Well never mind, woke up after 5 hrs of sleep with anxiety and panic attacks and muscle spasms again… just laying here now wondering how this could get so bad… its almost like the fina is still in my system except I slept better even then. Man oh man, this is really bad… I’m thinking about going to the emergency room just so docs will look at me… but I doubt anything would come of it.
Sorry to hear this. Sleep is so important for our imbalanced systems.
Talk to your doc about something else. I use Elavil as needed (most Fridays when I can sleep in the next day) and it’s helped me get some restorative sleep.
Well, the GABA may not help me sleep at night but it definitely helps my mood and brain fog during the day… I even think it helps with my libido somewhat but not with ED. Probably because it doesn’t cross the blood/brain barrier.
I have dedicated the last few weeks to reading everything and anything about finasteride, endocrinology and how the endocrine system and the brain work together.
I’m a fairly educated individual, having studied at a major univeristy and done grad school at an even more prestigious instution… having used AAS in the past and knowing their effects, somewhat helped me put myself ahead of the curve in my research on the side effects of FINA.
Given my current hormonal status as I previously posted, it doesn’t seem to be an issue with low T, even though my estrogen hasn’t been checked yet which of course could be a potential culprit the more I learn about it the more I think this (at least for me) is an issue in the brain having to do with allopregnanolone insuffiency, which probably screwing up my dopamine and seratonin leading to my sleep, mood, ED and libido issues.
By taking the GABA I am essentially filling the receptors with a stand-by which has helped get my anxiety and “kill myself” feelings under control to some extent.
I am becoming more and more convinced as I read some peoples recoveries on this sight and the effects of GHB and Xyrem that one of these drugs maybe the cure for my current state.
What I don’t however understand is how if my body now has normal DHT levels than 5-AR II must be working again thus why is allopregnanolone not kicking in? Has 5-AR II been surpressed subjectively in certain parts of the body like the prostate and the brain but not the skin or aderinals? And if GHB or Xyrem were to work would it be required for life or can it kick start the bodies own return to homeostasis?
GHB is essentially impossible for me to get unfortunately… I do plan on going into the next endo appointment armed to the teeth with information on Xyrem and the recoveries made form using it. If anyone can help me with links to further information about positive effects from this drug please post links up.
CNS Drug Rev. 2006 Spring;12(1):53-76.
A new look at the 5alpha-reductase inhibitor finasteride.
Finn DA, Beadles-Bohling AS, Beckley EH, Ford MM, Gililland KR, Gorin-Meyer RE, Wiren KM.
Department of Veterans Affairs Medical Research, Portland Alcohol Research Center, 97239, USA. finnd@ohsu.edu
Finasteride is the first 5alpha-reductase inhibitor that received clinical approval for the treatment of human benign prostatic hyperplasia (BPH) and androgenetic alopecia (male pattern hair loss). These clinical applications are based on the ability of finasteride to inhibit the Type II isoform of the 5alpha-reductase enzyme, which is the predominant form in human prostate and hair follicles, and the concomitant reduction of testosterone to dihydrotestosterone (DHT). In addition to catalyzing the rate-limiting step in the reduction of testosterone, both isoforms of the 5alpha-reductase enzyme are responsible for the reduction of progesterone and deoxycorticosterone to dihydroprogesterone (DHP) and dihydrodeoxycorticosterone (DHDOC), respectively . [b]Recent preclinical data indicate that the subsequent 3alpha-reduction of DHT, DHP and DHDOC produces steroid metabolites with rapid non-genomic effects on brain function and behavior, primarily via an enhancement of gamma-aminobutyric acid (GABA)ergic inhibitory neurotransmission. Consistent with their ability to enhance the action of GABA at GABA receptors, these steroid derivatives (termed neuroactive steroids) possess anticonvulsant, antidepressant and anxiolytic effects in addition to altering aspects of sexual- and alcohol-related behaviors .[/b] Thus, finasteride, which inhibits both isoforms of 5alpha-reductase in rodents, has been used as a tool to manipulate neuroactive steroid levels and determine the impact on behavior. Results of some preclinical studies and clinical observations with finasteride are described in this review article. The data suggest that endogenous neuroactive steroid levels may be inversely related to symptoms of premenstrual and postpartum dysphoric disorder, catamenial epilepsy, depression, and alcohol withdrawal.
Well this is essentially what I did to myself by taking fina and letrozole at the same time…
ncbi.nlm.nih.gov/pubmed/9759700
Effect of dual inhibition of 5-alpha-reductase and aromatase on spontaneously developed canine prostatic hypertrophy.
Suzuki K, Okazaki H, Ono Y, Kurokawa K, Suzuki T, Onuma E, Takanashi H, Mamiya Y, Yamanaka H.
Department of Urology, Gunma University School of Medicine, Maebashi, Japan. kazu@news.sb.gunma-u.ac.jp
Abstract
BACKGROUND: Our aim was to assess the effect of dual inhibition of 5-alpha-reductase and aromatase on prostate glands.
METHODS: We investigated the morphological changes in the prostate gland and the changes in the hormonal environment after administration of finasteride and arimidex to intact canine specimens. The study consisted of four groups: a 5-alpha-reductase only group (5RI only, n = 5); a 5RI plus aromatase-inhibitor combination group (5RI + ARI combination, n = 5); a BPH control group (n = 3); and a castration control group (n = 3). Finasteride (1 mg/kg/day) and the same dose of arimidex were orally administered for 80 days.
RESULTS: In the 5RI group, a significant decrease in the serum dihydrotestosterone (DHT) level was found, and prostatic volume was significantly decreased. However, significant increases in serum testosterone (T) and DHT levels were observed, with a concomitant increase in prostatic volume in the 5RI + ARI combination group. Morphometric analysis showed that histopathological findings in the 5RI + ARI combination group were similar to those in the BPH control group.
CONCLUSIONS: Dual inhibition of 5-alpha-reductase and aromatase resulted in a significant increase in prostate volume, accompanied by a 3-10-fold increase in serum testosterone levels and a significant increase in testicular volume.
I really may have broken new ground as far as idiocy is concerned for running this one.
I’m hesitant to make bold proclamations regarding what is causing our condition.
But biased upon what I’ve done recently and the improvement I’ve seen I am inclined to say that the majority of our problems are arising from a lack of 5-AR II activity.
Going about trying to find ways to boost 5-AR II was what I have been doing the past few days… little did I realize that I had one way already with me. DHEA, I took a dose of 450MG and the morning erection quality was 100%. My sleep was slightly better as well.
I need to do some more work with it, but this does appear to be the culprit. Now finding a way to permanently up-regulate 5-AR II is another problem, as it would be somewhat annoying and maybe dangerous to stay on DHEA high dosage forever.
Broken_Pecker maybe you are right but I saw at old posts of JN he had high TT and DHT
why are you assuming its not kicking in?
“What I don’t however understand is how if my body now has normal DHT levels than 5-AR II must be working again thus why is allopregnanolone not kicking in?”
Our normal DHT lvls might not be normal at all:
From Xeno on another board:
Theory
The ‘Phantom DHT’ theory or the ‘Increased Testosterone Metabolism Theory’
(1) Fin inhibits 5-beta-Reductase, which controls the hepatic cyp3a4 enzyme involved in the metabolism of androgens and xenobiotics [1]. Fin is both a xenobiotic and a synthetic androgen [10], thus the reduced cyp3a4 enzyme is taxed to metabolise it.
(2) As fin inhibits its own metabolism there may be v.high serum levels and higher chances of side-effects, especially if taken with other drugs, alcohol.
(3) When fin usage ends, 5-beta-reductase will regenerate thus creating more cyp3a4 enzyme. I theorise this could lead to permanant increase in the metabolation of androgens as well. (this has been discussed in relation to the gulf war syndrome [9])
(metabolism = deactivation before being made water soluble for urination. Androgens can also be made water soluble for urination w/out deactivation from cyp3a4)
(4) higher testosterone metabolism will lead to more deactivated hydroxytestosterone (especially 6beta-hydroxy testosterone ‘6bOHT’) in serum. [2]
(5) the body should compensate for metabolism with more T production via LH [3] (possibly resulting in altered LH profile)
(6) the sudden metabolism and gap before T production catches up could lead to the ‘crash’. If T production never catches up T levels will be permanantly lowered.
(7) I theorise that a higher serum ratio of hydroxytestosterone/testosterone could interfere with the heomeostatis of testosterone in the body leading to symptoms of hypogonadism. (ie competing for the androgen receptor [7], transport throughout the body)
(8) 6bOHT is an excellent substrate of 5aR.[4] Thus higher levels of this will also inhibit normal production of dihydrotestosterone throughout the body. High levels of 6bOHT will create higher serum levels which interfere with 5aR throughout the body, not just the liver.
(9) 6bOHT is NOT an inhibitor of 5aR. Thus its reduction via 5aR will only take place where T normally produces its metabolites. It will NOT inhibit 5aR conversions of neurosteroids in the brain for example, or stop other 5ar metabolites.
(10) I propose the product of 6bOHT and 5aR is: 6b-hydroxy-5a-dihydrotestosterone, a deactivated version of DHT [5]
(11) I theorise that 6b-hydroxy-5a-dihydrotestosterone is detected in the blood as normal DHT. Due to the fact it is a difficult chemical to determine due to its unique properties (as was found in this paper [5]) and because the normal test for DHT seems insensitive (andractim & proviron also detected as DHT for example[8]). Thus the DHT found in blood tests is a ‘Phantom DHT’.
(12) The result of point (11) is apparantly normal DHT but v. low 3adiolG (lower even than when on fin) due to both T AND DHT being effected.
(13) Blood tests will show inhibition of other 5aR reduced metabolites due to ‘competion’ over 5aR in the liver.
(14) A urinary or blood test to determine the ratio of Hydroxy-Testosterone to Testosterone will discover if this has happened, or prehaps other markers of cyp3a4 induction.[6]
(15) Also…this enzyme, cyp3a4, will also increase metabolism of androgens such as DHEA and Androstendione as well as T (although T is metabolised most).
The body will compensate with LH to create more T & Androstendione from the testes and ACTH to create more DHEA from the adrenals. However, since each are also steps in the steroid pathway, this disruption can lead to altered levels (particularly DHEA as it has only one precursor and comes before Androstendione & T)
A pretty solid theory. Symptoms & Blood tests results match with the theory.
Read more from the MESO-Rx Steroid Forum at: forum.mesomorphosis.com/mens-health-forum/mainstream-media-finally-realizing-134300565-2.html#ixzz1E07JojNg
Its pretty interesting and I wonder if hydroxytestosterone could actually be showing up in tests as DHT… which would change the understanding of what is going on completely. If we are not producing “actual DHT” due to down regulation of 5-AR-2… the protocols for recovery will have to be adjusted accordingly. My urologist has already stated that it is very difficult to increase enzymes… I hope for our sake he is wrong.
I’ve got something that seems to be working consistently… I will post back in two weeks about my progress.
I’ve been running this for the last 10 days:
HMG 75 IU EOD
HCG 2000 IU Twice Weekly
Tamoxifen 5-10 mg ED
(just added) Clomid 25-50 mg ED
Thinking about running HGH, not sure if it will help anything permanently thou.
Gonna go for another 20 days then run clomid and tamoxifen low dose for about 30 days.
So far my morning erections are nearly pre-fin, or 17 year old kid quality.
Sex drive is still not really kicking, thou buprenorphine seems to help when your on it as far as libido, but its an opiate used for addiction treatment and is addictive itself so not really a viable option to use long-term and hard to get.
Brain fog has been considerably reduced, however I still do not feel anything like I used to in terms of thinking capacity and vigor. Sleep has gotten considerably better since using clonazepam, but isn’t what it should be either.
But my mood and depression have been horrendous… I keep thinking about if I don’t get fixed… and I think about how I should have taken advantage of my late teens/early twenties better, slept with more girls, tried to find someone back then (I’m single, about to turn 28 and now live in a place where ppl get married/have kids very young…). I’ve been getting really freaked out, and given the tools of the trade related to my profession, that’s really not good.
Been to 2 more docs. One is a GP who I “had” to go to because the specialists wanted me to have a GP. This guy is nice and fairly intelligent and all, but when I bring up the finasteride as being the main cause of my depression/suicidal thoughts, ED, total loss of libido, sleep and mood issues he looks at me with this almost “yeah ok” look on his face.
Then he talked about me finding god and basically accepting what has happened to me. Kinda got mad at him at this point.
The psychiatrist is just as bad… fails to recognize that finasteride is the cause of any of my symptoms. But gave me wellbutrin and some divalproex (suppose to help me sleep, hasn’t really done anything better than clonzepam)
Oh yeah forgot to mention as soon as I mention I used steroids once 5 1/2 years ago they jump right on that and assume that’s the cause of everything… then he tried to talk me into getting off the HcG/HMG and tamoxifen. I basically told him “no sorry, its the only thing that is somewhat helping me at this point. just because you think I have some sort of drug problem.” the guy doesn’t even know what HcG/HMG really does in males anyway.
So that was pointless. Still waiting on Jacobs to get back to me with bloodwork results:
This time I had 3-Adiol-G, estrogen, DHT, and bio-available testosterone run…
I expect my 3-adiol-g will come back low (especially since my acne is nil right now) I was however taking DHEA when I had the blood drawn so we shall see.
Since I live 2300 miles from all my friends and family I have little support where I am. My father flew down to see me this week cause he knows I’m going through some hard times… its really bad for him to see me in the mental state I’m in right now. I’m trying to set something up with maybe going to the Cleveland Clinic, Mayo or Johns Hopkins I have faith in Jacobs but I really want to try to throw everything at this I can. I am willing to undergo any drug/procedure to fix myself no matter how experimental.
Brain fog + depression spell low neurotransmitters, which spell low pregnenolone. Pregnenolone production (along with cortisol’s) has been downregulated by propecia in many of us. Supplement with enough pregnenolone and you’ll get rid of brain fog and depression without any doubt. Since you are already on clomid, it could even give you your libido back, if you are lucky.
articles.philly.com/2011-03-16/news/28698182_1_finasteride-balding-men-propecia
Get in on this lawsuit!
I took pregnalone a few times, didn’t seem to do much.
If you are taking oral pregnenolone, switch to transdermal (oral doesn’t work). If you are already on transdermal, then you are probably taking too little. How much are you taking? How to dose it is outlined in the link below. In a nutshell, if within 1-2h from taking it you feel “spacey feelings” or yawns, then you are taking too much. If, on the other hand, you still have brain fog after 3-4h from taking it, then it’s definitely too little.
Personally, I found that the dose I need to fill up my pregnenolone reserves is around 150 mg (transdermal). Under 65 mg, I don’t feel a thing. Note that high dosing is an “off label” use, so I think it should be done under the supervision of a doctor.
http://www.musclechatroom.com/forum/content.php?118-cortisol-boost-101 (it’s a sticky post on Dr Crisler’s forum)
It was oral, thanks I will look into this.
New Blood Test Results:
DHT: 35 (25-75)
3-ADIOL-G: 256 (260-1500)
Cortisol: 72.2 (4-50)
Testosterone:
Serum: 811 (250-1100)
Free: 188.8 (46-224)
BIOAVAIL: 445.8 (110-575)
SHBG: 16 (7-49)
Estradiol: 32 (13-54)
IGF 1: 305 (88-374)
Your sex hormones look fantastic – I assume that your prolactin is low as in one of your old tests. They probably look good because your high cortisol downregulates T and DHT metabolism, and therefore your body doesn’t need to crank up E2 or SHBG.
Now, despite good hormones, you feel like crap. In order to wake up your androgen receptors, you need to have also thyroid hormones in the high range (FT4 and FT3). Note, though, that supplementing with thyroid hormones will “consume” some of your cortisol, so you may want to supplement with some pregnenolone not to go too low. But, as a first step, you need to measure FT3, FT4, RT3, TSH (and, possibly, TT3 and TT4).
In theory, you should not be too far from feeling good. Let’s see if the theory works.
Provide some scientific evidence that such a concept exists, please.