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 would be silly to suggest that estrogen doesn’t have an important basic physiological role, but it’s far worse to rationalize away the impact it can have upon disease. Things can 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…”

“Estrogen synthesis takes place…in peripheral tissues in postmenopausal women…The aromatization of androgens into estrogens is the most important source of estrogens in the breast tissue…In postmenopausal women, estrogen production is constant…Consequently, the exposure of breast tissue to estrogen in postmenopausal women is continuous…This continuous exposure to high local levels of the estrogen could in part explain…findings on the association between the hormones and breast health outcomes in postmenopausal women…”

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.

“Progesterone may…have an antagonistic activity against estradiol, mediated through a decrease in the replenishment of the estrogen receptor, and also through increased 17 beta-hydroxysteroid dehydrogenase which leads to accelerated metabolism of estradiol to estrone in the target organ.”

“…progesterone can antagonise estrogen-induced growth in primary human breast tumours…progesterone lacks proliferative potential and importantly, is anti-proliferative in an estrogen-driven context…progesterone antagonised estrogen-induced tumour formation…tumour volume was inhibited by progesterone alone…”

“The second ovarian hormone, progesterone, is largely ignored in the literature, but is clearly low compared with what was normal earlier in life. Lower progesterone levels or the abnormal ratio of estrogen and progesterone also likely causes many perimenopausal symptoms.”

It helps to view the relationship between estrogen and progesterone from the point of view of stress, and the impact stress exposure can have 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 restriction. These and other stress promoting things, are generally involved in the development of estrogen issues.

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

“…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…”

“It is well established that estrogens markedly enhance the glucocorticoid response to acute stress in females…E(2) markedly enhanced plasma corticosterone responses and adrenal corticosterone content…”

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

Symptoms relating to digestion, sleep quality, mood stability, skin and hair condition, energy levels, weight regulation, sexual and brain function, as well as a variety of other measures including blood tests and things like pulse and temperature readings, can be used to measure overall stress, including both thyroid and estrogen issues.

The problem with chronic exposure to physiological stress is that it can create a situation in which 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. It’s like a three pronged attack.

The liver has the job of preparing for the removal of many potentially harmful or toxic substances from the body, and estrogen is one of them. When the liver is unable to do its job properly, estrogen levels have a greater potential to rise throughout the main 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 tends to slow, 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 – even 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. Estrogen also increases the inflammation promoting impact of exposure to bacterial endotoxin, further accelerating stress.

“…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…”

“Peak serum tumor necrosis factor-a (TNF-a) values as well as TNF-a mRNA in the liver after LPS [endotoxin] were twice as high in the estrogen treated group as in the untreated controls. Plasma nitrite levels and inducible nitric oxide synthase in the liver were also elevated significantly…estrogen treatment in vivo sensitizes Kupffer cells to LPS, leading to increased toxic mediator production by the liver.”

Some of the inflammatory things mentioned above can promote the aromatase enzyme – responsible for a great deal of 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 the activation of NFkB signaling and 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.”

“Cytokines, such as IL-6 and tumor necrosis factor (TNF)-α, have an important role in regulating estrogen synthesis in peripheral tissues, including normal and malignant breast tissues. The activities of the aromatase, estradiol 17β-hydroxysteroid dehydrogenase and estrone sulfatase are all increased by IL-6 and TNF-α. Prostaglandin E2 may also be an important regulator of aromatase activity in breast tumors.”

“A subclinical inflammatory state associated with elevated aromatase in the breast, adipocyte hypertrophy, and systemic metabolic dysfunction occurs in some normal BMI women and may contribute to the pathogenesis of breast cancer.”

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

“…a central role of estrogens in the promotion of human breast cancer is supported by many data. However, it has not been possible to identify breast cancer patients or women at risk by abnormally elevated estrogen levels in plasma. 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…”

“The predominant AA [arachidonic acid] metabolite produced in the COX pathway is prostaglandin E2 (PGE2) which has been shown to be cancer promoting in various tissues…PGE2 has been linked with breast cancer through its capacity to increase mRNA expression and protein levels of aromatase enzyme which converts androgens to estrogen in breast cancer cells…”

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 is a malignancy whose dependence on estrogen exposure has long been recognized…The induction of complete transformation of MCF-10F cells in vitro confirms the carcinogenicity of E2 [17beta-estradiol], supporting the concept that this hormone could act as an initiator of breast cancer in women.”

“…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…”

“This report concerns the evaluation of various estrogens…and aromatase activities in pre- and postmenopausal women with breast cancer….despite the low levels of circulating estrogens in postmenopausal patients, the tissue concentrations of these steroids are several-fold higher than those in plasma…”

Excessive exposure to estrogen has also been shown to be one of the causes of the damage to genes associated with the development of cancer and other inflammatory disease states.

“DNA damage in breast cancer is induced by prolonged exposure to estrogens, such as 17β-estradiol, daily social/psychological stressors, and environmental chemicals such as polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HCAs). DNA damage induced by estrogen and stress is an important factor in the pathogenesis and development of breast cancer…”

“…estrogen-induced proinflammatory cytokines, such as interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha)…generate reactive oxygen and nitrogen species (RO/NS)…leading to genotoxic damage, cell apoptosis, or cell growth…There is increasing evidence supporting that estrogen-induced alterations in the genome of cells is produced by oxidative attack…and..may be involved in tumor development…This…is supported by the findings of DNA modifications produced…by natural and synthetic estrogens in the target organs of cancer…Interaction of estrogen-induced oxidants and estrogen metabolites with DNA was shown to generate mutations in genes…”

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.”

“The identification of cytokines as having an important role in regulating estrogen synthesis in breast tissues has provided new insight into understanding some aspects of the etiology of breast cancer…breast cancer occurs more frequently in older, postmenopausal…and…obese women…IL-6 levels increase with aging…production of IL-6 and TNF-α may be influenced by body weight…conversion of androstenedione to estrone is increased in older, overweight subjects…changes in cytokine production that are related to obesity and aging, by increasing aromatase, E1-STS and estradiol dehydrogenase Type 1 activities, may account for the increased peripheral production of estrogens in such subjects…”

Although the quantity of progesterone produced and circulating in the body, is one of the most important factors protecting against harm from estrogen (removing estrogen from inside tissue, assisting excretion and limiting production and toxicity), this does not occur in isolation, and thus cannot 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.”

“Progesterone inhibited oestrogen-mediated growth of ERα+ cell line xenografts and primary ERα+ breast tumour explants…Assessment of tumour growth confirmed the previous finding that progesterone inhibited tumour formation…estrogen-stimulated ERα binding in the xenograft tumours was substantially altered by progesterone treatment…”

“…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…”

“Injection of 750 micrograms methyl eicosapentaenoic acid (EPA) or methyl 12(R),13(S)-dihydroxyeicosapentaenoic acid (12,13-diHEPE) into the ovarian artery of ewes on day 10 of the estrous cycle caused a reduction in serum concentrations of progesterone…”

Many foods can be considered estrogenic simply because they interfere with metabolic function. High PUFA containing products are a perfect example. They can 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 for metabolic support and stress protection. Niacinamide, taurine, thyroid, biotin and the antihistamine famotidine, have been shown to assist with glycogen storage and lower stress.

Avoiding excessive consumption of digestion interfering foods so as to reduce bacterial issues, can play a big part in helping 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-honored drugs such as aspirin and the older anti-histamine cyproheptadine, have proven in many cases to 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…”

“…frequent use of aspirin should protect against breakthrough synthesis of prostaglandins and thereby suppress aromatase activity. In other words, frequent use would be predicted to lead to a steady-state reduction in intramammary estrogen and thereby reduce the risk of breast cancer.”

Some other things which can protect against estrogen include methylene blue, thyroid hormone, high quality 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 under cooked 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…”

“…there is evidence that stress may also increase the risk of developing breast cancer…By increasing glucocorticoid production, stress favors…cytokine production and an increase in IL-6 levels…cytokines have an important role in breast cancer, possibly acting via stimulation of estrogen synthesis.”

“…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.

“Amongst women, oestrogen exposure is known to cause weight gain, primarily through thyroid inhibition and modulation of the hypothalamus…The influence of soy on contributing to weight gain has been recently established…Perhaps, in societies with particularly high dietary saturation of soy, this works to “feminise” the males. If such a fact was substantiated, the soy exposure would allow men in those communities to artificially imitate the female pattern of weight gain. Interestingly, the United States, the largest consumer of soy products per capita in the entire world, belong to a select group in which male obesity rates outstrip those of their female counterparts…”

“Serum estrone (E1) and 17beta-estradiol (E2) were noted to be 2-fold elevated in a group of morbidly obese men. Urinary E1 and E2 production rates were elevated in proportion to the degree of obesity…peripheral conversion of T to E2 and androstenedione (delta) to E1 were all increased in obese men in proportion to the percentage above ideal weight…”

I’m not a doctor or a scientist, and I realize that there will always be people carrying out scientific studies (and interpreting study results) in such a way as to be able to put forward a completely different case. That’s why it is so important to be able to take a step back and look at the overall picture of metabolic function and energy production. One ‘scientific breakthrough’ will never be enough.

And the truth is, estrogen will be involved one way or another, in the interplay between proper metabolic function and stress exposure. Understanding how ongoing excessive stress and thyroid suppression are 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.

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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.

A Novel Antiestrogenic Mechanism in Progesterone Receptor-transfected Breast Cancer Cells

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.

Progesterone receptor modulates estrogen receptor-α action in breast cancer

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.

Increased estrogen production in obese men.

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

Estrogen potentiates adrenocortical responses to stress in female rats.

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

Comparison of estrogen concentrations, estrone sulfatase and aromatase activities in normal, and in cancerous, human breast tissues.

Concentrations of estrone, estradiol, and estrone sulfate and evaluation of sulfatase and aromatase activities in pre- and postmenopausal breast cancer patients.

Metabolic Obesity, Adipose Inflammation and Elevated Breast Aromatase in Women with Normal Body Mass Index

Current Evidence Linking Polyunsaturated Fatty Acids with Cancer Risk and Progression

The Estrogen Hypothesis of Obesity

Antiestrogen action of progesterone in breast tissue.

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.

Estrogen-induced generation of reactive oxygen and nitrogen species, gene damage, and estrogen-dependent cancers.

Circulating dehydroepiandrosterone-sulphate decreases even with a slight change in oestradiol.

Estrogens in the breast tissue: a systematic review

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

The endocrinology of perimenopause: need for a paradigm shift.


Unique metabolites of eicosapentaenoic acid interfere with corpus luteum function in the ewe.

Endogenous estrogen and postmenopausal breast cancer: a quantitative review.

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

Treatment of postmenopausal osteoporosis

Estrogen- and stress-induced DNA damage in breast cancer and chemoprevention with dietary flavonoid

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

The endocrinology of perimenopause: Need for a paradigm shift

17beta-estradiol promotes breast cancer cell proliferation-inducing stromal cell-derived factor-1-mediated epidermal growth factor receptor transactivation: reversal by gefitinib pretreatment.

Genotoxicity of the steroidal oestrogens oestrone and oestradiol: possible mechanism of uterine and mammary cancer development.

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

Estrogen production via the aromatase enzyme in breast carcinoma: which cell type is responsible?

Estrogen regulation of mammary gland development and breast cancer: amphiregulin takes center stage

Does high polyunsaturated free fatty acid level at the feto-maternal interface alter steroid hormone message during pregnancy?

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.

How does estrogen enhance endotoxin toxicity? Let me count the ways.

Host microenvironment in breast cancer development: Extracellular matrix–stromal cell contribution to neoplastic phenotype of epithelial cells in the breast

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

Impact of fatty acids on human UDP-glucuronosyltransferase 1A1 activity and its expression in neonatal hyperbilirubinemia

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.

Association of Frequency and Duration of Aspirin Use and Hormone Receptor Status With Breast Cancer Risk

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

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

17-Beta-estradiol induces transformation and tumorigenesis in human breast epithelial cells.

Chronic stress increases estrogen and other steroids in inseminated rats.

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

The role of cytokines in regulating estrogen synthesis: implications for the etiology of breast cancer

Serum hormone levels in men with severe acne.

Anti-estrogenic effect of unliganded progesterone receptor is estrogen-selective in breast cancer cells MCF-7.

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

Estrogen-induced generation of reactive oxygen and nitrogen species, gene damage, and estrogen-dependent cancers.

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.

Correlation of blood sex steroid hormones with body size, body fat distribution, and other known risk factors for breast cancer in post-menopausal Chinese women.

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.

The anti-aromatase effect of progesterone and of its natural metabolites 20alpha- and 5alpha-dihydroprogesterone in the MCF-7aro breast cancer cell line.

In situ aromatization enhances breast tumor estradiol levels and cellular proliferation.

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.

Antiestrogen action of progesterone in breast tissue.

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


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