Neuroendocrinologist confirms persistent Finasteride side effects & Post-Finasteride Syndrome


Has anyone tested for copper, im going to this week.


letsconvenience did - and came back positive.


jeez, if copper toxicity were an answer for some us, that would truly amazing. chelation therapy anyone? It’s more effective and faster than any oral liver/system cleanser regimen. I’m speaking from experience.

please keep us updated if you’ve identified copper toxicity and plan to begin treatment/regimen.


Once again, can we keep this thread on topic (ie, in relation to what Dr. Jacobs has written).

If you wish to discuss other things like “liver cirrhosis” and “copper toxicity”, pls do so in other threads that already exist on those topics. Cheers.


Recently went to Dr. Jacobs.
He has a lot to offer. I would like to be able to explain more but he and I only talked for about an hour straight.
Great guy,
and seems like the one.
Great office space, demeanor, and location.
Again, his office and space is amazing, a great place to work on our issue.
I would encourage people to go see him.
We should also just gather the cash to try and pay him to simply spend some long nights in his office researching, reading this forum and all the information, researching, writing, and devising some plans of action to help us.

Go visit Dr. Jacobs because he apparently seems the most capable of helping our case because of his background in neuroscience as well.
NYC is a great place to visit too. 5th Avenue and all the flagship designer stores are just a block away too.

Mew, hop on a plane and go pay him a visit. Anything you say means nothing until you start working with someone.

We visited the forum while talking in his office, breezing through articles, brain-storming, thinking out loud, and talking about all the various factors that could be involved, as well as plans to try to test for and tackle every possible question mark. The guy has a great bit of energy and enthusiasm for tackling our situation it seems. He seems to have a great ability to multi-task and be flexible and open-minded. He also seems to be very under control and an easy person to access, keep in touch with, and work with.

I look forward to any updates!!

Greetings fellas!!! :smiley: :unamused:


lol welcome back boston :open_mouth: :confused: :laughing:


Very nice Boston…I think Dr. Mariano is another great option too…He seems to have a vast understanding of the human body…


Dr. Jacobs has updated his blog with a new post.

It has been added to the first post in this thread (October 14 – “Another Piece of the Post-Finasteride Hypogonadism Puzzle?” – )


Looks like awor was ahead of the Doctor on this one. Good job…


Bad news, as ever…


The way I see it, the advancement of a diagnosis is never bad news.


Guys, keep in mind this has not been proven yet, it is simply his thoughts on the matter and wondering if/where the issues may lie.

That said, he is certainly more qualified than any of us to make such statements, and his insights are of absolute value to understanding and investigating this problem further.

The fact he is focusing on the androgen receptor and epigenetics is a crucial point, but wether these areas are the absolute root cause still needs to be tested for. That is the next step – getting research scientists interested enough in this problem to undertake the type of testing we need to get more answers.


How does this explain that when i quit i was feeling great for 2 weeks then suddenly i was hornier than ever in my life and sex was all i thought about for 3 weeks while feeling completely dead in all aspects but sexually. I could hardly move with out hurting yet im having an erection?

I dont belive this is the awnser to our problems. Our problem involves so much more than this explains imo.

Think its great that finally someone is taking our problems seriously tho and we will eventually find a cure for this crap. Ive had days and weeks even of complete recovery so im sure we will be okay in the end!

common epigenetic effect interacts with a less common variant in the androgen receptor gene CAG repeat profile to cause its syndrome of crippling persistent post-finasteride hypogonadism.
I dont think this explains how are condition progressed and not all of our symptoms either.


From his tone however, it seems as if he maybe hasnt had much luck lately in treating people. I hope this is not the case as I am going to be seeing him soon.


Mikey428, would you mind briefly sharing what specifically you are seeing Jacobs for? (I have no way to privately message you) He is local to me and I am interested in seeing him about my ongoing prostate/ejaculation issues that urologists seem to be shrugging off.

Also, in general, is this something that Endos/Neuro-Endos will deal with? Am I barking up the wrong tree? I need to have initial blood work done, should I see an endo before or after to point me in the right direction? I’ve been reading all over the forums, but I’m still kind of lost as far as first steps to take now that I realize my issues are likely related to PFS.


I don’t want to paint all cases with the blood to say that it is more neuro issue than androgenic.
I have problems (well am devastated really) for 4 years and even now, 2 days of Tribulus improves my libido and erection considerably. Just that after a certain point it does not work…



I tried to create a thread but it has yet to be approved. Lemme tell you something, Dr. Alan Jacobs is a nice, guy, he’s a smart guy, but he don’t know jack sh!t about 5AR inhibition or why it causes long lasting effects. The problem is not any change in the androgen receptor structure, and if there is a change in the AR other than the reduction in AR quantity body wide, we should be looking at WHAT CAUSED THIS CHANGE. You wanna learn something? Read this.

I am reaching somewhat with the following hypothesis but wishful thinking is better than none at all, it is also a lot more complex than I currently comprehend but I’ve been living this for seven years and I am very perceptive to the situation. This theory fits real friggan well and would explain why we don’t recover, or do so very slowly. Also I am an accutane sufferer, but before you discount what I say, listen because what I have discovered may hold OUR future cure.

Both accutane and finasteride are 5AR inhibitors. Accutane by indirect competitive inhibition, and Finasteride by direct 5AR inhibition. 5AR is responsible for epithelial integrity. One of the problems I have consistently experienced after accutane is blood pressure spikes upon standing up after I have been laying down for a while, even a short time, feeling like I will pass out for a few seconds. This is happening almost every time I stand now. I have been taking a lot of vitamin D and was using the simplified methylation protocol to attempt to bring back rate of metabolism, so I have been pushing my sytem to respond - None of this matters yet but it will.

When I was searching for retinol uptake genes and RA synthesis/recycling genes, I found this blood pressue spike could be a problem of amyloid-beta plaque buildup as the result of reduced Transthyretin. Transthyretin is responsible for the transport of amyloid-beta protein so that it does not build up in the brain and lead to cognitive decline and eventually Alzheimer’s. Another one of the issues caused by buildup of Beta Amyloids is erectile dysfuntion. Here’s the kicker, TTR is also responsible for retinol and thyroxine transport into the brain.

Now what does this have to do with our favorite 5AR drugs? Transthyretin is produced in the choroid plexus epithelium of the brain. The epithelium of the entire body is modulated by 5 alpha reductase. If our brains suffered damage from accutane and during the process lost much of the ability to produce transthyretin, we lost the ability to transfer amyloid proteins, as well as not have the normal uptake of nutrients from the blood. That is a recipe for the problems we are experiencing. One of which is cognitive decline, different from brain fog but they are of the same nature. The damage from accutane would heal very slowly. Also with reduced TTR there would be a retinol uptake problem and therefore retinoic acid deficiency in parts of the brain. This would explain our loss of growth factors. When retinoic acid is not binding to CRABP2 and activating retinoic acid receptors, it is binding to FABP5 and activating kinase growth pathways like protein kinase B/ Akt. This is able to explain the decrease in Androgen Receptor quantity as the gh/igf1 axis and androgens are highly integrated. If the brain doesn’t have the necessary nutrients, it will not attempt to heal.

If you visit the “Significant Irreversible Hormonal Antagonism” section on max001.proboards, and go to ‘growth hormone igf1 axis’, you will find the following information on a study on rats -

“In rat pituitary GH3 cells, Retinoic acid <1 microM stimulated growth hormone secretion by 220%. 50 nM HCT stimulated GH secretion 3,5 times and in synergy GH secretion was stimulated seven times”


I still experience dry skin and scalp, with my worse problems being low energy and libido as well as some level of cognitive decline and as I try and fix my problems almost consistent brain fog and spikes in blood pressure when I stand from laydown. Loss of epithelial integrity means less endogenous transthyretin production in the choroid plexus and decreased nutrient uptake to the brain. This may be the origin of our problems and is the first palpable common ground between finasteride and accutane.

I wrote the above message for accutane sufferers. But the idea is still the same. Both of us have suffered damage to epithelium body wide. This means in the brain as well. If we have all lost the ability to produce transthyretin, this creates a loop where the brain will not heal as it does not receive the nutrients from the blood. TTR is responsible for transfer of retinol into the brain for conversion to retinoic acid. RA is needed for the differentiation of highly specific neuronal cells. Therefore the rate of recovery will be extremely slow if there is a deficiency here. You cannot test this with a standard retinol test. If you still have dry skin, you should realize there is a problem. I took accutane 7 years ago at the age of 15.5, and I still have dry skin and scalp, almost every day. The sooner this gets fixed the sooner we recover epithelial integrity of the brain and entire body. The reason our androgen receptor quantity is low, is because with damaged pathways of the CNS and reduction of neurosteroids, the brain cannot recover. This is why we are suffering.

Forget the research on androgen receptor structure, there is nothing that has changed that is not attributed to the damage that has occurred in our brains, along the pathways that are sensitive to 5AR. When this is eventually realized, that’s when I will donate my money. Our cure may be of the same origin, but you guys are taking it step by step and it’s going way too fucking slow. Hopefully you will see where I am coming from and if you agree we can start working together. This is information that should be relayed to the men who are holding the roundtable meeting this february, they make be able to make gigantic strides if I am right about this.


Has there been any progress in treatments? I see that nothing has been posted to this thread in quite a while.

My symptoms are not as severe as some people on here but libido, sensitivity, ED etc. are truly getting me down. Its been about a year since I went off and finally determined to find treatment but really have no idea where to start.


Hi there,

This was just general thought I have on PFS. I have also been suffering from the persistent sexual dysfunction associated with this drug for the last 8 years. Along with many people who have taken Finasteride or similar 5a-reductase inhibitors such as acne medication Isotretinoin as well as SSRI’s. It appears this problem is far more common than it appears. Which is likely the result of many males being embarrassed or ashamed of reporting it.

It seems that this problem is caused be a fundamental change in the brain, which is seemingly permanent. If this is the result of an epigenetic change or malfunction of a receptor etc. it seems incredibly unlikely that any pharmaceutical treatment will become available any time soon. As this would likely require a drug or cell based treatment which alters the expression of cells etc. Not to mention the 10+ years associated with developing novel drug treatments.

Although it may sound drastic, I can’t help but think that Deep Brain Stimulation (DBS) is far more likely to be a viable treatment option. Many of the neuropsychiatric disorders currently being treated with DBS involve the mesolimbic dopamine reward circuitry, including Parkinson’s, schizophrenia, addiction, depression, etc. and by the sounds of most sufferers’ symptoms I would suspect that Finasteride along with Isotretinoin etc. have somehow impaired the dopamine circuitry as evidenced by studies of the nucleus accumbens in PFS sufferers. Dopamine is heavily involved in motivation and reward and what are generally called “appetitive” behaviours, including sexual behaviour.

Given that DBS was recently used for Anorexia, it seems highly plausible that a strong case could be made for its use in sexual dysfunction, a condition which affects a surprising number of people and is arguable far more problematic than Anorexia. I would argue that of all the symptoms that a PFS sufferer may face, persistent sexual dysfunction, is by far the most debilitating and disturbing. If this single aspect of the condition could be treated, I’m sure most sufferers would find life far more bearable and the likelihood of suicide would be greatly reduced. Especially as treating the dopamine circuitry, is likely to simultaneously treat aspects of both depression and anhedonia which many PFS sufferers have to endure.

The PFS foundation may be the only organisation in the world at this moment with enough legitimacy and following to pursue and raise interest into this research area. Again though it seems like a drastic treatment, I can’t help but feel that pursuing a pharmaceutical treatment is likely to take far longer, be far less effective and harbor far more side effects than DBS. I’m sure many would agree with me, that when dealing with a condition such as this, time truly is of the essence. Each extra year without treatment is an extra year of possible suicides and suffering.

Many Thanks,



Dr. Allan Jacobs’s latest post on PFS, from 5 years ago, has not been included in this thread, so I thought I would add it. I must say I am not impressed by it at all, especially his claim that somehow depression and anxiety are the main causative factor for PFS in 50% of sufferers. I am posting the text below so everyone can make their own conclusions. … drome.html

Clinical Experience in the Evaluation and Treatment of 300 cases of Post Finasteride Syndrome

In April 6, 2010 I blogged here on A Neuroendocrine Approach to Finasteride Side Effects in Men. Now I am reporting on how we’ve done over the past 3 years caring for around 300 men sufferring from Post Finasteride Syndrome (PFS).

First, the group of 300 + men presenting with sexual dysfunction while on finasteride, or recently or not-so-recently off it, did all show a similarly abnormal hormonal profile called hypogonadotropic hypogonadism or HH, which means low testosterone along with low LH and FSH, the pituitary hormones that stimulate the gonads. However, the group was otherwise not monolithic. In fact, I found three groups into which these men could be separately categorized.

10% of the the guys actually had a different reason to have HH, completely unrelated to the finasteride. For example, they had a benign pituitary tumor or some other related pituitary condition partially blocking its function in the hypothalamic-pituitary-gonadal (HPG) axis, so they could not make LH and FSH, and thus their testicles stopped making testosterone.

50% of the guys came with a family history, or genetic load, for emotional conditions such as anxiety and depression. Then when the finasteride caused big-time sexual problems, they were so distressed that their mental anguish itself appearred strong enough to suppress their HPG axis such that they had a separate reason to not be able to raise their LH and FSH when their testosterone declined, presumably initially from the finasteride. This mechanism is no different than the dancers and marathon-running women who loose their menstrual cycles. Such huge stressors, whether physical or mental, cause the higher brain centers in the temporal lobes to put the brakes on fertility, as if it were not a good time to have kids if your own internal stiuation is so hectic to begin with. The emotional parts of the brain inhibit the HPG axis directly, again blocking LH and FSH from responding to the low sex hormones. In this situation it was unclear whether the finasteride, their emotional brains, or both were impeding these guys’ ability to get better.

Then there were the 40% of guys who had no other reason than PFS to have HH, and to be sexually impaired, physically perturbed and mentally distraught - the pure post finasteride syndrome.

The first group of guys got treated in the appropriate neurosurgical setting, or reassured that there was no treatment needed except to normalize their testosterone levels. The second group presented more of a problem as they needed to be shaken out of their despair first in order for their HPG axis to be released from the grip of their higher emotional brian centers and be able to start making appropriate amounts of LH and FSH, leaving the only variable left to deal with the finasteride. The best way to do this was to raise their testosterone levels directly and aggressively such that they felt great and trusted their bodies to be normalizable. Also, in many cases anti-anxiety medications were added and were very helpful. Gradually these guys’ minds eased and they were eventually given the option to taper off the hormone after 6-12 months to see if they would stay normal on their own, though very few have as of yet wanted to. The third group could most often be treated successfully by using medications to raise LH and FSH directly and letting their testicles follow suit and make more testosterone. Sometimes LH and FSH would not budge enough and direct testosterone replacement was necessary and did the trick as long as the dose was pushed high enough and estradiol was kept from rising, due to peripheral conversion (aromatization) of the testosterone, with a different medication.

PFS is an troublesome condition, however, my experience is that it is well worth applying the neuroendocrine approach to caring for these guys since it has been most often beneficial to them.