Posted by TH on April 12, 2019, at 16:17:42
In reply to Re: Tranylcypromine Tachyphylaxis, posted by Christ_empowered on April 12, 2019, at 10:29:03
Thank you for your reply.
I can see the potential value in augnenting with a stimulant (methylphenidate seems to be the most appropriate), however I would certainly still have some reservations about the strategy.
I would be worried that if down-regulation of receptors is the cause of ADT tachyphylaxis, that adding extra dopamine may only exacerbate the problem.
In addition, going in search of a stimulant prescription is no easy task, and a good way to get yourself labeled as a drug-seeker. To prevent abuse, our medical system only allows such a prescription can only be made by a qualified specialist, and only with a diagnosis of ADHD or narcolepsy. While I do have a friend who had been prescribed methylphenidate off-label for a mood disorder, and it did appear to help, it was only prescribed having exhausted all other options.
Having already been prescribed atypical psychotics, I do not see any further value in attempting to augment with them. In regards to "Californian rocket fuel", I had previously spent quite a period on a similar combination already with no positive effect.
The idea of adding lithium is possibly worth exploring, I have seen it suggested that any value as an augmenting agent should be apparent within four weeks, else it would be wise to discontinue. At the very least, this fixed time period makes it a more attractive option. I had also seen suggestions of using lamotrigine in a similar manner.
Another set of very unproven suggestions seem to target the glutamate system. Anecdotally I have read of sarcosine being useful as an augmenting agent, as well as memantine being used specifically in the hopes of preventing ADT tachyphylaxis. As best I can understand, this theory suggests that glutemic overactivation of the dorsal raphe causes down-regulation of other receptors. Another unrelated suggestion involved using kappa opioid agonists regularly to induce down-regulation of that receptor, as kappa opioid activation is believed to cause dopamine receptor down-regulation. Does anything have any input on any of these theories?
I would be inclined to first try blindly increasing my dose of tranylcypromine to 40mg daily in the hope that a solution could be that simple, but is this overly naïve?
poster:TH
thread:1103943
URL: http://www.dr-bob.org/babble/20190206/msgs/1103949.html