Estrogen Domonance
ED - Why so prevalent?
Why has estrogen dominance become so prevalent?
•
Too much Dietary / Supplementary Estrogen
• Overproduction of estrogen (ESTRADIOL
or ESTRONE)
• Estrogen-Mimicking /stimulating xenoestrogens
pervade modern day life
• Decreased PROGESTERONE production
in the body
• Stress
• Non-ovulatory cycles
• Impaired Liver Function
• Iodine deficiency
• Obesity, Cardiovascular Disease, Digestive Problems,
Insulin resistance
(1) Too
much Dietary / Supplementary estrogen
Excessive intake of plant estrogens
Any additional estrogen by prescription
or supplemented, will increase estrogen levels
and must be properly balanced with natural PROGESTERONE
- Typical sources of prescription estrogen
are birth control pills and hormone replacement therapy.
Estrogen-mimicking phytoestrogens
Over-consumption of
phytoestrogens , especially soy or flaxseed adds to
estrogenic
load. Certain plants contain plant
estrogens , which have an
estrogenic effect when eaten to excess. Soybeans,
soy products and flaxseed contain high levels of
phytoestrogens . According to a report
in The American Journal of Clinical Nutrition a small number of studies have shown
that high levels of soy can increase menstrual cycle length, decrease FSH (follicle-stimulating
hormone) and decrease LH (leutinizing hormone), affecting the reproductive cycle.
- High levels
of soy generating anti- estrogenic effect are equivalent
to drinking three 12-ounce glasses of soy milk /dayfor a month -
three 12oz glasses is 60g soy protein (equivalent to 45 mg of isoflavones);
- Excessive
soybean consumption inhibits the thyroid and is widely associated with hypothyroidism
- Asia has endemic hypothyroidism (China
has 100,000,000 cretins).
Moderate
phytoestrogen intake actually has an anti -Estrogenic
effect - phytoestrogens "dock
onto" estrogen receptors and have a
weak estrogenic effect, preventing
xenoestrogens and other
estrogens from "docking" and having
their stronger effect.
Women with diets containing moderate amounts of
phytoestrogens excrete more
estrogens into their urine and have lower
blood estrogen levels.
- Liver must
be able to eliminate unused excess estrogens - low/moderate intake of weak plant estrogens
may replace our own more potent estrogens
for receptor sites, but if the liver is incapable of eliminating them, then our
own estrogens will still act if there are
receptors to act upon.
It is now well-established that many
phytoestrogens
and hormone-disrupting chemicals exhibit an inverted-U "Dose
to inhibitory response" curve
Phytoestrogens
and hormone-disrupting chemicals disrupt/inhibit
hormones at low doses but not at high doses - What seems
to happen is that the hormone system becomes overwhelmed and stops
responding, so at high doses there is no observable effect. Traditional
toxicological testing at high doses may miss important effects that
only occur at lower doses.
The Inverted U "Dose to inhibitory
response" curve. Initially, as a
dose rises, the inhibitory response rises. However, at some point
as the dose continues to rise the response stops rising, then begins
to diminish and falls back toward zero.
Examples of the Inverted U Dose-response
curve:
- xenoestrogenic
BPA. A study of BPA found that low doses of BPA produced
a greater inhibitory biological effect than higher doses. (EHP Vol.
109, Jul. 2001, pgs. 675-680.).
- Phytoestrogens -
EHP-published study demonstrates that:
1. Phytoestrogens
at low doses inhibit the production of
estrogen
2. At higher doses the inhibitory effect disappears and
the phytoestrogens behave
like estrogen itself, adding
to the effect of the body's own natural
estrogen - the authors say
this may explain why low doses of
phytoestrogens protect against breast cancer.
[EHP Vol. 110, Aug. 2002, pgs. 743-748] .
Estrogenic
Pesticides. A study
of adult male guppy fish, exposed to certain pesticides in their
food (vinclozolin and DDE - both known to disrupt male sex hormones)
exhibited shrunken testes, a significant reduction in numbers of
sperm, and "a severe disruption in male courtship behavior." Some
of the measured effects were greater at a lower dose, demonstrating
an inverted-U dose-response curve [EHP
Vol. 109, Oct. 2001, pgs. 1063-1070]. The authors of the
guppy study did a literature search and found over 100 published
papers reporting an inverted-U dose-response curve.
(2) Overproduction
of Estrogen
(ESTRADIOL or ESTRONE)
TESTOSTERONE
converts to
ESTRADIOL via
the aromatase
enyme produced by fat cells;
Ovarian cysts or tumors.
Can lead to excess estrogen
production;
Obesity.
All body fat has an enzyme which converts adrenal steroids to
estrogen , so the more fat you have, the
more estrogen is produced; this
peripheral production of estrogen is the
most common cause of excess estrogen
Murray RK et al. Harper's Biochemistry. 23rd ed. Norwalk
CN:Appleton & Lange; 1993
Caffeine/Coffee/Alcohol/Nicotine.
One study (Fertility and Sterility 2001;76:723-729)
finds that drinking more than two cups of coffee daily may boost
estrogen levels in women and could exacerbate
conditions such as endometriosis and breast pain. The study included nearly
500 women aged 36 to 45 who were not pregnant, breast-feeding or takinghormones .
All women answered questions about their diets, smoking habits, height and weight.Researchers
measured the women's hormone levels during days 1 to 5 of their menstrual cycle.
Women
who consumed the most cholesterol and alcohol, and those who consumed more than
one cup of coffee a day had significantly higher levels of
estrogen - during the early follicular
phase of their menstrual cycle, according to the report in the October issue
of "Fertility and Sterility".
Caffeine intake from all sources
was linked with higher Estrogen
levels. Regardless
of age, body mass index (BMI), caloric intake, smoking, and alcohol and cholesterol
intake.Women who consumed at least 500 mg of caffeine daily (E.g. 4 - 5 cups
of coffee), had nearly 70% more estrogen
during the early follicular phase than women consuming no more than 100 mg of
caffeine daily (< 1 cup of coffee).
Smoking / Nicotine. Women aged 40 and
older and those who smoked had higher levels of follicle stimulating hormone
(FSH), which corresponds with fewer eggs remaining in a woman's ovaries. FSH
tends to increase withage. Thus, the observation that smokers have higher FSH
levels suggests that their ovaries are ``older'' than their chronological age.
(3)
Estrogen-Mimicking /stimulating xenoestrogens
(also called Endocrine Disruptors) pervade
modern day life
Xenoestrogens
(The Greek word xeno means foreign) are
industrially made compounds with a molecular structure so similar to
estrogen
that they have estrogenic
effects (i.e. stimulate
estrogen
receptors) in the body.
xenoestrogens
are having significant and serious effects on our health. Many endocrine-disrupting
contaminants, even if less potent than the natural products, are present in
living tissue at concentrations millions of times higher than the natural hormones.
They are being blamed for increasing rates in hormone-sensitive
breast, prostate and reproductive cancers, fibroids, cysts, reduced infertility,
menopausal problems, PMS and early puberty in children .These endocrine
disruptors create imbalances, especially in the reproductive, thyroid and adrenal
systems. They can increase growth of the endometrium and disrupt the reproductive
cycle. In the U.S., more than a quarter of all women are now having hysterectomies
by the age of 60. Even men are not exempt from their effects, with many being
diagnosed with BPH and complaining of declining sexual performance.
Xenoestrogens
are strong and long-lasting. These chemicals
bind permanently to receptor sites, accumulate in fat tissues, and disrupt nearly
every biological process. Small daily doses build up, leading to an unbalanced
endocrine system. Obesity and adrenal exhaustion (chronic fatigue/"stress")
follow.
The environmental background of
xenoestrogens
provides a continuous
estrogenic exposure.
Unfortunately these modern day "Estrogen
look-alikes"are nearly impossible to avoid since they are ubiquitously
present in our lives, in meat and dairy, food preservatives, personal care products,
household goods, herbicides, pesticides, fertilizers, plastics, and more. However,
it is possible to reduce your exposure to
xeno estrogens
if you know where to find them, so brace yourself for a depressing revelation
as these sources are revealed:
X-rated xenoestrogens - Endocrine Disruptors
(4) Decreased
PROGESTERONE production in the body
PROGESTERONE
is necessary to counterbalance estrogen
and
TESTOSTERONE
Women who do not ovulate during their cycle
will not produce any PROGESTERONE
that cycle. This
is a common occurrence and worsens the already disturbed
PROGESTERONE / estrogen
balance;
PROGESTERONE
production is reduced in menopause.
Only the adrenal gland is producing it, because a woman is
no longer ovulating.
• Recurrent early miscarriage
• No period
• Not ovulating
• Endometriosis
• PCOS
• PMS
• Cramps during menses
• Blood Clotting
• Swollen Breasts
• Fibrocystic breasts
Lack of available cholesterol for
PROGESTERONE
synthesis.
The
corpus luteum
depends almost exclusively on peripheral low-density-lipoprotein-carried
cholesterol (LDL-cholesterol)for making steroids.
Gwynne, J.T.; Strauss, J.F., III: The role of lipoproteins
in steroidogenesis and cholesterol metabolism in steroidogenic glands. Endocr.
Rev. 3: 299 (1982).
High
doses of vitamin E (>600IU) may be luteolytic
(degrade corpus luteum ) ,
probably by lowering LDL-cholesterol.
Suggests data from recent studies. Although a daily dose of 150
IU vitamin E raised mid-luteal serum PROGESTERONE
levels by 50% (luteotrophic effect), 300 and 600 IU daily doses were
associated with lower PROGESTERONE levels than control levels.
London RS et
al.: The effect of alpha-tocopherol on premenstrual symptomatology. A double-blind
study. H. Endocrin correlates. J. Am. Coll. Nutr. 3: 351 (1984)
Although such decreases in PROGESTERONE
levels were not significant, it is likely that dosage of
vitamin E greater than 600 IU will result
in greater PROGESTERONE suppression.
This may explain why PMT-A (most common type of premenstrual tension) symptoms
worsened with 600 IU of vitamin E whereas 150 IU showed an improvement of PMT-A
symptoms. London, R.S.; Sundaram, G.S.; Murphy,
L.; et al.: The effect of alpha-tocopherol on premenstrual symptomatology. A
double-blind study. J. Am. Coil. Nutr. 2: 115 (1983)
Inhibition of
PROGESTERONE synthesis by the prostaglandin PGF2a.
PGF2a is luteolytic (Degrades corpus luteum) in women
Dennefors BL et al. PROGESTERONE and adenosine 3',
5'- monophosphate formation by isolated human corpora lutea of different ages.
Influence of human chronic gonadotropin and prostaglandins. J. clin. Endocr.
Metab. 55: 102 (1982)
The
precursor of PGF2a is
arachidonic acid (AA) ,
present in animal fats, thus excess consumption of animal fats may cause luteal
deficiency - Luteal deficiency is a high risk factor for breast
cancer, and may be the mechanism whereby increased intake of animal fats predisposes
to breast cancer.
Cowan LD et al. Breast cancer incidence in women with
a history of PROGESTERONE deficiency. Am. J. Epidem. 114: 209 (1981).
Wynder EL et al. Nutrition and the etiology and prevention
of breast cancer; in Strax, Control of breast cancer through mass screening,
pp. 89-100 (Littleton, Colorado 1979)
The luteotropic effect (stimulating formation of
corpus luteum of
small doses of vitamin E (150
IU or less) could be due to the inhibitory effect of
vitamin E on the release of
AA from storage pool, in this manner decreasing the availability
of PGF2a precursors. The net effect of
vitamin E on
PROGESTERONE synthesis
would depend on the response of LDL-cholesterol and arachidonate
release from storage pools to various dosages of
vitamin E . It is possible that
blockage of arachidonate release is more sensitive to
vitamin E than suppression
of LDL-cholesterol, such that low dose of
vitamin E would decrease precursor
availability for PGF2a synthesis (a luteotropic effect) and high
dose of vitamin E would suppress
LDL cholesterol (a luteolytic effect).
(5) Stress
Stress reduces PROGESTERONE
function - when under stress, the adrenals pump out
CORTISOL, which blocks some
PROGESTERONE receptors and thus
prevents PROGESTERONE function.
Chronic stress uses up our available
PROGESTERONE. Chronic
stress will cause adrenal fatigue, prompting the body to go to "Plan
B"and use available PROGESTERONE
to make CORTISOL. However, in this
scenario, there is not enough PROGESTERONE
to make the needed TESTOSTERONE
for a woman's sexual response, never mind to oppose rising levels of
estrogen. No wonder a woman feels
lethargic and disinterested in sex when stressed!
(6) Non-ovulatory cycles
It is not uncommon for women to experience menstrual
cycles without ovulating as many as 10 years before menopause.
In those cycles enough estrogen
is made to create menstruation, but not enough
PROGESTERONE to balance it. Even
after menopause, the estrogen
ESTRONE, ccontinues to be produced
in the fat cells, while PROGESTERONE
production is greatly diminished, since the ovaries are no longer producing
and the job is left to the adrenal glands.
(7) Impaired Liver Function
A healthier liver takes up, degrades and
excretes excess estrogen ,
xenoestrogens
and sex hormone-binding globulin
(SHBG) in bile or urine. A weak liver that
fails to eliminate these surpluses in the body is often responsible for
hormonal abnormalities.
Excessive alcohol consumption.
Blocks the liver enzyme that breaks down
estrogen . Overindulging raises
estrogen levels in both
men and
women ;
Diseases of the liver.
Cirrhosis (lesions in the liver) or decreased enzyme
activity can lead to increased estrogen
levels;
Vitamin B6,
magnesium, zinc
and/or
B2 deficiency.
B6
is an important cofactor for enzymes necessary for the liver to conjugate
estrogens from the blood.
A B6
deficiency affects the liver's estrogen
clearance, keeping blood estrogen
levels high.
Biskind, M.S.: Nutritional deficiency in the etiology
of menorrhagia, cystic mastitis and premenstrual tension. Treatment with
vitamin B complex. J. clin. Endocr. Metab. 3: 227-234 (1943).
Biskind, M.S.; Biskind, G.R.: Effect of vitamin
B complex deficiency on inactivation of ESTRONE
in the liver. Endocrinology 31: 109-114 (1942).
Biskind, M.S.; Biskind, G.R.: Inactivation of
TESTOSTERONE propionate in the liver during vitamin B complex deficiency.
Alteration of the estrogen -androgen
equilibrium. Endocrinology 32: 97-102 (1945).
Biskind, MS.; Biskind, GR.: Biskind, L.H.: Nutritional
deficiency in the etiology of menorrhagia, metrorrhagia, cystic mastitis,
and premenstrual tension. Surgery Gynec. Obstet. 78: 49-57 (1944)
The
liver is primarily responsible for the conversion (by phosphorylation)
of dietary
B6 (pyridoxine )
to its active form PLP (pyridoxal-5'-phosphate).
Such activation is dependent on
magnesium ,
zinc and
B2.
I n a self-supporting role,
B6 stimulates
cell membrane transfer and utilization of
magnesium .
Abraham, G.E.; Schwartz, U.D.; Libran, M.M.: Effect
of vitamin B-6 on plasma and red blood cell magnesium levels in premenopausal
women. Ann. clin. Lab. Sci. 11: 333 (1981).
Increased
sugar intake will excrete magnesium.
Interfering with its role in providing PLP for metabolizing
estrogen;
Magnesium
also has a direct role in estrogen
conjugation. By increasing the activity
of an enzyme (glucuronyl transferase) involved in the liver's glucuronidation
of estrogens
Abraham GE. Nutrition and the premenstrual tension
syndromes, J Appl Nutr , 1984; 19:57-63
Aging and Certain Drugs.
Impair liver function;
(8) Iodine Deficiency
Iodine
Deficiency causes estrogen
imbalance. Iodine
directly controls how much estrogen
is produced by the body and in some cases the lack of
iodine might cause a surge in the production
of the estrogen ;
Iodine
supports natural cell death in the breasts
and ovaries in a woman's monthly reproductive cycle -
In preparation for pregnancy each month, there is a build up of cells in
the breasts and uterus. When conception does not occur, the body rids itself
of these then unneeded cells by a natural monthly "programmed cell
death", called apoptosis .Not having appropriate monthly
apoptosis can lead to fibrocystic breasts, polycystic ovarian syndrome or
endometriosis.
Some studies supporting anti- Estrogenic
effect of
iodine
Study
examining the geographic differences of some femalecancer rates.
Found that a low dietary
iodine intake may produce a state of increased effective gonadotrophin
stimulation, which in turn may produce a hyper-estrogenic
state characterised by relatively high production of
ESTRONE +
ESTRADIOL
and a relatively low (anti-carcinogenic) ratio of
ESTRIOL
/ ESTRONE
+ ESTRADIOL .
Stadel BV, Dietary iodina and risk of breast,
endometrial, and ovarian cancer, Lancet,1976;
Study
examining the effect of iodine
on breast cancer found that iodine deficiency has
an estrogenic
effect. By causing a functional increase
in breast estrogen receptor activities.
Stoddard FR etal, Iodine Alters Gene Expression in the MCF7 Breast
Cancer Cell Line: Evidence for an Anti-Estrogen
Effect of Iodine, 2008
(9) Obesity, Cardiovascular Disease, Digestive Problems,
Insulin resistance
Typically seen in a diet heavy in artificial ingredients
and refined sugar and flour
High fat, carbohydrate rich diet and resultant
weight gain raises estrogen levels.
An enzyme in fat cells converts adrenal hormones to
Estrogens .