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Hormone Myths versus Medical Evidence by Dr. Ron Rothenberg

There are many myths surrounding hormone replacement therapies, from the notion that thyroid hormone is dangerous for the heart, to the widespread belief that growth hormone replacement therapy (GHRT) increase the risk of cancer.  The aim of this article is to review the current medical literature surrounding these myths and to demonstrate the safety and efficacy of hormone replacement therapies.


Is thyroid hormone bad for the heart?  No.  Yes, it is true that hyperthyroidism is associated with atrial fibrillation; however optimizing thyroid hormone is associated with numerous benefits.

*Improves lipids

*Improves CHF

*Has a positive inotropic effect upon the heart

*Is vasodilatory

**Prevents maladaptive cardiac remodeling after acute MI

*Normalizes the QT interval, thus reducing the odds of lethal arrhythmias

*Improves C-reactive protein (CRP_ and homocysteine levels

*Improves arterial stiffness and endothelial dysfunction

It is important to remember that T3 is the active hormone and T4 is the prohormone.  The heart needs T3 as it is unable to convert T4 into T3.  Signs of low T3 in cardiovascular disease include:

Bradycardia, narrowed pulse pressure, and diastolic hypertension


Endothelial dysfunction

Elevated CRP and homocysteine

Iervasi et al found that low T3 is a strong predictor of death in cardiovascular patients.  In this study, low T3 was defined as <3.1 pg/mL free T3, which is interesting because it is within the confines of the reference range (2.3 to 4.2 pg/mL), albeit in the bad half of the reference range – remember, as anti-aging providers we want optimal levels, not reference range levels.  Results showed that low T3 was the strongest independent predictor of death – more than dyslipidemia and more than a poor ejection fraction.  Furthermore, the authors concluded that low T3 might be directly implicated in the poor prognosis of cardiac patients.

So, we can see that thyroid hormone is clearly not dangerous for the heart.  It is very important to measure free T3 and reverse T3 in cardiac patients, and it is equally important not to be afraid of optimizing T3 – it should be in the upper third of the reference range (3.5-4.2 pg/mL).  A patient’s life may well depend on it.  Treat mild hypothyroidism by optimizing free T3 to reduce all components of metabolic syndrome.  DO not rely on the TSH.  Look at the patient’s clinical picture and look at free T3, and remember that it is important to consider symptoms, not just numbers.


The bottom line is that testosterone does not cause prostate cancer to grow.  The notion that testosterone causes prostate cancer to grow was based on one case report from 1941 – one patient.  There is no relationship between testosterone, dihydrotestesterone, estradiol, and prostate cancer, and there are no reports of prostate cancer in men treated with testosterone after radical prostatectomy.

Results of a perspective study of 11,606 men by Khaw et al led the authors to conclude.  “In men, endogenous testosterone concentrations are inversely related to mortality due to cardiovascular disease and all causes.” The authors also write: “Prospective studies or supplementation studies, reviewed elsewhere, have not reported significant relationships of endogenous testosterone concentrations or of testosterone supplementation with prostate cancer.  Although in the present analysis, there are insufficient power to examine the relationships with prostate or other specific cancers, we observed an inverse relationship of endogenous testosterone concentrations with cancer mortality.”

Another study, this time a review of 18 prospective  studies that included 3886 men with incident prostate cancer and 6438 control subjects, examined the association between endogenous sex hormone sand prostate cancer risk.  NO associations were found between the risk of prostate cancer and serum concentrations of testosterone, calculated free testosterone, dihydrotestosterone, dehydroepiandrosterone sulfate, adnrosternedione, androstanediol glucuronide, estradiol, or calculated free estradiol.

So, there is plenty of evidence to show that testosterone does not increase the risk of prostate cancer.  There is also evidence showing that endogenous testosterone concentrations are inversely related to mortality due to cardiovascular disease and all causes, but is there any evidence to show treating men with testosterone after radical prostatectomy is safe?  Yes, there is.  Agarwal and Oefelein studies 10 hypogonadal patients treated with radical prostatectomy for organ-confined prostate cancer to determine if TRT could be administered safely without causing recurrent prostate tumor.  Results showed that after receiving TRT for approximately 19 months total testosterone levels and hypogonadal symptoms had improved significantly, and there were no prostate cancer recurrences or increases in PSA.  These results led the authors to conclude: “In highly select patients after radical prostatectomy TRT can be administered carefully and with benefit to hypogonadal patients with prostate cancer.”


This is just another hormone replacement myth.  In fact, TRT has quite the opposite effect on behavior.  Much of the bad press about TRT stems from media stories about anabolic steroid abuse – we are not concerned with abusing anabolic steroids, we are concerned with abusing anabolic steroids, we are concerned with restoring testosterone to physiologic levels.  Studies have shown that men who have their testosterone levels restored with TRT are less likely to suffer from depression, are less moody, more sociable and gregarious, and have more energy.  O’Connor et al investigated the effects of TRT on self- and partner-reported aggression and mood.  Eight hypogonadal men received 200 mg intramuscular testosterone biweekly for 8 weeks.  *Results showed that TRT led to significant reductions in negative mood (tension, anger, and fatigue).  Furthermore, there was no increase in self- and partner-reported aggression or mood disturbances.  Thus, we can conclude that TRT does not cause or worsen angry or aggressive behavior.



A paper by Jenkins et al entitled “Does growth hormone cause cancer?” concluded: “Extensive studies of the outcome of GH replacement in childhood cancer survivors show no evidence of an excess of d novo cancers, and more recent surveillance of children and adults treated with GH has revealed no increase in observed cancer risk.

If you look at the package insert for GH it says that it should not be used in patients with an active malignancy.  However, the Growth Hormone Research Society published a paper in the Journal of Clinical Endocrinology and Metabolism, saying that their is no data to support this labeling, and that current knowledge does not warrant additional warning about cancer risk.  The authors of this paper say that this line should be removed from the package insert because there is no evidence to show that GH increases cancer recurrence or de novo cancer or leukemia.  In conclusion, the notion that GH causes cancer is another myth.


A review by Popovic et al showed that some degree of hypopituitarism is found in 35-40% of TBI patients, and suggested that untreated TBI-induced hypopituitiarism contributes to the chronic neurobehavioral problems seen in many head-injured patients.   Preliminary data suggests that people suffering from TBI-induced hypopituitarism experience significant improvements in concentration, memory, depression, anxiety, and fatigue when treated with GH.  The authors of this review concluded that pituitary failure is poorly recognized and can occur even with minor head injuries.

Thus, all TBI, cerebrovascular accident, and subarachnoid hemorrhage patients should be evaluated for AGHD within a year of the event, and they should be treated if a deficiency exists.  In the future, it may be possible to treat all TBI patients with GH if they have symptoms of GH deficiency however at present patients need to have been given a  diagnosis of AGHD before they can be treated.


Progesterone is neuroprotective.  There is a basic science to support this and now there are human trials.  Pettus et al found that when progesterone is given after TBI it reduces the initial cytotoxic surge of inflammatory factors, decreases levels of nuclear factor kappa beta (NFKB), and decreases levels of inflammatory eicosanoids.  So, how does progesterone exert this neuroprotective effect?  The neuroprotective properties of progesterone are probably derived from the action of allopregnanoline (APa), a neuroactive roperties of progesterone are probably derived from the action of alloprenganolone (APa), a neuroactive metabolite of progesterone, which turns on neuronal stem cells.  Wang et al found that APa promotes the proliferation of roden neuroprogenitor cells (NPCs) derived from the hippocampus, and increases human neural stem cells (hNSCs) derived from the cerebral cortex.  Results also showed that APa regulates cell-cycle gene and protein expression.


Fournier et al compared the association between different forms of hormone replacement therapy more than 8,000 women.  Results showed that women treated with bioidentical  estradiol and progesterone were no more likely to develop breast cancer rates than women who had never used any form of HRT.  However, women treated with estradiol and progestin (Provera) had a 69% increased risk of developing breast cancer.

Other research has shown that more progesterone a woman is exposed to over the course of her life, the lower her risk of breast cancer.  So, let’s make it clear once and for all – progesterone and progestin are not the same.


There are many myths surrounding hormone replacement therapies, however form the evidence presented above, we can see that not one of them is true.  Hormone optimization provides us with an extremely powerful anti-aging tool to maximize quality of life.


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