Although it seems unrelated to the forum, I made this thread to show that the use of accutane has the potential to negatively influence brain metabolism and size. I have taken roche accutane twice, both for three month periods, at doses ranging from 40-100mgs a day, both times under doctor's supervision years ago before I was aware of any side-effects other than those commonly cited (chapped lips and birth defects).
3 months after the last treatment, I began to experience significant symptoms of depression for the first time in my life. I honestly have no idea if the accutane caused effects which are making me feel the way I do now, but given the growing number of cases that aren't unlike mine, I don't think the association is unfounded.
Some important things to take into consideration: I have a family history of major depression.
I have experienced no other "side-effects" that people report during/post accutane (ie dry skin, anger, sleep problems).
I would like to influence any person who is considering accutane; they should be aware that there are thousands (probably) of people who regret using it. I CERTAINLY regret ever using accutane, despite my uncertainties about its role in my case of depression.
These studies are mice and use doses that are rather high, but the first shows striking results. Does anyone have any recommendations for my case? I thought I would run it by some brainiacs here who might think of interventions given what was learned through these studies. SSRI's and talk therapy have not helped with my depression, indeed SSRI's made me excessively tired/sleepy only.
Program No. 114.2. 2004 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience, 2004. Online. J.D. Bremner, N. Fani, N. Ashraf, J. Votaw, M. Brummer, V. Vaccarino, M. Goodman, L. Reed, C.B. Nemeroff. FUNCTIONAL BRAIN IMAGING ALTERATIONS IN ACNE PATIENTS TREATED WITH ISOTRETINOIN Although there have been case reports suggesting a relationship between treatment with the acne medication isotretinoin (Accutane) 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 no studies to date have examined the effects of isotretinoin on brain function in acne patients. The purpose of this study was to assess the effects of isotretinoin on brain function in acne patients. Brain function was measured with [F-18]-2-fluoro-2-deoxyglucose (FDG) positron emission tomography (PET) before and after four months of treatment with isotretinoin (N=13) and antibiotic (N=15). Isotretinoin (but not antibiotic) treatment was associated with decreased brain metabolism in the orbitofrontal cortex (-21% change versus a +2% change for antibiotic) (p<0.05), a brain area known to mediate symptoms of depression. There were no differences in severity of depressive symptoms between the isotretinoin and antibiotic treatment groups before or after treatment. This study suggests that isotretinoin treatment is associated with changes in brain function.
Program No. 437.15. 2004 Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience, 2004. Online. S.A. Ferguson, F.J. Cisneros, J.P. Hanig, B. Gough, K.J. Berry. CHRONIC ORAL ACCUTANE (ACC), BUT NOT ALL-TRANS-RETINOIC ACID (ATRA), TREATMENT CAUSES BEHAVIORAL ALTERATIONS IN THE FORCED SWIM TEST The anti-acne drug, ACC (isotretinoin, 13-cis-retinoic acid), is associated with depression, suicide ideation and suicide. The potential confounds inherent in human research necessitated the current animal study. Here, male and female Sprague-Dawley rats (n=6/sex/dose) were gavaged with 0 (soy oil), 7.5, or 22.5 mg/kg/day ACC beginning on postnatal day 82. Previous work indicates that 7.5 mg/kg produces blood ACC levels similar to those of humans taking recommended ACC doses (1 mg/kg/day). As a comparison for in vivo isomerization of ACC, separate groups of rats were gavaged with 10 or 15 mg/kg/day ATRA (n=6/sex/dose). After 7 weeks of chronic treatment, a forced swim test was conducted on two consecutive days. Each rat was placed in an inescapable cylindrical tank of 25oC water for 10 (day 1) or 5 (day 2) min. Tests began ~ 1 hour post-gavage. Dive frequency and durations of active swimming, immobility (including floating), and climbing/struggling were measured. Neither ACC nor ATRA altered diving or swim durations. ATRA treatment had no effect on any other measured behavior. However, rats treated with 7.5 mg/kg ACC engaged in longer durations of climbing/struggling and shorter durations of immobility than controls (p<.05). This ACC treatment effect did not interact with test session (day) or sex, although there were significant main effects of session and sex, and the effect was not caused by alterations in locomotor activity (see accompanying abstract for lack of open field activity changes). In general, short immobility and long climb/struggle durations are indications of decreased depression (i.e., antidepressant treatment shortens immobility time). Thus, ACC doses which produce blood levels similar to humans cause behavioral alterations in a rodent assessment designed to assess depression.
Ann N Y Acad Sci. Sakai Y, Crandall JE, Brodsky J, McCaffery P. 13-cis Retinoic acid (accutane) suppresses hippocampal cell survival in mice. 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.
