MESO-Rx
Anabolic Steroids
post finasteride syndrome pct
- Thread starter Peterson
- Start date
KL8209
Member
Especially onions. Not sure about you but I can't ever get enough onions on my head.
Grab Bag
Well-known Member
Have you had your dht levels checked via bloodwork?
Grab Bag
Well-known Member
In the absence of bloodwork, have you considered that these symptoms may not be related to the fina? What you are describing are also symptoms of depression, or symptoms of low T, or symptoms of a thyroid disorder. I really hope you visit a doctor or get a blood panel on your own, because there are a ton off potential issues here which most likely have nothing to do with PFS, which I believe is a psychological condition as much as anything. I’m not trying to put you down, just hope you get the help you need, and feel you may be barking up the wrong tree here.
Well, I was completely healthy before taking fina so it seems very weird that fina is not the cause of all these problems. There are thousands of other men who have the same experience with fina as me. Everything points to fina but I will have my blood checked though.
If my bloodwork shows normal values, what would you suggest me to do?
Grab Bag
Well-known Member
Honestly I’m not sure what you should do if bloods come back normal. You may as well try some kind of pfs pct at that point if you feel it will help you. Everyone has a right to be in charge of their own health as they see fit, in my opinion.
Did the finasteride coincide w any major emotional life event? Have you ever tried any counseling? Is it possible there’s a psychological element here? I’m not saying this IS the answer, just saying it may be a possibility. This may sound crazy, but at one point in my life I had a bunch of physical symptoms from something, couldn’t figure out what the hell was going on, and then started some self work and it unintentionally cleared up the physical issues I was having. You never know man, and if you feel like shit you should pursue all options.
Any other related medical history, or is it really just finna with no other culprits?
The reason I am a little skeptical of pfs is that I did a lot of research on it before I started taking fina years ago (zero sides personally). I was super freaked out after I read the pfs accounts, but then I talked to a few friends who had been using it w zero side and figured I’d give it a try. I didn’t have any ill effects, so did a little research and read some things that made me pretty skeptical of the whole pfs in normal healthy people. I do believe it could be damaging to someone very unhealthy, with a messed up endocrine system, but it seems like the health risk to a healthy person w a fully functional endocrine system is low, hence why I think some blood work and further investigation may be in order.
Grab Bag
Well-known Member
Read this guys post, and one thing stuck out to me: “Differences...
I was previously in very bad shape... meaning that I was really overweight. I now workout almost daily and am in pretty great shape.”
If I’m reading this correctly (as in reading through the lines), this guy was obese and lost a ton of weight and that cured his pfs. A lot of the stuff I have read is like this... people who have other major health issues but think the finasteride is to blame.
No don't have any other medical history at all also no emotional or psychological problems.
It's clear to me that blocking an important male hormone like DHT will cause side effects sooners or later. New studies are coming out regularly, everything indicates to fina as pure hormonal poison.
Here's an article about fina last year;
https://www.reuters.com/investigates/special-report/usa-courts-secrecy-propecia/ (https://www.reuters.com/investigates...recy-propecia/)
A REUTERS SERIES
https://www.reuters.com/investigates/section/homepage/ (Court let Merck hide secrets about a popular drug’s risks)
Lawsuits claim baldness drug Propecia causes sexual problems and depression. The judge sealed evidence – uncovered by Reuters – suggesting the maker downplayed the side effects. A widow wants the truth out.
Also know Merck has a very shady past too:
Approval by the FDA should mean that the substance in question is reasonably safe for use in the wider population. Sadly, despite FDA approval, many drugs have had to be subsequently withdrawn from the market after wider use showed severe consequences which were not adequately assessed or communicated by the very institution that was supposed to protect the public from such outcomes. Take another Merck (makers of propecia) drug, Vioxx, which was approved by the FDA. Withdrawn from the market after five years, it caused approximately 100000 heart attacks and thousands of deaths. The revelations that resulted from the ensuing scrutiny offer a chilling insight into the machinations of a pharmaceutical company that nakedly prized its profit margin above its duty not to harm its consumers. It also exposed the FDA’s rank inadequacies in preventing such a tragedy from happening in the first place. https://www.ucsusa.org/manipulating-...out-drug-vioxx
“Merck Manipulated the Science about the Drug Vioxx”
Scientists from the pharmaceutical giant Merck skewed the results of clinical trials in favor of the arthritis drug, Vioxx, to hide evidence that the drug increased patients’ risk of heart attack.
Tragically, Merck’s manipulation of its data—and the FDA’s resulting approval of Vioxx in 1999—led to thousands of avoidable premature deaths and 100,000 heart attacks.?Dr. David Graham, the Associate Director for Science and Medicine in FDA’s Office of Drug Safety, https://www.finance.senate.gov/imo/media/Doctor/111804dgtest.pdf. before the Senate Finance Committee that the FDA's failure to recall Vioxx earlier had resulted in as many as 55,000 premature deaths from heart attacks and stroke, calling it the equivalent of allowing "two to four jumbo jetliners" to crash every week for five years. Even years after discontinuing use of the drug, patients who have taken Vioxx continue to experience complications. https://www.newscientist.com/article...aths-cover-up/
“Drug giant Merck accused of deaths cover-up”
When a study suggested that Vioxx was more dangerous than a rival drug, for example, the company is alleged to have decided not to publish the results or properly inform the FDA.
Egilman says the documents also contain an email in which a Merck employee tells a co-worker that “this is a very serious result and you will hardly be surprised by the idea of keeping this VERY TIGHT for the moment”. https://www.news.com.au/news/drug-company-drew-up-doctor-hit-list/news-story/eb55ca36e081d497730629e6c8559abf?sv=1f029b17d33bdbde184dbc4c4fed7126
“Vioxx maker Merck and Co drew up doctor hit list”
An international drug company made a hit list of doctors who had to be “neutralised” or discredited because they criticised the anti-arthritis drug the pharmaceutical giant produced.
The email, which came out in the Federal Court in Melbourne yesterday as part of a class action against the drug company, included the words "neutralise", "neutralised" or "discredit" against some of the doctors' names.
"We may need to seek them out and destroy them where they live," a Merck employee wrote, according to an email excerpt read to the court by Julian Burnside QC, acting for the plaintiff.
https://www.nytimes.com/2007/11/09/b...s/09merck.html
“Merck Agrees to Settle Vioxx Suits for $4.85 Billion”
Three years after withdrawing its pain medication Vioxx from the market, Merck has agreed to pay $4.85 billion to settle 27,000 lawsuits by people who claim they or their family members suffered injury or died after taking the drug, according to two lawyers with direct knowledge of the matter. https://www.finance.senate.gov/imo/media/Doctor/111804dgtest.pdf.
Some more studies:
DHT is biologically important for sexual differentiation of the male genitalia during embryogenesis, maturation of the penis and scrotum at puberty, growth of facial, body, and pubic hair, and development and maintenance of the prostate gland and seminal vesicles. It is produced from the less potent testosterone by the enzyme 5?-reductase in select tissues, and is the primary androgen in the genitals, prostate gland, seminal vesicles, skin, and hair follicles.[2]
Dihydrotestosterone - Wikipedia
Finasteride, sold under the brand names Proscar and Propecia among others, is a medication used mainly to treat an enlarged prostate or hair loss in men.[2] It can also be used to treat excessive hair growth in women and as a part of hormone therapy for transgender women.[3][4] It is taken by mouth.[2]
Finasteride - Wikipedia
https://ethics.harvard.edu/blog/risk...not-be-trusted
The bar for “safe” is equally low, and over the past 30 years, approved drugs have caused an epidemic of harmful side effects, even when properly prescribed. Every week, about 53,000 excess hospitalizations and about 2400 excess deaths occur in the United States among people taking properly prescribed drugs to be healthier.
Prescription drugs are the 4th leading cause of death.
This evidence indicates why we can no longer trust the FDA to carry out its historic mission to protect the public from harmful and ineffective drugs. Strong public demand that government “do something” about periodic drug disasters has played a central role in developing the FDA.2 Yet close, constant contact by companies with FDA staff and officials has contributed to vague, minimal criteria of what “safe” and “effective” mean.
Other than thousands upon thousands of anecdotal reports from different men of severe adverse reactions to the drug appearing on the internet in the decades since it was approved for sale, evidence of objective differences between PFS patients and control groups has now been established.
https://journals.plos.org/plosone/ar...0237#abstract0
The ratio of AR positive stromal cells % to serum testosterone concentrations was 2-fold higher in cases than in controls (P?=?0.001). Our findings revealed that modulation of local AR levels might be implicated in long-term side effects of finasteride use. This provides the first evidence of a molecular objective difference between patients with long-term adverse sexual effects after finasteride use versus drug untreated healthy controls in certain tissues.
Neuroactive steroid levels and psychiatric and andrological features in post-finasteride patients. - PubMed - NCBI
We also reported abnormal somatosensory evoked potentials of the pudendal nerve in PFS patients with severe ED, the first objective evidence of a neuropathy involving peripheral neurogenic control of erection.
Data obtained on neuroactive steroid levels also indicate interesting features. Indeed, decreased levels of pregnenolone, progesterone and its metabolite (i.e., dihydroprogesterone), dihydrotestosterone and 17beta-estradiol and increased levels of dehydroepiandrosterone, testosterone and 5alpha-androstane-3alpha,17beta-diol were observed in CSF of PFS patients.
Finally, finasteride did not only affect, as expected, the levels of 5alpha-reduced metabolites of progesterone and testosterone, but also the further metabolites and precursors suggesting that this drug has broad consequence on neuroactive steroid levels of PFS patients.
https://www.jsm.jsexmed.org/article/...817-9/fulltext
Using novel ultrasound technology, 96% of men with PFS and ED demonstrated heterogeneity in their corporal tissue at maximal pharmacologic erection. This new protocol is able to show that PFS men complaining of ED may have an underlying biologic pathophysiology.
So, three objective differences in men with PFS
- Double the androgen receptor expression compared to non-PFS control group
- Cerebrospinal fluid readings of PFS patients showed significantly lowered levels of several hormones and neuroactive steroids and “abnormal somatosensory evoked potentials of the pudendal nerve were reported”
- Ultrasounds of PFS patients’ genitals showed evidence of a potential biologic pathophysiology
Btw, it took decades for post SSRI syndrome to be taken serious, last year it was finally officialy recognized and SSRI's are a lot longer on the market.
https://www.psychologytoday.com/us/b...ical-condition
Some more studies:
The Steroidogenesis Inhibitor Finasteride Reduces the Response to Both Stressful and Rewarding Stimuli.
Abstract
Finasteride (FIN) is the prototypical inhibitor of steroid 5?-reductase (5?R), the enzyme that catalyzes the rate-limiting step of the conversion of progesterone and testosterone into their main neuroactive metabolites. FIN is clinically approved for the treatment of benign prostatic hyperplasia and male baldness; while often well-tolerated, FIN has also been shown to cause or exacerbate psychological problems in vulnerable subjects. Evidence on the psychological effects of FIN, however, remains controversial, in view of inconsistent clinical reports. Here, we tested the effects of FIN in a battery of tests aimed at capturing complementary aspects of mood regulation and stress reactivity in rats. FIN reduced exploratory, incentive, prosocial, and risk-taking behavior; furthermore, it decreased stress coping, as revealed by increased immobility in the forced-swim test (FST). This last effect was also observed in female and orchiectomized male rats, suggesting that the mechanism of action of FIN does not primarily reflect changes in gonadal steroids. The effects of FIN on FST responses were associated with a dramatic decrease in corticotropin release hormone (CRH) mRNA and adrenocorticotropic hormone (ACTH) levels. These results suggest that FIN impairs stress reactivity and reduces behavioral activation and impulsive behavior by altering the function of the hypothalamus-pituitary-adrenal (HPA) axis.
The Steroidogenesis Inhibitor Finasteride Reduces the Response to Both Stressful and Rewarding Stimuli. - PubMed - NCBI
Fina has a strong effect on neurosteroid activity in the brain:
Neurosteroids like 3?-androstanediol (derived from DHT) and allopregnanolone (derived from progesterone) activate the GABAA receptor in the brain; because finasteride prevents the formation of neurosteroids, it functions as a neurosteroidogenesis inhibitor and may contribute to a reduction of GABAA activity. Reduction of GABAA receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.[61][62][63]
https://www.bmj.com/content/365/bmj.l1204
Fina raises chance of diabetes
The risk of type 2 diabetes was increased by approximately 30% over 11 years in men with benign prostatic hyperplasia who received one of the 5?-reductase inhibitors on the market, finasteride or dutasteride compared with tamsulosin
Additional monitoring might be required for men starting these drugs, particularly in those with other risk factors for type 2 diabetes.
Finasteride-Induced Inhibition of 5?-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study
Finasteride-Induced Inhibition of 5α-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study
https://www.ncbi.nlm.nih.gov/pubmed/31937082 11
Abstract
BACKGROUND:
Combination therapy with 5 alpha-reductase inhibitor (5-ARI) and alpha-blocker can be considered as a gold standard intervention for medical management of lower urinary tract symptoms related to benign prostatic hyperplasia (LUTS/BPH). On the other hand, 5-ARI monotherapy and in particular Finasteride alone is currently getting focus of attention especially due to lack of systematic reviews investigating efficacy outcomes and/or adverse events associated.
OBJECTIVES:
Aim of the present critical review was to analyze current knowledge of clinical efficacy and incidence of adverse events associated with 5-ARI treatment for LUTS/BPH.
MATERIALS AND METHODS:
A systematic review of clinical trials of the literature of the past 20 years was performed using database from PubMed, Cochrane Collaboration and Embase. A total of 8821 patients were included in this study and inclusion criteria for studies selection were: data from randomized clinical trials (RCTs) focusing their attention on the clinical role of Finasteride monotherapy for symptomatic BPH. Parameters of research included prostate specific antigen (PSA), prostate volume (PV), International Prostate Symptom Score (IPPS), postvoid residual urine (PVR), voiding symptoms of IPSS (voiding IPSS), maximum urinary flow rate (Qmax), and adverse events (AEs).
RESULTS:
Overall 12 original articles were included and critically evaluated. Sample sizes of patient actively treated with finasteride varied from 13 to 1524 cases analyzed in a single study. Follow-up after treatments ranged from 3 to 54 months. The effect of finasteride in reducing prostate volume (PV) was moderate (standardized mean difference (SMD) effect between 0.5 to 0.8 for all trials evaluable) while the effect on IPSS score and Qmax was considered significant (SMD in the 0.2 to 0.5 variation range). No severe AEs and/or psychiatric disorders were retrieved among the studies. Sexual health dysfunctions were significantly influenced by finasteride therapy when compared with placebo treated patients.
CONCLUSIONS:
Although significant clinical benefits of finasteride monotherapy were demonstrated, the effective size of the available reports included in the analysis is limited. Additional head-to-head studies would be needed to re-evaluate clinical efficacy and safety of 5-ARI in combination or not with alpha blockers.
https://www.sciencedirect.com/scienc...06453018305067
“Finasteride treatment causes several alterations in the hippocampus,” the section of the brain responsible for processing long-term memory and emotional responses, according to a new study conducted at the University of Milano, and the Cajal Institute and Carlos III Health Institute, both in Madrid.Oct 1, 2018
There are tons of studies:
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://peerj.com/articles/3020.pdf
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.notion.so/Bibliography-of-research-on-adverse-effects-of-finasteride-22927dda82e94d6ba50f64b2e5e00552
Anyway, you can get pfs after a couple of pills or 5-10 years, I've read more than enough about this to know you are never safe if you take fina or duta.
https://www.psychologytoday.com/us/b...ical-condition
Some more studies:
The Steroidogenesis Inhibitor Finasteride Reduces the Response to Both Stressful and Rewarding Stimuli.
Abstract
Finasteride (FIN) is the prototypical inhibitor of steroid 5?-reductase (5?R), the enzyme that catalyzes the rate-limiting step of the conversion of progesterone and testosterone into their main neuroactive metabolites. FIN is clinically approved for the treatment of benign prostatic hyperplasia and male baldness; while often well-tolerated, FIN has also been shown to cause or exacerbate psychological problems in vulnerable subjects. Evidence on the psychological effects of FIN, however, remains controversial, in view of inconsistent clinical reports. Here, we tested the effects of FIN in a battery of tests aimed at capturing complementary aspects of mood regulation and stress reactivity in rats. FIN reduced exploratory, incentive, prosocial, and risk-taking behavior; furthermore, it decreased stress coping, as revealed by increased immobility in the forced-swim test (FST). This last effect was also observed in female and orchiectomized male rats, suggesting that the mechanism of action of FIN does not primarily reflect changes in gonadal steroids. The effects of FIN on FST responses were associated with a dramatic decrease in corticotropin release hormone (CRH) mRNA and adrenocorticotropic hormone (ACTH) levels. These results suggest that FIN impairs stress reactivity and reduces behavioral activation and impulsive behavior by altering the function of the hypothalamus-pituitary-adrenal (HPA) axis.
The Steroidogenesis Inhibitor Finasteride Reduces the Response to Both Stressful and Rewarding Stimuli. - PubMed - NCBI
Fina has a strong effect on neurosteroid activity in the brain:
Neurosteroids like 3?-androstanediol (derived from DHT) and allopregnanolone (derived from progesterone) activate the GABAA receptor in the brain; because finasteride prevents the formation of neurosteroids, it functions as a neurosteroidogenesis inhibitor and may contribute to a reduction of GABAA activity. Reduction of GABAA receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.[61][62][63]
https://www.bmj.com/content/365/bmj.l1204
Fina raises chance of diabetes
The risk of type 2 diabetes was increased by approximately 30% over 11 years in men with benign prostatic hyperplasia who received one of the 5?-reductase inhibitors on the market, finasteride or dutasteride compared with tamsulosin
Additional monitoring might be required for men starting these drugs, particularly in those with other risk factors for type 2 diabetes.
Finasteride-Induced Inhibition of 5?-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study
Finasteride-Induced Inhibition of 5α-Reductase Type 2 Could Lead to Kidney Damage—Animal, Experimental Study
https://www.ncbi.nlm.nih.gov/pubmed/31937082 11
Abstract
BACKGROUND:
Combination therapy with 5 alpha-reductase inhibitor (5-ARI) and alpha-blocker can be considered as a gold standard intervention for medical management of lower urinary tract symptoms related to benign prostatic hyperplasia (LUTS/BPH). On the other hand, 5-ARI monotherapy and in particular Finasteride alone is currently getting focus of attention especially due to lack of systematic reviews investigating efficacy outcomes and/or adverse events associated.
OBJECTIVES:
Aim of the present critical review was to analyze current knowledge of clinical efficacy and incidence of adverse events associated with 5-ARI treatment for LUTS/BPH.
MATERIALS AND METHODS:
A systematic review of clinical trials of the literature of the past 20 years was performed using database from PubMed, Cochrane Collaboration and Embase. A total of 8821 patients were included in this study and inclusion criteria for studies selection were: data from randomized clinical trials (RCTs) focusing their attention on the clinical role of Finasteride monotherapy for symptomatic BPH. Parameters of research included prostate specific antigen (PSA), prostate volume (PV), International Prostate Symptom Score (IPPS), postvoid residual urine (PVR), voiding symptoms of IPSS (voiding IPSS), maximum urinary flow rate (Qmax), and adverse events (AEs).
RESULTS:
Overall 12 original articles were included and critically evaluated. Sample sizes of patient actively treated with finasteride varied from 13 to 1524 cases analyzed in a single study. Follow-up after treatments ranged from 3 to 54 months. The effect of finasteride in reducing prostate volume (PV) was moderate (standardized mean difference (SMD) effect between 0.5 to 0.8 for all trials evaluable) while the effect on IPSS score and Qmax was considered significant (SMD in the 0.2 to 0.5 variation range). No severe AEs and/or psychiatric disorders were retrieved among the studies. Sexual health dysfunctions were significantly influenced by finasteride therapy when compared with placebo treated patients.
CONCLUSIONS:
Although significant clinical benefits of finasteride monotherapy were demonstrated, the effective size of the available reports included in the analysis is limited. Additional head-to-head studies would be needed to re-evaluate clinical efficacy and safety of 5-ARI in combination or not with alpha blockers.
https://www.sciencedirect.com/scienc...06453018305067
“Finasteride treatment causes several alterations in the hippocampus,” the section of the brain responsible for processing long-term memory and emotional responses, according to a new study conducted at the University of Milano, and the Cajal Institute and Carlos III Health Institute, both in Madrid.Oct 1, 2018
There are tons of studies:
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://peerj.com/articles/3020.pdf
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.ncbi.nlm.nih.gov/pubmed/...?dopt=Abstract
https://www.notion.so/Bibliography-of-research-on-adverse-effects-of-finasteride-22927dda82e94d6ba50f64b2e5e00552
Anyway, you can get pfs after a couple of pills or 5-10 years, I've read more than enough about this to know you are never safe if you take fina or duta.
Old
New Member
Dutasteride is a stronger 5α-Reductase inhibitor than Finasteride [ ~95% reduction of DHT verses ~70% ]. And reports of sexual dysfunction, during and after, are more prevalent.
DHT is vital for sexual development and function. It is also vital for proper brain function. The above would indicate that a pharmaceutical action with neurological changes is more likely then just 'emotional' problems. Even though, both, but even more so with Dutasteride, emotional side effects also occur.
It is very convenient to blame another person's problem as being psychological because only a minority are affected this way.
Messing with the brains neurotransmitter - and YES, androgens are also neurotransmitters - is asking for trouble ... even if it is just the 'vulnerable few'. The major metabolite of DHT is pro-pleasure, pro-sexual, anti-anxiety, and anti-seizure.
So ... what is more important:
DHT is vital for sexual development and function. It is also vital for proper brain function. The above would indicate that a pharmaceutical action with neurological changes is more likely then just 'emotional' problems. Even though, both, but even more so with Dutasteride, emotional side effects also occur.
It is very convenient to blame another person's problem as being psychological because only a minority are affected this way.
Messing with the brains neurotransmitter - and YES, androgens are also neurotransmitters - is asking for trouble ... even if it is just the 'vulnerable few'. The major metabolite of DHT is pro-pleasure, pro-sexual, anti-anxiety, and anti-seizure.
So ... what is more important:
- One's brain and sexual function?
- Or vanity of hair loss (hey try Minoxidil - it is a topical 5-ARI)?
- Or paranoia about prostate cancer (of which both finasteride and dutasteride are known to 'hide' the most serious forms)?
Grab Bag
Well-known Member
Thank you for posting all these links. I will take a look at them.
Looks like another one is getting better thanks due to steroids, DHT supplementation.
Using steroids in the right combination has brought me back to 90% within a week (UPDATED)
Does somebody know if this is a lifetime commitment? Or could he do a PCT and keep the benefits?
Using steroids in the right combination has brought me back to 90% within a week (UPDATED)
Does somebody know if this is a lifetime commitment? Or could he do a PCT and keep the benefits?
master.on
New Member
Did you get bloodwork?
Testosterone, estrogen, LH, FSH, even hematocrit to rule out anemia and thyroid tests total T4, T3, TSH to rule out a thyroid dysfunction.
Your problem may not even be finasteride related.
Proviron can help a bit with its DHT-like effects, while being minimally or no suppresive for most people.
ORAL minoxidil is a liquid hair transplant. No need for finasteride.
No I haven't done any bloodwork yet. But everything points to finasteride, perfectly healthy before.
I'm aware of oral minox but that's not really good either, especially for the heart.
master.on
New Member
Without bloodwork you're just guessing.
Guess what? Many conditions can cause a finasteride-like syndrome.
Yeah I'm sure a drug that I took for 2 years and blocks one of the most important male hormones has nothing to do with it.
It's fina. Sadly bloodwork doesn't show much with pfs patients but I will get it done.
master.on
New Member
Then you can try some low dose Proviron to see if it helps.
Even if it doesn't, most people don't get suppressed from it.
Start with 25 mg. Best to cut the tabs in half and take 2x daily or more.
A new very interesting recovery.
He had pfs for 11 fucking years and recovered with proviron.
Took finasteride for 5 months. I felt fine while taking it but it gave me gyno so I stopped. After stopping, I got ED, extreme fatigue, brain fog, no libido and lethargy. I tried just about everything over 11 years. I also tried testosterone treatment but it had almost no effect regardless of dosage.
I read a case study by Neurologist David Clark (https://carrickinstitute.com/hormones-causing-brain-fog-and-fatigue-video-case-review-ci-tv-2/ (link 21)) where someone had similar symptoms but there was no mention of finasteride or PFS. His issue wasn’t the hormones being too low but rather too high which caused receptor issues so they decided to down regulate them.
My take on PFS is that the receptors become hyper sensitive due to getting so little DHT for a long period of time. So when things compensate or go back to normal, they are too sensitive and you end up in a miserable state.
I decided to test that by supplementing DHT (proviron) and despite it being a general feel-good hormone for most, I felt absolutely dreadful when taking it. My symptoms increased by 10x and I couldn’t function but it made me realize I was on to something. I felt like my options were either to permanently decrease DHT in some way or decrease the sensitivity of the receptors.
The receptors likely became hyper sensitive by getting so little DHT for a prolonged period of time while taking finasteride. So I tried the opposite to reverse the situation. I took a large amount of DHT (proviron) for 7 weeks at 200 mg per day to reduce receptor sensitivity to DHT.
At first, I felt absolutely miserable when doing so, it is the worst I’ve felt in my life and I was unable to do almost anything but after some weeks it became more tolerable as the receptors lost some of their sensitivity.
After stopping 7 weeks later (when I ran out of my proviron), things felt off for a few weeks but then after around two months I got back to my pre-PFS state. Now and for the past six months, I feel great, my libido is great, mental issues are gone, ED is gone. This after having PFS constantly for 11 years. My life is finally back.
Cured after 11 years
He had pfs for 11 fucking years and recovered with proviron.
Took finasteride for 5 months. I felt fine while taking it but it gave me gyno so I stopped. After stopping, I got ED, extreme fatigue, brain fog, no libido and lethargy. I tried just about everything over 11 years. I also tried testosterone treatment but it had almost no effect regardless of dosage.
I read a case study by Neurologist David Clark (https://carrickinstitute.com/hormones-causing-brain-fog-and-fatigue-video-case-review-ci-tv-2/ (link 21)) where someone had similar symptoms but there was no mention of finasteride or PFS. His issue wasn’t the hormones being too low but rather too high which caused receptor issues so they decided to down regulate them.
My take on PFS is that the receptors become hyper sensitive due to getting so little DHT for a long period of time. So when things compensate or go back to normal, they are too sensitive and you end up in a miserable state.
I decided to test that by supplementing DHT (proviron) and despite it being a general feel-good hormone for most, I felt absolutely dreadful when taking it. My symptoms increased by 10x and I couldn’t function but it made me realize I was on to something. I felt like my options were either to permanently decrease DHT in some way or decrease the sensitivity of the receptors.
The receptors likely became hyper sensitive by getting so little DHT for a prolonged period of time while taking finasteride. So I tried the opposite to reverse the situation. I took a large amount of DHT (proviron) for 7 weeks at 200 mg per day to reduce receptor sensitivity to DHT.
At first, I felt absolutely miserable when doing so, it is the worst I’ve felt in my life and I was unable to do almost anything but after some weeks it became more tolerable as the receptors lost some of their sensitivity.
After stopping 7 weeks later (when I ran out of my proviron), things felt off for a few weeks but then after around two months I got back to my pre-PFS state. Now and for the past six months, I feel great, my libido is great, mental issues are gone, ED is gone. This after having PFS constantly for 11 years. My life is finally back.
Cured after 11 years
Old
New Member
Sound like worth a try. Although proviron is NOT DHT, it is a derivative.
As for receptor desensitivity, that is a continual myth. ARs increase in the presence of androgens, so 'net' sensitivity of the cell is increased, not decreased. With the case of neurons, a whole cascade of 'wiring' changes occur. In the end this technicality doesn't matter since what DOES matter is that it worked.
So if you want to try proviron instead of DHT ... why not. It is easier to get.
Interesting the guy got gyno from finasteride. Clearly, lowering DHT with these drugs carries risks beyond the obvious. Doctors have used DHT for treatment resistant gyno.
Wish you success! Please let us know how things work out.
Very interesting video.
This is his article with all the studies he's talking about:
Is Post Finasteride Syndrome Real? | How To Diagnose And Reverse It
He's also saying proviron is possibley the best treament for pfs.
Could you guys watch/read this and till me your opinions?
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