Estrogen Overload In Young Girls

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Estrogen Overload In Young Girls

 

 

 

In a recent study of 17,077 American girls, at age three, 3% of

African-American girls and 1% of white girls showed breast and/or

pubic hair development. At age seven, 27.2% of the former and 6.7%

of the latter showed such secondary development. At age eight 8,

48.3% of African American and 14.7% of white girls exhibit such

development.

 

Amazingly, three percent of three-year old girls also showed such

precocious developemnt. This indicates a tremendous estrogenic

overload and no one can predict what kind of trouble it spells for

those girls.79

 

Estrogenic activities have been shown in chemicals in common use,

including pesticides, plastics, petroleum products, polystyrene, and

PAHs (polycyclic aromatic hydrocarbons).80,81 Chemical companies

usually pooh-pooh the health hazards of their chemicals, claiming

that minute amounts of are safe. However, in a recent study, some

plastic compounds were shown to have hormonal activity at

concentrations as low as two parts per billion. The author discussed

this serious issue in his book RDA: Rats, Drugs and Assumptions.67

 

To complex layers of hormonal dysregulations must be added the

impact of many environmental pollutants that often goes

unrecognized. The studies of endometriosis in Rhesus monkey

following chronic exposure to 2,3,7,8-tetrachlorodibenzo-e-dioxin by

Rier et.al..82 are of special interest. Endometriosis occurs in

Rhesus monkeys spontaneously and resembles its human counterpart,

both pathologically and clinically.

 

Endometriosis is generally believed to be caused by estrogen

dysregulation, and the role of environmental pollutants in its

pathogenesis is rarely appreciated. Rier et al observed a direct

dose-response correlation between chronic dioxin exposure and the

incidence and severity of endometriosis in Rhesus monkeys.

Specifically, they documented the presence of endometriosis with

laparoscopy and biopsy in 71% of the exposed (25 ppt) monkeys while

similar lesions were encountered in only 33% of control monkeys not

exposed to dioxin. There are several target genes for the action of

dioxin, including several growth regulatory genes involved in cell

differentiation and inflammatory response. Notable among them are

genes for cytochrome P-450, plasminogen activator inhibitor-2, and

interleukin-1b.

 

In a related study, a higher incidence of endometriosis in humans

was correlated with exposure to PCBs.83 Dioxin and PCBs belong to an

ever-lengthening list of pesticides and industrial pollutants that

have been clearly shown to cause a wide range of hormonal

dysregulation in humans, mammals, birds and fish.84

 

It is noteworthy in this context that the World Health Organization

in 1990 reported the average per person daily dioxin intake of 133

picograms (mainly through polluted fish, meat, and poultry) in

industrialized countries. The data strongly suggested that maternal

exposure to dioxins before and during pregnancy can result in fetal

mortality with overt effects on the mother.85 It may be added here

that dioxin binds to eryl hydrosulfate receptors and forms adducts

directly with DNA to cause its toxicity.86

 

5.Empirical Eevidence of Functional Inter-Relationship and

Interdependences of Gonadal and Nongonadal Hormones

 

Empirical experience with patients with CFS, fibromyalgia, and

chronic autoimmune disorders makes it clear that disorders of

nongonadal endocrine systems, such as thyroid and adrenal glands,

cannot be separated from those of seemingly gonadal origin. The data

for 24-hour urinary excretion of adrenal metabolites and selected

data for thyroid hormones are included in this article to underscore

that point. Indeed, in the amenorrhea subgroup, all 12 patients

showed clearly abnormal urinary profiles.

 

http://garynull.com/cms/index.php/plain/documents/amenorrhea_oligomen

orrhea_and_polymenorrhea_in_cfs_and_fibromyalgia_are_caused_by_oxidat

ive

 

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