I suppose it wouldn’t hurt… but I’ve done numerous diets over the years since I was 18 and its just my personal opinion that a change in eating habits won’t effect hormone metabolism to a great degree.
Depends on the root problem, ultimately.
Looks like I am having one of those “recovery” phases tonight… everything seems to be firing good right now (70%) mentally and sexually. Too bad the girl I’ve been talking to is 45 mins away working right now.
Hopefully it lasts a little while thou I know how short these recovery phases usually are.
“If you subtract the placebo group, 3% to 4% of patients may have some sexual side effects, and they go away when you stop the drug,” says Patrick Walsh, MD, the University Distinguished Service Professor of Urology at Johns Hopkins in Baltimore, who also reviews studies for the journal Urology. “This is bizarre.”
“I’ve never seen a patient who had sexual side effects and when he stopped them he was impotent forever,” says Walsh.
From this article:
men.webmd.com/news/20110309/sexual-side-effects-of-hair-loss-drugs-persist?page=2
I sent him a email regarding the his comments and offered for him that I come out to JHU so he can “study” my case. I sent it from my work email so hopefully that provides a little bit more levity to my words. (I am a federal government official)
And his reponse…
“Ask Merck - do you know what your blood levels were before you took the drug. I believe that you have problems but the placebo effect can be very strong. Merck should have the answer. Thanks for contacting me.”
And my rebuttal:
"Dr. Walsh;
No, I do not know what they were. All I know is I was a normal 22 year old before I took this stuff. I could get erections without difficulty and had a sex drive. There is no placebo effect in my case I didn’t even know there were any side effects when I started the drug because my doctor did not inform me of any. Merck doesn’t have the answer, I already contacted them months ago about this. I have the 3-Adiol-G levels of a HERMAPHRODITE yet I was born and developed naturally as a male. What explanation could they have for this… I doubt they know of any way to fix it either or else there wouldn’t be thousands of us on propeciahelp.com with the same problem still."
More from the doctor:
“If you had a problem with 5 alpha reductase your DHT would be low - it is not - you have a normal hypothalamic pituitary testicular axis and normal 5 alpha reductase activity. Your medical problem is arising from something else.”
And my response:
"Well the mayo clinic says 3adiolg is a marker for 5ar2. So I guess its their info that is wrong.
3adiolg 256 (260-1500)"
That proves everything IMO.
He doesn’t even know what he’s talking about.
How fucked is this world when self-professed experts aren’t even tuned in?
Your response could have been better mate. 3-ADIOL-G is the primary intercellular marker of 5ARII, it being a metabolite of DHT. Serum DHT means relatively little if it’s not being metabolised correctly.
What a douche.
Accutane but it appears the same thing happened to us… is this caused by the lack of circulating DHT?
J Clin Endocrinol Metab 1995 Apr;80(4):1158-61
Effect of oral isotretinoin treatment on skin androgen receptor levels in male acneic patients.
Boudou P, Soliman H, Chivot M, Villette JM, Vexiau P, Belanger A, Fiet J.
Department of Hormonal Biology, St. Louis University Hospital, Paris, France.
An oral daily dose (mean /- SD, 0.75 /- 0.05 mg/kg) of isotretinoin was administered for 3 months to six male patients with acne (scores of 4 and 5 according to Rosenfield). The therapy resulted in complete resolution of acne in four patients and improved acne significantly (score 1) in two patients. In accordance with recent findings, no change in serum testosterone and significant decreases in 5 alpha-dihydrotestosterone, 5 alpha-androstane-3 alpha,17 beta-diol glucosiduronate, and androsterone glucosiduronate levels were observed after treatment. Androgen receptor status was investigated in back skin biopsies obtained in acne areas before and after 3 months of isotretinoin treatment. The treatment did not modify the binding affinity constant of skin androgen receptor (0.44 vs. 0.32 nmol/L), but it did induce a 2.6-fold decrease in its binding capacity constant (62 vs. 24 fmol/mg cytosolic protein), as assessed by Scatchard plot and confirmed immunologically by Western blot analysis. These data clearly showed that skin androgen receptor was sensitive to oral isotretinoin administration in acneic patients. The decrease in skin androgen receptor levels (this study) and the recently reported suppression of skin 5 alpha-dihydrotestosterone production by isotretinoin treatment appeared consistent with the involvement of androgen receptor and 5 alpha-dihydrotestosterone in the pathogenesis of acne. Indeed, sebum production is under androgen control, and an abnormal response of the pilosebaceous unit to androgens appears to be implicated in the pathogenesis of acne. These observations were consistent with the absence of sebum in complete androgen-insensitive patients and normal sebum production in male pseudohermaphrodites.
Yes it could have been better I sent a reply with a better explanation.
But this is what we have to do, attack the nay-sayers with proof. Don’t be afraid to challenge them on the grounds that they are wrong. These people are walking around as if we don’t exist.
If everyone on earth used finasteride this problem would be no mystery because we’d probably have a 100 million people around with it.
In fact I suggest we start mass emailing endocrinologists, derm’s, urologists, and even general prac’s with this information. Especially now with Merck adding “erectile dysfunction that continues after discontinuation of the drug” to its side effect list. They need to pull this drug from the market for anything less than severe prostate issues.
Surprise, surprise… his responses have ceased to flow in.
I just want to get a quote from him discrediting Mayo’s description of what 3-Adiol-G is measure of.
Oh and here’s his email in case anyone else wants to shoot him some more information.
Yes, I remember reading Walsh’s response in that piece. What an ass. I’ll email him as well.
The sort of things he says are pretty frightening considering he’s at Johns Hopkins.
How about asking him why Sweden and England both recognize permenant sexual dysfunction or the Irwig study.
Ok, Jacobs thinks I may have cushings syndrome because on my Dexamethasone Supression test my cortisol remained high along with my ACTH.
So I’m getting an MRI in the next few days.
i agree… I ask Jacobs about my low 3adiolg all the time but he doesn’t usually spend much time talking about it. Perhaps they don’t consider 3adiolg to be very important…
No we dont.
I see both Shippen and Jacobs. Jacobs seemed interested in 3 adiol G (obviously since he orders the lab for all of us) while Shippen just said its nice to have but of little consequence.
“Of little consequence” only means he doesn’t know what to do with it.
I have read that boosting free testosterone levels can help 3-adiol-G levels for example.
I think it’s good to have, at very least for comparative purposes futher down the line (when we are, hopefully, feeling better!!)
3-Adiol-G went up to 442 (260-1500) from 256. 1.5 months between tests. Do I feel much better? Not substantially.
I’ve taken so much “stuff” its difficult to tell what may have caused this… However I am still taking my tribulus supplements.
So more then 4 months off now.
Still have ZERO libido, I can get erections with manual stimulation and the erections are about 75-85%… Cialis helps some but I am still avoiding female contact… thou I’ve met a few recently and I am not sure about proceeding with them in this state.
Sleep has gotten somewhat better.
But at the rate my sides are improving I should be healed in about 15 years.
Thinking back to how I used to be… it is deeply heart breaking. To think that if it wasn’t for a few dumb decisions about putting this drug into my body my life world be entirely different right now…