Dear Lynne, it is a truly great day to see your post here. For all that don’t know Lynne, let me introduce her: She is a legend, and a warrior, like I have seldom met in my life. Many years ago, Lynne took Lupron (leuprolide), which belongs to the drug class of GnRH analogues. Despite having become very ill from Lupron, Lynne is fighting for recognition of the Lupron problem like a lion. She has approached politicians and media for many years. Through her relentless work and effort, she has achieved a significant media presence for the Lupron Victims. If you have a moment, please take a look at her website. It represents everything she knows about Lupron persistent side effects, and many of the actions she was involved in. The site is massive.
Lupron acts as an agonist at the pituitary GnRH receptor level. Agonism (activation) of GnRH receptors initially results in the stimulation of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. However, after several weeks, pituitary GnRH receptors become desensitized resulting in decreased LH and FSH secretion, leading to hypogonadism and thus a dramatic reduction in estradiol and testosterone levels regardless of sex. Lupron is used to treat prostate cancer, breast cancer, endometriosis, uterine fibroids, and early puberty. It is administrated by injection (IM or under the skin). Lupron is poison in its purest form. Because it decimates estrogens and androgens at a systemic level (as opposed to fin which “just” reduces DHT in cells which express 5αr2/3), the effect is brutal. So are the side effects. Take your average PFS patient, multiply the side effects by factor X in both breadth and depth, and you’ve got an average Lupron Victim.
What I initially found fascinating, is that Lupron has no direct interaction with 5ar, but still produces a very similar side effect pattern (including post-drug crash in some cases), just much more severe on average, as stated above. For me this is clear evidence that our problem is not about 5αr (or DHT for that matter), but about an (epigenetic?) effect that is triggered by androgen ablation. Finasteride of course is also about androgen ablation, just much more site specific. Anti-depressants have also been shown to have potentially strong anti-androgenic properties through the induction of 3α-HSD, turning DHT into the weak androgen 3α-Androstanediol (often abbreviated as 3α-diol). The effect of this inactivation is a little weaker than the strong effect of finasteride for example, and the distribution of 3α-HSD is not identical to 5αr2/3 either. Nevertheless, the syndromes are quite similar (PSSD). And let’s not forget about Accutane (isotretinoin), a potent 5αr1 inhibitor. Again, different distribution across the body, but still results in a similar phenotype.
Even the most conservative scientists should get it: There clearly is something bigger going on here. Unfortunately, certain PFS engaged scientists are captured in their narrow field of expertise and scientific dogma, which dictates keeping variables to a minimum, preferentially one (finasteride). This is hurting our cause, even though not all in our community have yet come to realize this. Even though science is clearly not the only route to explore, it is the route that @axolotl and I are focused on. The critical success factor for this route is critical mass. We are fighting hard to gain that visibility and critical mass. Our Lupron Victim friends hopefully are going to help us get closer to that critical mass, out of mutual interest.
I am very much looking forward to some Lupron Victims joining in on the conversation here with our wonderful community. I am convinced that we can benefit and gain strength from each other.
Again, a warm welcome to our Lupron Victim friends.