what are you main symptoms then?
Yo tengo miccion frecuente debito a falta de vasopresina inducida por pfs
I want to see people here who feel their symptoms are not covered by Lupron. We are trying to connect dots.
I think the last post in my member’s story sums it up quite well.
In any case, after reading the images you posted (and Leuprorelin’s wikipedia article) I agree, both have simmilar symptom profiles, but maybe it’s because leuprorelin messes with hormones too, and not necessarily because of brain damage.
Could you provide the links from where the images are from anyways?
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Some of my symptoms are in that list…heart palpitations, insomnia, muscle loss. Others I don’t see…collagen and fat loss, sunken eyes, pale dry wrinkled skin, eyebrow loss, gum recession, fatigue.
There have been studies and research papers showing decreased brain activity and liaisons after the use of Fin. Also almost all of the hormones coming from pituitary are decreased. My vasopressin, LH, FSH and TSH are almost bottomed. On the other hand cortisol which is always above normal.
I will be happy to see people challenging my theory and proving it wrong with researches/evidences. The sooner it is debunked the less time I will be wasting here.
Where will you go if it’s debunked?
I will be happy and then go back to reading research papers and forums etc. What else you can do?
I thought you meant ‘here’ like this site.
Please guys help me find at least one side effect which is different between Lupron and pfs. This will prove that Lupron issues and pfs are two different things.
So far I find the complete list of sides from PFS under Lupron as well. Since we know how Lupron works this does not prove pfs is actually damage to our brain?
I agree, they are suffering just like us.
I tried to add following more symptoms to my first post which are common in both pfs and Lupron users but could not add to the post so putting them here.
11- thyroid issues
12- water retention
13- pancreatitis
14- adrenal gland issues
15- Colon issues.
16- Pancreatitis.
17- Fibromyalgia
Lupron has antiandrogenic properties, just like Finasteride, Accutane, SSRIs, Saw Palmetto etc. Since the existing evidence suggests that our problem is caused by alteration to androgenic signaling following androgen deprivation, it is not surprising that all these antiandrogenic substances cause similar symptoms in a subset of patients across these patient communities. Awor already discussed this over a decade ago.
So, yeah, some Lupron patients likely experience the same symptoms caused by the same condition.
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Is there any known treatment for people damaged by LUPRON ?
Anti-androgenic? it is GnRH agonist hormone.
Lupron (Leuprolide Acetate) is an injectable medication which reduces the production of hormones (estrogen and progesterone) by the ovaries. Lupron works by blocking the effect of Gonadotropin Releasing Hormone (GnRH) on the pituitary gland in the brain
Yes, antiandrogenic.
Testosterone is an androgen. If a substance reduces an androgen, e.g testosterone, it has antiandrogenic properties. Finasteride, Leuprorelin (Lupron), Isotretinoin (Accutane) and SSRIs all have antiandrogenic properties. That’s the common factor between them.
Lupron is generally used when one don’t want those hormones, like prostate cancer.
While I can’t find any publications on this, the only thing I can think would help is hormone replacement therapy. But for obvious reasons it’s contradictory to use at the same time as Lupron.
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As regards men, the advice is to go to the gym to reverse or at least mediate the physical. Side effects, as well as fatigue.
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Nonalcoholic fatty liver disease induced by leuprorelin acetate
Abstract
Leuprorelin acetate is an agonist of gonadotropin-releasing hormone, used as a first choice treatment in patients with prostate carcinoma. The impact of leuprorelin therapy in liver function and metabolism is largely unknown. We report about a patient who had been treated for 32 months with leuprorelin acetate, who developed a nonalcoholic fatty liver disease (NAFLD), associated with a focal lesion at the IV hepatic segment where histologic features appeared to be more severe. The patient, in addition to NAFLD, presented a marked iatrogenic hypotestosteronemia and full-criteria meeting the diagnosis of metabolic syndrome, including insulin resistance. The radiologic and clinical findings, the histopathologic features, and the absence of any hepatic abnormalities before treatment, support a causal role of leuprorelin in inducing metabolic derangement that, most likely secondary to androgen-deprivation, were, in turn, responsible for the development of NAFLD. In conclusion, this is the first case report of NAFLD with focal fatty liver associated with leuprorelin therapy. Patients in leuprorelin should be carefully monitored for the development of liver disease.