There is no shortage of information and opinions concerning hormone treatments or the “best” way to test for hormone deficiencies, not to mention how to use hormones or confirm if a hormone intervention is working.
However, the hormone receptors are really the thing that should be examined. Regardless of the testing method, the specific hormone, or its intended result, all hormone action occurs at the receptor sites.
WHAT ARE RECEPTOR SITES?
Receptors are protein structures designed to grab passing hormones. Receptors for hormones that poke through the cell membrane and are called membrane receptors. Other receptor sites are inside the cell (intracellular receptors) in the cytosol(the liquid found inside cells) and more receptors are in the cell nucleus. The number of receptors are not stagnant, and varies according to nutrients and the environment.
Once a receptor captures a hormone, that cell receives instructions for an action, such as cell replications, manufacturing other proteins, moderating cell activity, and programming abnormal cell death. A single hormone can produce action within minutes of binding. Receptors manipulate the cell’s action by upregulating or down-regulating the production of proteins.
Conventional practitioners insist that as long as a hormone receptor site receives a hormone-whether it is identical to the human hormone or not – all hormones and hormone-like substances should be considered equal. This thinking completely ignores the research identifying different affinities for different hormone receptors. As an example, the hormone estriol is generally considered a week estrogen. This is because the binding of estriol on a receptor, in comparison to estradiol binding on the same receptor, produces less response.
In sharp contrast, the receptor for estrogen in the urinary tract, bladder, and vaginal tissue have a much greater affinity for estriol. A study published in the New England Journal of Medicine demonstrated dramatic differences in effectiveness in treating urinary tracts in elderly women with recurrent infection. Clinically, estriol also shines when treating vaginal dryness, outperforming estradiol and other estrogens.
For example, receptors have an affinity and are not very discriminating about binding and can be affected by synthetic hormones as well as the “real thing.” Receptor site activity can be blocked or accentuated. For example, medroxyprogesterone acetate (synthetic), a progestin rather than real progesterone, not only interferes with progesterone receptors but can block testosterone and cortisol receptors also.
Dr. Friedman, a theoretical biologist, describes the hormone’s “big picture” and also offers a theory on what he calls the Hormone Receptor Model. He believes that his model answers questions about how breast and prostate cancer initiate, and how this information can be used to target very specific treatment based on bioidentical hormones (particularly testosterone) to change the course of these diseases. Dr. Friedman states that breast and prostate cancer are fundamentally identical in their causes, presentation, and progression.
Dr. Edward Friedman’s book is titled “The New Testosterone Treatment: How You and Your Doctor Can Fight Breast Cancer, Prostate Cancer, and Alzheimer’s”.
Bcl-2
Bcl-2 is a protein produced by hormone stimulation in the cell nucleus of cancer cells. This protein is of high importance in the discussion of breast and prostate cancer. Cancerc cells are immortal’ they escape the normal program for cell death called apoptosis. The Bcl-2 protein shields cancer cells from their normal cell destruction.
Estrogen Receptors
Estrogen Receptor Beta (ER-Beta) stimulation has a positive result, which is that the production of the Bcl-2 protein is down-regulated, thus depriving cancer cells of their immortality. Moreover, it also has an anti-inflammatory effect.
Estrogen Receptor Alpha (ER-Alpha) increases inflammation and the production of the Bcl-2 protein. When breast cancer tissue is examined and reported as estrogen receptor-positive, that information is incomplete. We need to know the concentrations of the different estrogen receptors. A dominance of ERBeta receptors is good. One feature of cancer cells is that the further the cancer progresses, the more ERAlpha receptors are available.
A synopsis of Dr. Friedman’s treatment program includes the following:
He suggests that vitamin D (which is a hormone) should always be considered first and foremost with a diagnosis of breast cancer or prostate cancer. there is no downside to ensuring that vitamin D levels are optimized and activation of the vitamin D receptor helps destroy cancer cells.
He also states that ample amounts of testosterone are very protective against both breast and prostate cancer.
He advises on the use of an aromatase inhibits to hamper the conversion of testosterone to estrogens, which can lead to more activation of ER-alpha receptors.
He believes that stimulation to the ER-Beta receptors Premarin with its predominance of estrone, clearly is a therapy that shifts the stimulation to the ER-Alpha receptors.
Be very aware that anyone considering this treatment should work with a specialist. Preferably a naturopathic doctor or alternative care specialist who understands this treatment. I am interested in reading Dr. Friedman’s book.
While breast cancer is one of the most common cancers diagnosed among women, there are many established risk factors including age, genetic alterations, family history, mammographic breast density, menstrual and menopausal history, radiation exposure, and life style. In particular, the hormones, estrogen and/or progesterone, are known to be capable of increasing breast cancer risk. Both ER-dependent and ER-independent pathways have been proposed for biological responses of estrogen. Estrogen binding to receptors results in their translocation to the nucleus, where they act as transcription factors leading to altered gene expression. ER-dependent carcinogenic action of estrogen involves ER-mediated aberrant regulation of estrogen responsive genes that lead to increased cell proliferation and accumulation of DNA damage ultimately causing cell transformation. The ER-independent pathway involves cytochrome P450 (CYP) mediated oxidative metabolism of estrogen resulting in generation of genotoxic metabolites and ROS. Since a large number of studies have demonstrated an inverse association between consumption of fruits and vegetables and the risk of breast cancer through suppression of ER signaling and reduction of oxidative stress, naturally occurring dietary compounds and phytochemicals have received increasing attention for treatment of prevention of breast cancer. This review aims to summarize the potential of bioactive natural products in the prevention and treatment of estrogen-mediated and ER-positive breast cancer.
NOTE: Please be aware that our body makes its own hormones. When levels become deficient or changed then there are synthetic and compounded bioidentical hormone replacements that are provided to balance what is lost or deficient.
Women’s International Pharmacy (https://www.womensinternational.com) provides a vast amount of information on hormonal health as well the compounded forms of bioidentical hormone replacement therapies. I have been on the bioidentical hormones for many years. Provided by prescription through my own naturopathic doctor and compounded through my local compounding pharmacy. I have many articles on my site explaining why these formulas are better then synthetic one size fits all hormone replacement therapies.
