, and socioeconomic groups as well as all ages of women, from girls as young as 10 or 11 to women in their 60's and 70's.1 The terrible impact on young women is evident in the dramatic 250% increase in hysterectomies for endometriosis for women aged 15 to 24 between 1965 and 1984. The same period saw an increase of 186% for women aged 25 to 34.

Whhy do gynecologists remove uteri of teenagers for endometriosis without searching for factors that cause endometriosis? I consider it a serious ethical lapse—an intellectually inexcusable and morally regrettable acts of professional misconduct. Strong words! Yes. Later in this chapter, I present a careful review of available scientific facts concerning endometriosis that shed as much light on my gender devolution model as do considerations of PCOS. I will let the readers decide whether or not my words are unjustifiably strong.

My patients in good health in the ninth and tenth decades of life have revealed something important to me. They have sharp memories of the years of menarche, first meeting their future husbands, and events related to the birth of their children. Nearly all report little or no symptoms attributable to menstruation, endometriosis, or ploycystic overy syndrome. This contrasts sharply with my patients in the second or third decades of life who in nearly all instances report moderate to severe menstrual symptoms. How may this sharp difference be explained? It seems to me that the pandemics of disabling premenstrual syndrome, endometriosis, polycystic ovary syndrome, and related menstrual derangements are varying clinical expressions of gender devolution.

Gender Twisters

An important issue here is the delayed consequences of exposure to minute quantities of gender twisters, including the well-recognized endocrine disruptors. Specifically, I proposed that the pandemic of cancer of the breast is unleashed by synthetic hormones and exobiotics, which simulate the effects of gonadal hormones. I devoted Breast and Prostate Cancer—Eco-Monsters and Onco-Monsters (2006) to this vast subject.

Significant evidence of gender-skewing has also been observed in animal kingdom.38,41 For example, female-to-female pairing and other changes in reproductive behavior have been reported in gulls exposed to higher amounts of DDT and DDE in Santa Barbara as well as in Roseate terns exposed to PCBs in Massachusetts.

For detailed discussions of the molecular biology of hormones and relevant citations, I refer the reader to "Darwin and Dysox Triology,"the 10th, 11th, and 12th. Volumes of my textbook entitled " The Principles and Practice of Integrative Medicine."

Related Tutorials

* Polycystic Ovary Syndrome - Part 1: A Body State of Evolution In Reverse

* Polycystic Ovary Syndrome _ Part 2: Surgical Removal of Cystic Ovaries

 

 

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