Lupron and other GnRHa (Gonadotropin-Releasing Hormone agonist) drugs are strongly suspected of causing life-altering, even debilitating, persistent side effects.

GnRHa drugs act as a form of chemical castration by abolishing the initial chemical signal that ultimately leads to the production of testosterone and estrogen, decreasing their concentrations in the body many-fold. Appropriate levels of “sex hormones” are essential for maintenance of multiple physiological systems in both women and men, meaning profound pharmaceutical ablation of these hormones may result in consequences which span far beyond reproductive health alone.

In addition to their role of relaying GnRH signals in the pituitary gland, GnRH receptors have also been found to be expressed in lymphocytes, ovaries and testes, breast tissue, placental tissue, and prostate tissue. This suggests GnRH influences the immune system directly, as well as exerting effects on the reproductive system which are auxiliary to its prime function of promoting estrogen and androgen production.


Lupron and estradiol deficiency

In an article entitled “Lupron, Estradiol and the Mitochondria: A Pathway to Adverse Reactions” Chandler Marrs, CEO of Lucine Health Sciences and founder of Hormones Matter, examines Lupron side effects which are plausibly linked to severe negative impacts caused by such a drastic reduction of sex hormones. She questions the safety and sensibility of the casual use of Lupron as a diagnostic tool and as a go-to treatment option for pain associated with reproductive disorders, stating that there isĀ “little research indicating its efficacy in reducing pain and no research delineating its effects on disease progression”.

Pointing out the fact that hormone receptors are expressed in nearly every cell in the body, she further clarifies the involvement of estradiol in either directly or indirectly stimulating mitochondrial genesis, mitochondrial membrane integrity, and their ability to synthesize ATP, the fundamental source of chemical energy for all living things. There is an indispensable lesson in recognizing the broad scope of health issues which may develop due to impaired hormone signalling to the mitochondria. Lupron side effects such as disorders of the brain and nervous system, chronic fatigue, muscular atrophy, cardiovascular problems, loss of bone mineral density, and gastrointestinal symptoms have all been linked with mitochondrial dysfunction.

Mitochondrial dysfunction and androgen deficiency

While Chandler Marrs’ analysis of Lupron focuses on the impact of estradiol deficiency on mitochondria, a 2011 publication in Hormone Molecular Biology and Clinical Investigation authored by biochemistry professor and Post-Finasteride Syndrome researcher, Abdulmaged M. Traish, considers a similar viewpoint centered around androgen deficiency. Professor Traish and his cohorts meticulously explain the detrimental effects of testosterone deficiency, and accordingly, androgen deprivation therapy, on mitochondrial function. Of note, the presence of androgen-responsive genes in both mitochondrial DNA, and mitochondria-associated nuclear DNA, is discussed and an impartial description of pathological processes linking testosterone deficiency to mitochondrial dysfunction is provided. Mitochondrial dysfunction is cited as a common trait shared by multiple health problems related to low testosterone such as metabolic syndrome, muscle atrophy, cardiovascular damage, and sexual dysfunction.


Lupron and androgen deficiency

Lupron and drugs with similar mechanisms of action are utilized as androgen deprivation therapy in the context of prostate cancer treatment. By their very nature, they should be capable of causing the deleterious effects of low testosterone.
The substances discussed at have all been acknowledged to influence androgen metabolism, or significantly decrease androgen levels, in some way and many members experience long-term side effects which are generally associated with androgen deficiency. This occurs despite a supposed return of normal hormone levels. Could impaired hormone signaling and resulting mitochondrial dysfunction be heavily involved in our symptoms?