Hormone Receptors are THE Thing!

Testing for hormones to define how to use them, or how to confirm successful interventions, fails because ultimately we need to know what happens at the hormone receptor. Whether we test the serum or saliva or urine, the real action of hormones occurs at the receptors.  

All hormones are alike

Conventional practitioners are insisting that if a hormone receptor receives a hormone, whether it is identical to human or not, then all hormones and hormone like substances have to be considered equal.  But research identifies different affinities for specific hormone receptors. For example, the estrogen called estriol is generally considered a weak estrogen. Binding of estriol on a receptor in comparison to estradiol binding on the same receptor produces less response. In sharp contrast, the hormone receptors for estrogen in the urinary tract, bladder and vaginal tissue have a much greater affinity for estriol. An early study published in 1993 in the New England Journal of Medicine demonstrated dramatic effectiveness of estriol with the urinary tract and stopping recurrent infection. Clinically, estriol shines when treating vaginal dryness, outperforming estradiol and other estrogens.  

What are hormone receptors?

Hormone receptors are protein structures designed to snag hormones.  Receptors for hormones poke through the cell membrane. These are called membrane receptors.  Other receptors are inside the cell (intracellular receptors) in the cytosol. Hormone receptors are in the cell nucleus. Once a receptor captures a hormone, cells receive instructions for their work.  This work includes cell replication, manufacturing other proteins, moderating cell activity and programming cell death of abnormal cells. A single hormone can produce action within minutes of binding.  Hormone receptors oversee manipulating the cell’s work by up-regulating or down-regulating production of proteins. 

Hormone receptors are promiscuous. 

Hormone receptors can be affected by synthetic hormones as well as the real thing.  Receptor activity could be blocked or accentuated.   Numbers of receptors are not stagnant but vary according to food and environment.  Medroxyprogesterone acetate, a progestin rather than real progesterone, will not only interfere with progesterone receptors but can block testosterone and cortisol receptors too.  Since testosterone has such a positive effect on potential breast and prostate cancer (below), this might explain why this synthetic hormone is associated with increases in breast cancer as reported in the Women’s Health Initiative study. 

The New Testosterone Treatment

In his book, The New Testosterone Treatment: How You and Your Doctor Can Fight Breast Cancer, Prostate Cancer, and Alzheimer’s, Dr. Edward Friedman, a theoretical biologist put together the “big picture” and offers the Hormone Receptor Model.  He believes his model answers the questions about how breast and prostate cancer initiates. Specific treatment, based on bioidentical hormones, particularly testosterone may change the course of these diseases.  He states that breast and prostate cancer are fundamentally identical in their causes, presentation and progression. 

Direct to Consumer Hormone Testing

Introducing Bcl-2

Bcl-2 is a protein which is produced by hormone stimulation in the cell nucleus in cancer cells.   This protein is of high importance in the discussion of breast and prostate cancer.   Cancer cells are immortal.  They escape the normal program for cell death.  The Bcl-2 protein shields cancer cells from their normal cell destruction,

Hormone Receptors Include Vitamin D Receptors

Vitamin D should always be considered first and foremost during the presentation of breast or prostate cancer. Activation of the vitamin D receptor helps destroy cancer cells by at least 4 different mechanisms. There is no downside to ensuring that vitamin D levels are optimized. 

Estrogen receptor Beta (ER-Beta)

Stimulation of the beta receptors with estrogen has a positive result.  Production of the Bcl-2 protein deprives cancer cells of their immortality. More, there is an anti-inflammatory effect.

Estrogen receptor Alpha (ER-Alpha) increases inflammation and the production of the Bcl-2 protein. Breast cancer cell reported as estrogen receptor positive yields information is incomplete. We should know all the types and concentrations of receptors.  If there is a dominance of ER-Beta, it would be a good thing. A feature of cancer cells is that the more the cancer progresses, the more ER-alpha receptors are available.

Types of estrogen and binding properties. 

Estradiol binds to both alpha and beta receptors with equal strength. Estrone binds to alpha receptors 5 times more tightly than to beta receptors and estriol binds to ER-beta 3.2 times more tightly than will bind to ER-alpha. The amount of Bcl-2 being produced is dependent upon which estrogen is binding, how strongly it is binding and finally the amounts of each type of receptor. Hence estrone is potentially more pro cancer and estriol has potential to be more anti-cancer. 

Progesterone Receptors

Progesterone receptors A increases Bcl-2 and stimulation of this receptor is tied into BRCA1 and BRCA2 mutations. According to Dr. Friedman, the small number of women with this mutation with have increased amounts of progesterone receptor A. In turn, this leads to an increased Bcl-2 production protecting cancer cells. Progesterone receptor B also diminishes the production of Bcl-2 when activated.

Androgen receptors

The membrane androgen receptor behaves differently in men and women. In women, stimulation of this receptor causes a decrease in Bcl-2 and in men there is an increase in Bcl-2  Stimulation of the intracellular androgen receptors decrease Bcl-2 and also causes of the production of other anti-cancer proteins in both men and women.  However, if there is a shortage of testosterone to stimulate the intracellular receptors, the shortage favors more cancer cell growth. 

Dr. Friedman considers testosterone in ample amounts very protective for both breast and prostate cancer. He advises on the use of aromatase inhibitors to diminish the amount of conversion of testosterone to estrogens. If aromastase is excessive, more activation of ER-alpha receptors occurs. (The hormone progesterone is an aromaste inhibitor.) Estriol is underused and could be supplemented generously to shift stimulation to the ER-beta receptors Dr. Friedman believes. Premarin, with its predominance of estrone clearly is a therapy that shifts the stimulation to the ER-alpha receptors. 

Dr. Rebecca Glazer

Dr. Rebecca Glazer published strong evidence that testosterone can be protective and perhaps even effective in treatment for breast cancer.  She presented the results of the 1268 women receiving testosterone treatment along with an aromatase inhibitor.  She is observing a dramatic decrease in breast cancer incidence in her study group.  

In Conclusion

Dr Friedman offers some very thought-provoking ideas using bioidentical hormones in treatment of breast and prostate cancer.   His theory is not yet tested but some practitioners have incorporated some of the features.   He feels this method is not intended to be a “cure” but a means to control the cancer.  The only downside is instead of suffering from the disfigurement and secondary effects of cancer surgery and radiation and the debilitation of hormone deprivation and chemotherapy drugs, restoring hormones to more youthful levels yields zestful living while living with cancer.