Isotretinoin, tetracycline and circulating hormones in acne.
Palatsi R, Ruokonen A, Oikarinen A. Source: Department of Dermatology, University Central Hospital, Oulu, Finland.
Isotretinoin, used to treat severe acne, has been shown to induce hormonal changes, especially to reduce 5 alpha-reductase in the production of the tissue-derived dihydrotestosterone (DHT) metabolite 3 alpha-Adiol G. However, the effects of isotretinoin on other pituitary, adrenal or gonadal hormones have not been thoroughly elucidated. In the present study, isotretinoin administered at a dose of 0.5 mg/kg/day for 4 weeks caused no marked changes in the serum levels of pituitary, adrenal or gonadal hormones or 3 alpha-Adiol G in patients with severe papulopustulotic acne (n = 19). After 12 weeks of therapy, there was a decrease in the levels of the precursor androgens androstenedione, testosterone and 3 alpha-Adiol G in 6/9 patients. Acne improved after 4.5 months in all but 2 male patients, who had very low serum hormone binding globulins (SHBG) and a high free androgen index (FAI). Isotretinoin did not affect the elevated LH/FSH ratio in a patient with the polycystic ovarian syndrome (PCOS); nor did it change the high FAI or low SHBG in the male patients. For comparison, tetracycline had no effects on the serum hormonal levels of patients with mild acne (n = 19) after 7 days of treatment. This study confirms that the effects of isotretinoin on the serum hormone levels are small and unlikely to be of relevance for the resolution of acne or the suppression of sebum excretion.
Functional brain imaging alterations in acne patients treated with isotretinoin.
Bremner JD, Fani N, Ashraf A, Votaw JR, Brummer ME, Cummins T, Vaccarino V, Goodman MM, Reed L, Siddiq S, Nemeroff CB.
Department of Psychiatry and Behavioral Sciences, Emory Center for Positron Emission Tomography, Emory University School of Medicine, Atlanta, GA, USA. email@example.com
Am J Psychiatry. 2008 Dec;165(12):1614.
Although there have been case reports suggesting a relationship between treatment with the acne medication isotretinoin and the development of depression and suicide, this topic remains controversial. In order for isotretinoin to cause depression, it must have an effect on the brain; however, the effects of isotretinoin on brain functioning in acne patients have not been established. The purpose of this study was to assess the effects of isotretinoin on brain functioning in acne patients.
Brain functioning in adults was measured with [(18)F]fluorodeoxyglucose positron emission tomography before and after 4 months of treatment with isotretinoin (N=13) or an antibiotic (N=15).
Isotretinoin but not antibiotic treatment was associated with decreased brain metabolism in the orbitofrontal cortex (-21% change versus 2% change for antibiotic), a brain area known to mediate symptoms of depression. There were no differences in the severity of depressive symptoms between the isotretinoin and antibiotic treatment groups before or after treatment.
CONCLUSIONS: This study suggests that isotretinoin treatment is associated with changes in brain functioning.
13-cis Retinoic acid (accutane) suppresses hippocampal cell survival in mice.
Sakai Y, Crandall JE, Brodsky J, McCaffery P. Source: UMMS/E.K. Shriver Center, 200 Trapelo Rd., Waltham, MA 02452, USA.
Use of the acne drug Accutane (13-cis retinoic acid, [13-cis RA]) has been associated with severe depression. This association has been considered controversial because no causative link has been found between 13-cis RA and this disorder. A recent hypothesis has suggested that atrophy of the hippocampus can result in depression. We now show, in a mouse model, that endogenous RA generated by synthetic enzymes in the meninges acts on hippocampal granule neurons, and chronic (3-week) exposure to a clinical dose of 13-cis RA may result in hippocampal cell loss. In humans this may be conjectured to be the mechanism by which Accutane contributes to depression.
So essentially, for those of you who actually take the time to read the papers I post, Accutane has a very similar anti-androgenic effect on the brain as Finasteride. I’m betting our fMRIs will look very similar to the ones in that paper I posted. Possibly even worse as they don’t really emphasize sexual decimation. So, it could be that Finasteride has really damaged parts of our brain, similar to how Accutane does.
Btw, I remember reading an article about how a study showing brain damage via PET scan (somewhat similar to fMRI) was used in court against Roche (maker of Accutane) and Roche still one the case. Here is an article about Merck, which is much much more powerful than Roche: theconversation.com/the-most-pow … merck-3187 .
I know its early and we’ve yet to see the fMRI results. But if we have the same brain damage, what do we do?
Also, the “depression” mentioned in many of these studies could also include sexual dysfunction. It could just be that they left it out because of the resistance of doctors and scientists to believe that medication can cause such long lasting side effects.
Well here is the problem, if it was actual brain damage, and not some imbalance. How do we explain how some people would get to be , let’s say subjectively feeling 90% better? Some claim COMPLETE reversal of the veins in the penis and shrunken penis as well. So clearly, unless these people are lying, this condition by some means is reversible or highly treatable. I Also am not the same as I was a year ago, I don’t have testicle pain anymore, I am getting more sensitivity back, I have more sexual thoughts and am able to fantasize about sex. If this was true brain damage I’m not sure how these improvements would have happened.
I’m no expert but I believe if brain cells are destroyed then other parts of the brain can replace those cells. Stroke victims have to re learn stuff they could already do such as speaking etc. As I understand it you can never recover 100% after brain damage. Mentally I have recovered about 90% but I’m slower than I use to be and can not feel much emotion it does feel like part of brain has been destroyed.
The ability of the brain to repair itself may depend on how severe the brain damage is in the first place. Maybe the brain can repair itself partially, but maybe you can help it repair itself. The shitty thing though is that I think the hippocampus is the part of the brain that signals brain repair. So if you damage the hippocampus maybe your fucked. The cannabis oil is interesting. Also, maybe more people should try cerebrolysin for longer.
One thing I want to say and I hope many people see is this: YOU CANNOT EXPECT TO RECOVER BY TRYING SOMETHING A FEW TIMES. Some people took finasteride for years (I think Finatruth said he took it for 9 years) before they developed PFS. You may need to try something for a while or try a megadose. I bet if you took 10 mg or even 1 mg finastider with a compound that will help it penetrate the BBB, then you’ll get PFS.
dgreene- yeah but my crash after 9 years parallels many peoples crash after 1 pill, so I think time has nothing to do with it. Almost seems at some point there is an imbalance that occurs and then boom!
Errr…I attempted to raise a similar issue the other day and you shot me down. Although, I began my point by arguing the polar opposite: What if our scans show normal activity?
Anyway, I think it’s worth noting that Isotretinoin is a chemo drug, which can induce post-chemo cognitive impairment (aka “chemo brain”). Perhaps the findings in the second post are akin to recent chemo brain studies. Although quite how this phenomenon occurs, is not yet known.
I personally think that Isotretinoin has the potential to do more damage than Fin, but that’s all relative.
Scattered among the many drug forums on the web, are personal accounts from Accutane sufferers who report normal brain activity from PET and CT scans. Others claim to have discovered abnormalities upon seeking a second opinion. There does not seem to be any collective concrete findings.
They claim that this accounts for the “depression”. I’m wondering though if its whats actually causing the sexual dysfunction as well. I wonder if Dr. Bhasin has seen these. They must suspect something since their ordering fMRIs…
I mean, 12 months ago i really thought I had brain damage, when I crashed I was confused, couldn’t remember simple tasks, forgot passwords, would go to work without my contacts in my eyes and wonder why I couldn’t see etc. it was horrible, as time went on I suffered bad name recall and word association but that’s improving every month! In fact I was so fluid the other day with my thoughts and didn’t once pause to try to come up with the right word.
I am still more convinced then ever that our problems stem from too much estrogen
(Or estradiol for us) in the brain. I am thinking that I’d there is nothing to counter the estrogen in our bodies than it wouldn’t matter if we had high or low levels of estrogen, it could simply be un-opposed estrogen