Soy No More

You don’t need to guzzle cartons of soy milk and snack on edamame or soy protein bars all day long to develop a problem with estrogen, although it probably won’t help matters. The truth is you don’t even need to be a woman. Oh, and before you rush out for a blood test, there’s some things you oughta know.

It’s silly to suggest estrogen doesn’t have an important basic physiological role, but it’s far worse to rationalise away it’s impact upon disease. Things become really dangerous the minute you start talking about so called estrogen deficiencies and estrogen replacement treatment methodologies.

“Perimenopause, rather than a time of declining estrogen, is characterized by…major hormonal changes…erratically higher estradiol levels, decreased progesterone levels…there is an urgent need to change…understandings, language and therapies…”

Biologically speaking, progesterone has been shown to be a basic anti-estrogen substance, and the ratio of progesterone to estrogen appears to be central to protection against estrogen’s harmful effects.

It helps to view the relationship between estrogen and progesterone from the point of view of stress and its impact upon thyroid function and metabolism. While you’re at it, you may as well include some discussion about serotonin, the polyunsaturated fats, and of course sugar. These and many other stress promoting things, are involved in the development of estrogen issues.

Anything that interferes with thyroid metabolism and promotes stress, will likely eventually cause estrogen levels in the body to increase, as a result of increased production and accumulation. To put it a little more simply, stress is estrogenic.

“…results indicate that exposure to a relatively acute stressful event immediately and persistently enhances serum estradiol…”

“…findings suggest that homeostatic regulation involves complex mutual interactions between the reproductive axis, HPA axis and the immune system, in which estrogens and CRH [Corticotropin-releasing hormone] may be playing central roles.”

“The most striking finding in the…hypothyroid rats was the dramatic enhancement of oestradiol formation…”

Much like with stress in general, working out whether or not estrogen levels are excessive can be assisted greatly by an awareness of certain indicators of metabolic performance, and the state of the different anti-stress or anti-estrogenic factors, some of which have already been mentioned.

The problem with chronic exposure to physiological stress is that it can create a situation in which far more estrogen is produced, elimination of excess estrogen is being interfered with, and biological protections against estrogen’s most damaging effects are less and less available.

The liver has the job of preparing for the removal of many toxic substances from the body, and estrogen is often one of them. When the liver is unable to do its job properly, estrogen levels rise throughout the greater system.

“Estrogens are eliminated from the body by metabolic conversion to estrogenically inactive metabolites that are excreted in the urine and/or feces…the metabolism of estrogens mainly occurs in the liver.”

When thyroid metabolism is suppressed by stress, liver function slows and this reduces detoxification capability. Stress also inhibits digestion, allowing greater amounts of toxins to pass through intestinal barriers, placing even more strain on the liver. As a result of this, estrogen detoxification and excretion is hindered allowing it to recirculate into the system.

Estrogen itself can overload and interfere with liver function, making the development of a vicious circle of gradually worsening conditions – with increasing exposure to more and more of the substances of stress and inflammation – more likely.

Stress can become a problem because of emotional trauma, extreme exercise, inadequate diet, as well as hereditary issues and lots of different environmental poisons and toxins. Two things which can have a powerfully damaging effect upon metabolic function, include sugar restriction and excessive consumption of polyunsaturated fats.

When sugar is restricted and stress is high, glycogen stores can be diminished quickly. When this happens polyunsaturated fats (stored in tissue from previous consumption) are released into the system as free fatty acids, worsening estrogen issues.

Polyunsaturated fats are highly inflammatory and they interfere with thyroid/energy system function in numerous different ways. On top of this (and because of this) they inhibit digestion and cause damage to the liver.

This can result in a pronounced increase in systemic levels of estrogen, and when the polyunsaturated fats interact with estrogen, they act on it in such a way as to make it more toxic and harmful.

When stress suppresses thyroid metabolism (including digestion and liver function), bacterial endotoxin levels tend to rise, promoting the release of serotonin. Estrogen enhances serotonin’s ability to wreak havoc on metabolism, adding to stress levels, stimulating the release of cortisol, adrenalin, prolactin, nitric oxide and free fatty acids, as well as a variety of other substances of inflammation.

“…findings suggest that estrogen can facilitate serotonergic transmission by enhancing serotonin synthesis and/or decreasing serotonin reuptake…”

“…we observed that…serotonin/prolactin was lowest when aromatase was maximally inhibited…Serotonin correlated best with theoretical aromatase activity and neural conversion of T to E, which in turn would promote neural ER activation.”

“Our study defines a contribution of estrogen through its regulation of eNOS expression and nitric oxide production to vascular hyperpermeability and intensified anaphylactic responses…”

Many of the inflammatory things mentioned above promote the aromatase enzyme – which is responsible for the production of estrogen – and systemic inflammation can change the form of estrogen, so that it remains in the tissue where it accumulates and does the most damage.

“…chronic low-grade inflammation is associated with…elevated levels of aromatase, the rate-limiting enzyme in estrogen biosynthesis…This occurs not only in the visceral and subcutaneous fat, but also in the breast fat.”

The polyunsaturated fatty acids (PUFA) promote tissue storage of estrogen, and more PUFA inside fat cells is likely to encourage aromatase activity, increasing estrogen production inside the cell.

“The concept of available, i.e., non-SHBG bound sex steroid seems to offer a better understanding than total serum steroid levels do. We demonstrated that sex steroid protein binding is decreased by free fatty acids.”

“…there existed a positive tissue/plasma gradient for…estrone…and estradiol…tissue and plasma estrogen concentrations were not correlated…fat tissue is an important steroid hormone reservoir…it is the site of active aromatase…”

Continuous and prolonged exposure of tissue to estrogen is known to be a driving force behind the development of many forms of cancer, although it’s difficult if not impossible to exclude the involvement of excess (unopposed) estrogen levels in the development of metabolic/degenerative disease in general.

“…breast cancer tissue E2 [estradiol] levels are 10-fold to 50-fold higher in postmenopausal women than predicted from plasma levels…factors…present to alter breast tissue E2 levels independently of plasma concentrations…may be the local production of E2 in breast tissue through the enzyme aromatase…”

Unfortunately most blood tests used to determine estrogen levels are misleading. Instead of detecting tissue bound estrogen, all they do is help fuel dangerously misleading and hugely profitable belief systems which suggest the possibility of estrogen deficiencies and the need for supplementation.

“…tissue/plasma ratio of E2 ranged from 1.45 to 20.36 with very high values in early follicular phase and the lowest in mid-luteal phase…In postmenopausal women, the tissue concentration of E2 was not significantly lower than in menstruating women in follicular phase…Neither in these women nor in menstruating women was there a close correlation between tissue and plasma levels…a certain amount of these steroids is bound to tissue even if plasma levels are low.”

Although the quantity of progesterone produced and circulating in the body, is one of the most important factors protecting against harm from estrogen (removing it from inside tissue, assisting excretion and limiting production and toxicity), this cannot really be separated from ideas relating to stress and thyroid energy system performance.

“Women in the PD [progesterone deficiency] group had 5.4 times the risk of premenopausal breast cancer as compared to women in the NH [nonhormonal causes] group…Women in the PD group also experienced a 10-fold increase in deaths from all malignant neoplasm compared to the NH group.”

“…transdermal progesterone…effectively reverses postmenopausal osteoporosis…The safety of supplemental progesterone is impressive.”

Progesterone production is dependent upon metabolic performance, making the suppression of thyroid function due to continuous exposure to stress (including from lack of sugar and exposure to polyunsaturated fats) especially relevant.

Apart from making estrogen more powerful and injurious, the polyunsaturated fats directly interfere with progesterone synthesis, and can suppress thyroid function to such an extent that it enables the promotion of stress related conditions (and substances) which help to worsen the ratio of estrogen to progesterone, and promote inflammation and disease.

“…arachidonate inhibition was dose-dependent in the tissue steroid hormone receptors, except for dose-dependent potentiation of the brain cortical estrogen receptors.”

“…unsaturated fatty acids such as oleic acid (18:1), arachidonic acid (20:4) and docosahexaenoic acid (22:6) inhibited the binding between androgen receptor and 3H-R1881…”

Many foods can be considered estrogenic simply because they intefere with metabolic function. High PUFA products are a perfect example. They inhibit thyroid and digestion, promote bacterial toxin production and cause damage to the liver.

Popular ‘health’ foods made from soy (containing phytoestrogens) can be understood to be directly carcinogenic.

“…dietary soy isoflavones enhanced the growth of bone micro-tumors…soy isoflavones stimulate BC [breast cancer] with bone micro-metastasis in mice and further investigations are needed regarding their consumption by BC survivors.”

“…at low concentrations, genistein and zearalenone produce proliferative effects on human breast cancer cells.”

It is common to hear talk of restricting sugar to deal with ‘estrogen dominance’ issues, but sugar and protein are fundamental ingredients necessary for effective estrogen reduction as well as progesterone production and overall thyroid performance.

In fact, things that improve thyroid energy metabolism in general, help make existing estrogen less dangerous (shifting it from the stronger form estradiol, to estrone), whilst also reducing overall estrogen production, and improving the ability of the liver to more efficiently excrete it.

A general multi-pronged stress preventative approach, can be a powerful way to avoid estrogen excess, and can help to avoid the development of ‘estrogenic’ metabolic conditions.

There are lots of different approaches or tactics which have been used to promote great improvement in overall metabolic energy system performance, and many of them are cheap and easily available for experimentation.

In order to minimize the potentially damaging effects of stress, it’s a good idea to use food (and some other things) in a manner which encourages glycogen storage and helps to maintain stable blood sugar supply.

Glycogen storage capability is a topic all by itself but a consistent supply of fructose and sucrose from sweet juices, honey or white sugar is one of the important things. Niacinamide, taurine, thyroid, biotin and the antihistamine famotidine can all potentially assist greatly.

Avoiding digestion interfering foods so as to reduce bacterial excess, can help free up the liver to carry out detoxification functions more effectively and get rid of unwanted estrogen.

Increasing exposure to daylight (and therapeutic red light) and avoiding too much blue light especially in the evenings, can improve sleep quality and protect against estrogen and stress in general.

Tried, tested and time-honoured drugs such as aspirin and the older anti-histamine cyproheptadine can be a useful addition.

“Treatment of human breast cancer cells…with cyproheptadine decreased…estrogen-dependent cell growth. Our findings suggest that cyproheptadine can be repurposed for breast cancer treatment…”

“…If cyproheptadine acts by antagonizing serotonin, these studies suggest that serotonin may be involved in hypoglycemia induced cortisol secretion in man.”

Some other things which can protect against estrogen include methylene blue, thyroid hormone, protein, vitamin B1 and B2, caffeine, pregnenolone, progesterone, vitamin E, raw carrots, activated charcoal, well cooked mushrooms, certain antibiotics, niacinamide and more.

A diet avoiding the polyunsaturated fats and difficult to digest fibrous and starchy beans, grains and legumes and undercooked vegetables, including smaller more regular meals, with sufficient protein and nutrients from milk, cheese and gelatin, and plenty of sugar from sweet ripe fruits, juices, white sugar and honey, is one possible approach to protecting against stress, and improving hormonal balance.

Saying something is estrogenic is basically synonymous with saying that it is stressful and vice versa. A simple blood test for Prolactin gives an accurate picture of tissue bound estrogen as well as serotonin levels.

“exposure to the stressors enhanced estradiol beyond basal levels…Glucocorticoid levels were elevated in response to both stressors…”

“…serotonin stimulates the secretion of prolactin…aromatase activity correlated significantly with prolactin…”

It’s not a small deal. Estrogen excess has been connected to many conditions other than cancer, in both men and women. Depression, schizophrenia, MS, Alzheimer’s, obesity, osteoporosis, allergy and anaphylaxis, infertility, gynecomastia, erectile dysfunction, acne, varicose veins, PCOS, endometriosis, narcolepsy, addiction, epilepsy, ‘autoimmunity’ and more.

Truth is, one way or another estrogen will always be involved. Understanding how stress and thyroid suppression is intertwined with changes in hormonal and biochemical conditions (and metabolic performance in general) can give powerful insight regarding ways to improve quality of life and prevent the onset of common diseases of aging and degeneration.

See More Here

Comparison of plasma and myometrial tissue concentrations of estradiol-17 beta and progesterone in nonpregnant women.

Induction of proto-oncogene BRF2 in breast cancer cells by the dietary soybean isoflavone daidzein

Dietary soy isoflavones increase metastasis to lungs in an experimental model of breast cancer with bone micro-tumors.

Diet and disease–the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet.

Dietary Estrogens Stimulate Human Breast Cells to Enter the Cell Cycle

Cytochrome P450-mediated metabolism of estrogens and its regulation in human.

Serotonin in trigeminal ganglia of female rodents: relevance to menstrual migraine.

Inflammation, dysregulated metabolism and aromatase in obesity and breast cancer.

Androgens and estrogens in relation to hot flushes during the menopausal transition.

Alcoholic liver injury: Influence of gender and hormones

Inhibition of estrone sulfatase and 17 beta-hydroxysteroid dehydrogenase by antiestrogens.

Inhibition of Hypoglycemia-Induced Cortisol Secretion by the Serotonin Antagonist Cyproheptadine

Tissue-specific synthesis and oxidative metabolism of estrogens.

Acute stress persistently enhances estrogen levels in the female rat.

Hormonal contraceptives masculinize brain activation patterns in the absence of behavioral changes in two numerical tasks.

Analgesic use and sex steroid hormone concentrations in postmenopausal women

Novel interactions of vitamin E and estrogen in breast cancer.

Possible relevance of steroid availability and breast cancer.

Breast cancer incidence in women with a history of progesterone deficiency.

Regulation of MCF-7 Breast Cancer Cell Growth by β-estradiol Sulfation

The endocrinology of perimenopause: need for a paradigm shift.

The regulation of adenohypophyseal prolactin secretion: effect of triiodothyronine and methylene blue on estrogenized rat adenohypophysis.

Treatment of postmenopausal osteoporosis

Induction of PGE2 by estradiol mediates developmental masculinization of sex behavior.

Osteoporosis reversal with transdermal progesterone.

Sex differences in corticotropin-releasing factor receptor signaling and trafficking: potential role in female vulnerability to stress-related psychopathology

Unconventional endocannabinoid signaling governs sperm activation via the sex hormone progesterone

Estrogen increases the severity of anaphylaxis in female mice through enhanced endothelial nitric oxide synthase expression and nitric oxide production

Evidence of direct estrogenic regulation of human corticotropin-releasing hormone gene expression. Potential implications for the sexual dimophism of the stress response and immune/inflammatory reaction.

FSH-induced aromatase activity in porcine granulosa cells: non-competitive inhibition by non-aromatizable androgens.

Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor.

Menopausal hormone therapy and breast cancer: what is the true size of the increased risk?

50 years of hormonal contraception—time to find out, what it does to our brain

Inhibition of SIRT1 deacetylase suppresses estrogen receptor signaling

Regulation of the sperm calcium channel CatSper by endogenous steroids and plant triterpenoids

Preliminary evidence of altered steroidogenesis in women with Alzheimer’s disease: Have the patients “OLDER” adrenal zona reticularis?

The role of dopamine in methylene blue-mediated inhibition of estradiol benzoate-induced anterior pituitary hyperplasia in rats.

Functional state of the hypophysis, adrenal cortex and gonads in patients with gynecomastia.

The effect of vitamin deficiency on estradiol inactivation in the liver.

Estrogen Mediates Metabolic Syndrome-Induced Erectile Dysfunction: A Study in the Rabbit

Direct effects of prolactin on corticosterone release by zona fasciculata-reticularis cells from male rats.

Serum hormone levels in men with severe acne.

Caffeine and Caffeic Acid Inhibit Growth and Modify Estrogen Receptor and Insulin-like Growth Factor I Receptor Levels in Human Breast Cancer.

Estrogen-mediated effects on depression and memory formation in females

Effects of aromatase inhibition and androgen activity on serotonin and behavior in male macaques.

Genomic agonism and phenotypic antagonism between estrogen and progesterone receptors in breast cancer

alpha-Tocopherol administration produces an antidepressant-like effect in predictive animal models of depression.

Elevated serum estradiol/testosterone ratio in men with primary varicose veins compared with a healthy control group.

Methylene blue as an endocrine modulator: interactions with thyroid hormones.

The regulation of adenohypophyseal prolactin secretion: effect of triiodothyronine and methylene blue on estrogenized rat adenohypophysis.

Effect of methylene blue on estrogen-receptor activity.

Fat tissue: a steroid reservoir and site of steroid metabolism.

Inhibitory effect of fatty acids on the binding of androgen receptor and R1881.

Identification of Cyproheptadine as an Inhibitor of SET Domain Containing Lysine Methyltransferase 7/9 (Set7/9) That Regulates Estrogen-Dependent Transcription.

Arachidonic acid as a possible modulator of estrogen, progestin, androgen, and glucocorticoid receptors in the central and peripheral tissues.

Influence of thyroid hormone on androgen metabolism in peripuberal rat Sertoli cells.

Menstrual Phase as Predictor of Outcome After Mild Traumatic Brain Injury in Women


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