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Do not stop finasteride cold turkey! A strong argument to taper to very low doses.

Discussion in 'Dealing with Side Effects' started by ham373, Nov 2, 2014.

  1. ham373

    ham373 New Member

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    I have very good reasons to suggest that a slow tapering (slower than almost everyone considers doing) has a good chance of reducing the chance of post-finasteride syndrome. Apart from requiring patience there is no down side.


    The short summary:


    1. Very small doses of finasteride (like 0.04mg) inhibits DHT quite a lot.

    2. A single dose of finasteride inhibits DHT for 4-7 days for a tiny dose (like 0.04mg to 0.2mg) and even longer for a 1mg dose.

    3. The post-finasteride syndrome has many of the hallmarks of a hormonal axis shut down, and may be due to the surge in DHT caused by abrupt stopping the drug.

    4. Like in other hormonal shutdowns this risk can be minimised by a very slow tapering regime.

    5. There is no discernible downside to tapering. If you have been on the drug for x years then three months (or so) tapering cannot add a lot of risk and it may be beneficial.

    6.A slow tapering regime for finasteride involves the following in broad outline:

    a.going to about 0.25 mg a day straightaway (this inhibits DHT the same as 1mg/day),

    b.then going to 0.25mg every second day, third day and then fourth day.

    c.At this point you should reduce the dose, while dosing every fourth day. An eight of a tablet is 0.125mg.

    d.Ideally you would get down to about 0.04mg every fourth day which might be done by very careful cutting up of eights of a tablet.

    e.From every fourth day on 0.04mg, space this out to 5, 6, 7, 10 and 14 days.

    f.There is even rationale to go to even more smaller doses - like 0.02mg and 0.01mg at these intervals - but this is likely too difficult.

    g. Timing: step a. can be done straight away. step b. can be done over a couple of weeks. steps c.to f. should be done as slowly as you can stand. It is very likely that when you get to 0.125 mg every fourth day you will notice an improvement in your side effects and you might also be able to discern a time line of worse symptoms about 24-36 hours after a dose that improves over the next 2-3 days.

    This is not the time to quit cold turkey! This is the time to go slow. This period should remove any doubt in your mind where the side effects have come from. But you need to wean off slowly to give a chance to safely land your hormonal system.

    It is tough to put a drug into your mouth that you realise is doing you harm, but it is far tougher to risk the prolonged side effects that might come from stopping quickly.

    - - - Updated - - -
     
    #1 ham373, Nov 2, 2014
    Last edited: Nov 9, 2014
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  2. ham373

    ham373 New Member

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    I'm going to expand on 3. first because this will explain why tapering might do anything at all:

    I apologise for the endocrinology 101 stuff but it's important:

    The most studied hormonal axis in man is the hypothalamic-pituitary axis (HPA axis) and it acts as a good model for other axes like the hypothalamic-pituitary-gonadal axis (HPG axis).

    Simple pictures of both below will show you how similar the mechanics are.

    HPA_Axis_Diagram_(Brian_M_Sweis_2012).jpg

    For the HPA axis, the hypothalamus secretes CRH which stimulates the pituitary gland to produce ACTH which in turn stimulates the adrenal gland to produce cortisol (CORT). Levels are roughly maintained by feedback inhibition of cortisol to the adrenal gland and hypothalamus.



    722423-fig1.jpg


    For the HPG axis, the hypothalamus secretedGnRH which stimulated the pituitary toproduce LH and FHS which in turnsimulated the testes to produce a number of gonadal hormones includingtestosterone. Testosterone and other gonadal hormones (like dihydrotestosterone(DHT)) produce feedback inhibition to the pituitary and hypothalamus.

    - - - Updated - - -

    Glucocorticoids (drugs that act like cortisol which is the human glucocorticoid) are amongst the most widely used drugs in medicine. When people have inflammatory disorders – like severe arthritis or severe asthma they often receive glucocorticoids (because it is a potent anti-inflammatory). These glucocorticoids (like prednisone or dexamethasone - there are many different trade names) are man-made and are more potent versions of cortisol.

    So they do what cortisol does only stronger. The beneficical part of this is they strongly suppress inflammation (good treatment for the arthritis, asthma etc). They also produce a number of side effects.

    But the main thing of interest here is that these synthetic glucocorticoids strongly suppress the HPA axis. That is, they strongly inhibit the secretion of CRH and ACTH at the hypothalamus and pituitary and therefore shut down the secretion of cortisol from the adrenal gland. That is totally fine because you have a huge amount of these glucocorticoids in your body when you're being treated so you don't need your own supply.

    - - - Updated - - -

    But when you stop it’s a different story.

    It has been known for years (since the 1960s) that if you stop these synthetic glucocorticoids abruptly then the HPA axis tends to stay shut down. Studies vary as to what percentage of people will experience this - some suggest 100% (for at least a small period of time if the dose has been big enough for long enough).

    What varies between people is how long the axis stays shutdown for. For some people there is recovery in a couple of weeks, others four weeks, some it takes as long as months.

    What influences this? How high the dose of glucocorticoids were, how long they were given for, how abruptly they were stopped.

    Ok, so what's this got to do with finasteride?

    Finasteride lowers levels of DHT so if anything it should increase the activity of the HPG axis (because there is less feedback inhibition), right?

    There probably is an upregulation of the sensitivity of the HPG axis while you are on the drug (this is why those studies of androgen receptors in foreskin tend to show increased levels of androgen receptors, etc).You have levels of DHT that are around 20-30% of usual levels meaning there is less signal hitting the system and hormonal systems normally upregulate to make up for this (this is how biochemistry generally works).

    - - - Updated - - -

    OK, but what's this got to do with dexamethasone?

    When you stop finasteride, your levels go back to approximately normal over 2-4 weeks (see graph below).

    This is a study that shows men being given different doses of finasteride each day for two weeks. At day 14 they stopped getting the drug. Their serum DHT levels were measured (at intervals) for the 14 days of receiving the drug and for 16 days after stopping, giving a total of 30 days.

    You can see that after day 14 their levels of DHT rise back towards normal over this period. Extrapolating the graph you might guess that their levels of DHT would return to normal in about another 2 weeks, meaning they would probably get back to normal about 4 weeks after stopping the drug.


    stop fin caption.jpg stop fin.jpg


    That sounds good, right? It is and that is why people likely report feeling a lot better a week or so after quitting (probably the time taken for enough DHT to be back in the system for people to be able to feel the difference) and report their side effects diminishing and then disappearing. In fact, some people report feeling fantastic.

    One thing to point out here is that hormone levels (like DHT) coming back from their reduced levels is not the same 80% increase as on the way down. Now you are going from 20-30% of normal levels back up to 100%. This is actually a four or five fold increase. That is a massive increase in hormone levels. It is kind of like getting a big dose of dexamethasone - only this affects your hpg axis.

    - - - Updated - - -

    It is plausible that this rapid increase in DHT (not forgetting all the other hormones that are influenced by 5AR) has the same effect on the HPG axis as dexamethasone has on the HPA axis. That is, the surge in DHT causes shut down of the HPG axis.

    This would fit with the improvement felt by men coming off it over 7-14 days (approx) followed shortly after by a 'crash'.

    - - - Updated - - -

    What I am suggesting is that the coming off finasteride might be an important factor in causing the post-finasteride syndrome.

    Logically speaking there are basically two broad possibilities for what causes this syndrome:
    (1) Something the drug does to you while you are on it (affects neurosteroids, the androgen receptor, etc, etc, hypotheses abound)
    (2) Something that happens upon stopping it

    (or perhaps a combination of (1) and (2))

    The reason why (2) seems to be plausible is the time line of events that most men report -

    - experiencing side effects while on the drug
    - a resolution of side effects a few days after stopping
    - followed by a 'crash' a few days or weeks after this
    - the symptoms following this 'crash' are variable in severity and variable in how long it takes to resolve. They also seem to be worse than the side effects experienced on the drug AND they seem to have a different hormonal signature (ie in post-finasteride syndrome men seem to have a hypogonadotrophic hypogonadism, while men on the drug have low DHT (of course) and a slightly higher than normal testosterone and basically normal LH and FSH)


    This time line of symptoms seems to fit the shutdown of the axis cause by a surge in returning hormones.

    I think (1) is important because it probably increases the sensitivity of the system to DHT and other hormones, thus creating a perfect storm - a rapid and large increase in hormone affecting an already overly sensitive system; making it more likely to be shut down.
     
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  3. mr.patches

    mr.patches Established Member

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    To say PFS may occur for stopping the treatment suddenly brings much more light to the matter. Interesting read.
     
  4. Fanjeera

    Fanjeera Senior Member

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    I personally think this theory makes no sence. Don't think you've come up with something new. Endocrinologists think about that kind of basic stuff beforehand (it's what you learn in medschool every year over and over again) and finasteride has been shown not to suppress the endocrinal axis: http://www.ncbi.nlm.nih.gov/pubmed/1322427 ; http://www.ncbi.nlm.nih.gov/pubmed/8957695 ; http://www.ncbi.nlm.nih.gov/pubmed/8077369 ; http://www.researchgate.net/publica...in_patients_with_benign_prostatic_hyperplasia; http://www.ncbi.nlm.nih.gov/pubmed/7615107
    Negative feedback is attained with just testosterone. And if anything, finasteride suppresses the axis: http://www.ncbi.nlm.nih.gov/pubmed/9589555
     
  5. ham373

    ham373 New Member

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    Thanks for taking an interest.

    Mr patches - did you ever use finasteride/try tapering? What made me think about this issue was the period of resolution of symptoms that a lot of men report when coming off finasteride. This makes me think the use of the word 'persistent' to describe the side effects is somewhat erroneous- actually they resolve and then come back, seemingly more strongly. So maybe the side effects on finasteride are of a different origin to the post-finasteride problems

    Fanjeera, I don't think I have come up with anything knew - it is nothing that hasn't been said by guys for a few years. But I think tapering off the medication makes a lot of sense and I hope to explain why I think that and hope that if it makes sense people who are considering stopping finasteride might do it in a tapered fashion because it might reduce the risk (or severity) of post finasteride issues.

    You make fair points but I am not suggesting that finasteride suppresses the HPG axis - as you say it does not.

    I am saying the opposite - coming off finasteride quickly might suppress the HPG axis as your DHT (and others) shoot up quickly.

    Your papers on the effects of finasteride emphasise the point that hormones are not greatly altered whilst on finasteride (except of course DHT goes down and testosterone goes up a bit). This is a contrast to the levels of hormones found in people with post-finasteride syndrome - suggesting a difference in the cause of the side effects on finasteride and the post-finasteride syndrome.

    There are various hormones that have a feedback inhibitory effect on the HPG axis - you're right testosterone is one, but so does DHT. In fact, it does so stronger than testosterone.

    What I am suggesting is that the rapid increase in DHT on stopping finasteride feeds back and inhibits the HPG axis causing it to shut down.

    Perhaps my HPA axis analogy is a bit confusing but it is the axis that we most often suppress in hospital and the feedback inhibition acting on it is very well recognised and the similarity to PFS is one of the things that drew my attention originally.
     
  6. ham373

    ham373 New Member

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    I think this may be right nottoolanymore - with this idea in mind, a slow tapering off might give your androgenic system time to recalibrate itself to new levels of hormones without the big whack you get in a couple of weeks of coming off it
     
  7. Fanjeera

    Fanjeera Senior Member

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    Link a study please! I just proved the opposite: only testosterone itself suppresses the axis. When you give a person finasteride and therefore cause a LACK of DHT, the HPG axis either remains unchanged or is suppressed. Therefore, rise in DHT doesn't suppress the axis. The following fall in T will actually cause an upregulation of the axis like one study I cited said. It's the other way around.
     
  8. ham373

    ham373 New Member

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    [FONT=Arial Unicode MS, Arial Unicode, Arial, URW Gothic L, Helvetica, Tahoma, sans-serif]Dihydrotestosterone is a more androgenically potent derivative of testosterone (which means it acts more strongly on androgen receptors - responsible for many of the male-defining properties of hormones - determining deepness of voice, hair growth, prostate development and function etc), while being anabolically less potent (i.e. not producing the same effect on lean muscle mass as testosterone).

    The feedback inhibition system works by androgens - DHT, testosterone - acting on the androgen receptors present in the hypothalamus and pituitary and initiating a feedback mechanism by which GnRH pulses, and LH and FSH are inhibited.

    The increased affinity for DHT for androgen receptors as well as the increased duration of its binding underlies the increased androgenic potency of DHT compared with Testosterone.

    It is even thought that the conversion of testosterone to DHT by 5-alpha reductase is done so in areas where increased activation of androgen receptors is needed - i.e. in the prostate, testes, skin and also the brain (why you need it in the scalp skin is beyond me?). In other words, one of the key properties of DHT seems to be its ability to more powerfully activate androgen receptors.

    But one last point, I mention DHT explicitly above, but it is known that 5-AR is involved in the metabolism of a number of active steroids, which presumably also increase when 5-AR inhibition is lifted. I know much less about the effects of these hormones on different endocrine axes (and there may be synergistic effects) but the point is that there will be major hormonal changes as 5-AR inhibition is lifted and rapid changes of hormonal levels plausibly cause major perturbations, including axis shutdowns.

    Tapering off the medication would reduce the rapidity of these hormonal shifts and so would plausibly reduce any perturbation that resulted, including perhaps the axis shutdown (or similar) that may underlie the post-finasteride syndrome.


    References:
    [/FONT]

    [FONT=Arial Unicode MS, Arial Unicode, Arial, URW Gothic L, Helvetica, Tahoma, sans-serif]"Dihydrotestosterone, an A-ring reduced steroid which is not convertible to estrogen, was demonstrated to be more potent than testosterone in suppressing serum LH levels while equipotent to testosterone in suppressing FSH" ([/FONT]http://www.sciencedirect.com/science/article/pii/0039128X72901158)

    "the levels of human FSH beta mRNA in monolayer cultures of pituitary cells were decreased by 24-hour treatments with 10 nM testosterone propionate or 5 alpha-dihydrotestosterone to 13 and 26% of control values, respectively, in the absence of GnRH." (http://www.ncbi.nlm.nih.gov/pubmed/7544877)

    "It was later shown that two gonadal steroids, 17β-estradiol (E2) and 5α-dihydrotestosterone (DHT), could directly target the pituitary to modulate the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in these frogs [2-4]." (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC548137/)

    "the affinity of binding of dihydrotestosterone was, on the average, about 2-fold greater than that of testosterone. [[SUP]3[/SUP]H]Testosterone also exhibited a 5-fold faster dissociation rate from the receptor than [[SUP]3[/SUP]H]dihydrotestosterone....

    Our results suggest that the weaker androgenic potency of testosterone compared to that of dihydrotestosterone resides in its weaker interaction with the androgen receptor, most clearly demonstrable as an increase in the dissociation rate of testosterone from the receptor...

    ...a metabolic amplification step, namely the in situ conversion of testosterone to dihydrotestosterone." (http://press.endocrine.org/doi/abs/10.1210/endo-126-2-1165)

    "Inhibition of pulsatile LH secretion by all three steroids indicated that testosterone as well as its androgenic and oestrogenic metabolites can inhibit the LRH pulse generator in the hypothalamus. Additional feedback on the pituitary was indicated by the dampened LH responses to exogenous LRH." (http://www.ncbi.nlm.nih.gov/pubmed/6342323)
     
  9. ham373

    ham373 New Member

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    I take your point nottool. It is true that finasteride doesn't block 100% of anything and I think it seems certainly true that it does not have bad effects for everyone - while on it or after coming off it - but it does seem to affect a portion of people quite badly on it and afterwards. In part, I think this may be due to the rapid changes of hormone levels that occur when stopping it abruptly.

    At the same time, what you say about propecia's effectiveness is probably also true and losing your hair can be pretty crappy.

    It is about balancing the risks and benefits - for some people hair loss might be so devastating that taking a pill that plays around with your hormones - perhaps permanently or for long periods of time in some people - might be worth the risk. For others they might decide that using less effective agents that have less risk associated might be more prudent.

    The main thing is that the risks are understood clearly so people can come to their own well-informed decision. At the moment, I don't think there is a clear understanding of what percentage of people that use this drug experience the moderate and sometimes severe side effects that occur on and after this drug.

    At the same time, there are also a bunch of people currently on the drug who are experiencing side effects who are concerned about the long term effects of the drug and would likely benefit from some means of reducing their chances of long term effects.

    It is a rather frightening place to be in - having side effects to a drug that you hear can cause worse effects if you stop it. Quite a double bind. This is why I am a broken record about the advantages of tapering off the drug. Perhaps, for people like you, who did not experience problems coming off this is overkill and involves needless irritation in the form of dividing up pills, or dissolving them in alcohol, etc but perhaps for others this might save them months or years of awful effects that seem to occur in an (unknown) percentage of people.

    So, I'd like to query your equation of propecia and happiness. Actually, having said this would you use propecia again to prevent further hair loss?
     
  10. Fanjeera

    Fanjeera Senior Member

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    The question is whether the tissue has 5ar2 or not. Hypothalamus obviously doesn't have 5ar2 in it and so doesn't get very much DHT anyway. And like it's said in the study you posted, 1/3 of normal testosterone is needed to have an effect on the hypothalamus, but 2 to 4 times the normal level of dht: http://www.ncbi.nlm.nih.gov/pubmed/6342323
    So testosterone obviously is the one mediating negative feedback. DHT definitely can do it too, but it doesn't in a whole human organism. It gets binded quickly everywhere else because of its higher affinity for the androgen receptor. You've still got it all wrong. The exact opposite happens after quitting the drug. What's your specialty?
     
  11. ham373

    ham373 New Member

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    Fanjeera - you seem to really, really dislike the idea off DHT being one means of a feedback mechanism forthe HPG axis.


    I have to say I appreciate your critical reading as this is helpful in gathering all the details together.So thanks for giving me a grilling one-man peer review. For the record, though I don't think it changes the validity of the references I've provided, I am a medical doctor and near completing aPhD in neuroendocrinology.


    However, I am not convinced that your intent is entirely constructive and I'm not sure your reputational comment 'wrong' is all that helpful. If you think that stopping finasteride leads to an overactive HPG axis or similar then I suggest you provide evidence to bolster that proposition.


    I suspect most people would like to understand what causes the endocrine effects that seem to occur after stopping finasteride, and what people might do to reduce their chances of experiencing this terrible syndrome.


    It is clear that you have an opinion on the matter- do you think that it is largely due to damage on the drug rather than damage that occurs upon stopping it?


    And would you think it better, were someone to decide they wanted to come off the drug, to stop abruptly rather than tapering off? Have you used finasteride? And are you still on it or have you stopped using it?


    Before getting to your specific queries, I'll just briefly restate my frame.


    I began from the general observation that the post-finasteride syndrome looked very similar to the axis shutdown you get with high levels of glucocorticoids.


    The idea of tapering fits in with the general and sound principle in endocrinology that minimsing the rate at which hormones are modified is likely to reduce the impact on the finely tuned balancing mechanisms that exist in the body.


    The following is a non-exhastive list of enzymes that are metabolised by 5-AR:


    -In the glucocorticoid family-5-alpha-Dihydrocortisol; 5-beta-Dihyrdocortisol; 3-alpha,5-alphaTetrahydrocortisol; 3-alpha,5-beta-Teatrahydrocortisol; 3-alpha,5-beta Tetrahydrocortisone
    -In the andrgoen family -5-alpha-dihydrotestostrone (DHT); 3-alpha,5-alpha androstanediol;5-alpha Dihydroandrostanedione; 3-alpha,5-alpha-Androstanedione
    -Progesterone metabolites-5-alpha-Dihydroprogesterone; 3-alpha, 5-alpha-teatreprogesterone(Allopregnenolone)
    -Aldosterone metabolites -5-alpha-Dihydroaldosterone; 3-alpha, 5-alpha-Tetrahydroaldosterone


    I provide this list only to indicate that there are a lot of pathways controlled by 5-AR, not just test->DHT, and all of these pathways are then activated as finasteride is stopped and 5-AR activity is restored.


    Though people focus on DHT for obvious reasons actually all these enzymes have effects on the brain and different endocrine axes in the body.


    As to your specific concerns:


    Testosterone is certainly not the only hormone with the ability to inhibit the HPG axis as part of feedback control - several other hormones do so, including oestrogen,progesterone, inhibin and DHT.


    I have provided a number of references above indicating that DHT inhibits the secretion of LH and FSH from the pituitary (one level at which feedback can be transduced)


    One study you focused on did use higher levels of DHT than testosterone to inhibit the axis but this is not to say that lower levels would not do so as well, as is well demonstrated by the other studies. Indeed, it as been shown again andagain that DHT is a more androgenically potent hormone than testosterone.


    Though I am sure that you understand that study of hypothalamic release of GnRH in the human is made difficult by needing access to the hypophseal cicrulation (that is the circulation that connects the hypothalamus to the pituitary near the base of the brain) there are several convincing means of establishing the ability of DHT to inhibit hypothalamic release of GnRH (also known as LH-RH or LH-releasing hormone):


    1) The hypothalamus does express the 5-AR-2 enzyme
    GT-1 cells are hypothalamic cells that specifically secrete GnRH (LH-RH)


    Fromhttp://www.sciencedirect.com/science/article/pii/S0960076098001502
    "Inadulthood, thetype 2 gene appears to be specifically expressed in localised brainregions, like the hypothalamusandthe hippocampus.
    The5α-Rtype 2 is present in the GT1 cells, a model of LHRH-secretingneurons. These cells also contain the androgen receptor, which isprobably involved in the central negativefeedbackeffect exerted by androgens on the hypothalamic–pituitary–gonadalaxis.The physiological significance of these and additional data will bediscussed.
    Itis known since a long time that both the hypothalamus and thehippocampus are major targets of sexsteroidactions. The hypothalamusis particularly rich of intracellular receptors for gonadal steroidsand this brain region, through the effector system of the LHRHsecreting neurons, is the primary site of the control of thehypothalamic–pituitary–gonadalaxis.
    Theandrogen-responsive machinery here described in GT1 cells probablyrepresents the site for the intracerebral negativefeedbackeffect of androgens on the hypothalamic–pituitary–gonadal axis;in fact, DHTis a potent, direct suppressor of LHRH gene expression in GT1 cells[36]."
    2) In men with a 5-AR-2 deficiency forgenetic reasons you can also see strong evidence for reducedinhibiton of the HPG axis by the absence of DHT


    In these people you see:
    "(i) increased plasma levels of LH and anincreased LH pulse amplitude with a normal LH frequency (Canovatchelet al., 1994);
    (j)plasma FSH levels may be elevated. "
    (http://www.sciencedirect.com/science/article/pii/S0303720702003684)- in other words, evidence in humans of impaired feedback on the HPGaxis (despite increased leves of testosterone).


    To be more precise, in these 5-AR-2 deficient men:
    "Mean plasma levels of LH areapproximately twice normal. The elevated mean LH occurs despite anelevated mean plasma testosteorne level (Canovatchel et al,1994). Furhermore, data from pulsatility studies have demonstratedthat there is an increased LH pulse amplitude, with a normal LHfrequency, which suggests a role for DHT in the negative feedbackcontrol of LH (Canovatchel et al, 1994). Plasma FSH concentrationsare also elevated in these subjects (Imperato-McGinley et al,1979a). While some of the elevation of FSH is undoubtedlyattributable to cryptorchidism and seminiferous tubular damage, arole for DHT in the feedback control of FSH cannot be ruled out(Fratianni et al, 1993)."
    (http://www.sciencedirect.com/science/article/pii/S0950351X98804783?np=y#)


    Further:
    http://www.hindawi.com/journals/au/2012/530121/
    "IntracellularT is converted to dihydrotestosterone (DHT), the preferred ligand forandrogen receptor (AR) transactivation, by the enzyme 5alpha-reductase (5α-R)
    Inthe 1960s, 5α-reduction was shown to be an irreversible reaction andDHT was found to be a more potent androgen than T in prostatebioassays [26].
    5α-R1-3is ubiquitously expressed [10,11,13,20,55].5α-R1 and 5α-R2 are expressed differently in liver, genital andnongenital skin, prostate, epididymis, seminal vesicle, testis,ovary, uterus, kidney, exocrine pancreas, and brain (Table 2,Aumuller et al.)
     
  12. Fanjeera

    Fanjeera Senior Member

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    How do you explain the fall in LH and FSH while taking finasteride then? http://www.ncbi.nlm.nih.gov/pubmed/9589555
    The people with pfs are not all saying they got it after stopping the drug. A lot are saying they got side effects on the drug which just stayed. And hormones have been shown to be totally normal after quitting finasteride.
    No 5ar2 in human hypothalamus, but 5ar1 (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC294929/pdf/jcinvest00029-0377.pdf).

    Last study on the permanence of the side effects: http://www.ncbi.nlm.nih.gov/pubmed/25268732
     
  13. Luke1985

    Luke1985 New Member My Regimen

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    Hi Ham373.
    I've been on Propecia for about 5 months. Have decided to stop as I've started getting severe anxiety panic attacks over nothing And I've never had any panic attacks before going on this drug. I have no other side effects and everything seems to be working normally downstairs. I'm not a very aggressive man usually so don't know if this suggests I already have low DHT. I could really use your help in tapering off.

    I went on the 5mg version of the drug and cut it up into 1.25mg. Sometimes the pieces of tablet i cut up were bigger sometimes smaller. I read your post and the all the other ones of men who have developed post finesteride syndrome and I'm terrified! I've tried to follow what you've suggested by weaning my self off but the panic attacks are so bad when i have a dose I'm not very good at it. So far I've been off it for two week. I missed a couple of days and had a half dose twice. Then missed three days and had a half dose. Then five days, and i cut the tablet up with raiser and I think I would have had about .05mg.

    I really want to get off this as the anxiety is affecting me a lot, but really don't want to get the long term side effects.
    I had a range of blood tests done the other day, based on what these forums suggest but apparently everything falls within the normal levels. What do I do? Should i continue to taper off and how?
    Also this guys seems to have another theory - what do you think?
    (www.pfshealing.com/key-to-curing-post-finasteride-syndrome-inflammation/)
     
  14. holyhead

    holyhead Member

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    Let me tell you I took this junk for only a few months..Had terrible sides and feelings while on the drugs..I tried to stop gradually by taking it only once or twice a week..After your hormones return to normal I declined like you wouldn't not believe..Been off year and a half and have...Massive weight gain over 40lbs of fluid like filled flab on waist thighs and stomach..Complete hair change looks like sh*t now it's so dry like burnt up straw hair..Depression and wanting to kill myself daily..It's catastrophic for healthy male if you get pfs from it..Trying to get on clomid now anything to relieve symptoms basic ly your test crashes and won't swing back..And estrogen dominance worsens.
     
  15. Luke1985

    Luke1985 New Member My Regimen

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    Well it's been a month and a bit since i've been off since my last post. I've gone off finasteride completely. Feeling so much better. I've looking into products and food that increase estrogen and tried to limit these. Been working out hard and doing sprints. Mentally I'm getting better every day. Been taking zinc, magnesium, vitamin d and Ashwagandha. Feeling a lot better. And another thing. Stopped looking at p**rn, this does crazy stuff at messing up your dopamine receptors in your brain. So stop looking at the crap online and your brain slowly resets.
     
  16. rdandy

    rdandy New Member My Regimen

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    Any updates from OP on this one?
     
  17. Pigeon

    Pigeon Senior Member My Regimen

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    OP could be right, I didn't taper off and had long term sides.
     
  18. Manochoice

    Manochoice Experienced Member My Regimen

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    Like? Still have them?
     
  19. Pigeon

    Pigeon Senior Member My Regimen

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    The usual sides, ED, loss of libido. Fina totally nuked my libido. Had a very high libido before finasteride.

    And yeah still have them although it got better but FAR from cured. This is 2 years after quiting finasteride. (also took finasteride for 2 years)

    And I'm doing a regimen to counter these sides, will make a thread if it helps.
     
  20. Manochoice

    Manochoice Experienced Member My Regimen

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    Damn man! Sorry to hear that! Hopefully you'll recover! Did your libido and ED improve?
     

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