I have a diagnosis of ADHD for which I’m currently using methylphenidate, which works almost perfectly. Or to be specific, the instant-release form works well; extended-release formulations have a high chance of either not helping much (lower doses) or making me all jittery or causing a state most concisely described as “stimulant autism”, a hyperfocus on some random thing that might or might not be completely useless (higher doses). I also have a prescription for diazepam which originally was intended to alleviate phobia-ish things related to some medical procedures, but which has had the surprising side effect of turning me to a honest-to-azathoth superhero when a mild dose of sedatives is combined with a stronger than normal dose of stimulants.
These two things had my doctors utterly baffled and they couldn’t provide much of an explanation for them, other than trying pregabalin as a non-addictive anxiolytic which didn’t have the desired effect. And my doctors weren’t even particularly mediocre ones, they gave me a modafinil prescription and everything. On the other hand they also told me to try atypical antipsychotics for sleep which had the predictable effects so they clearly aren’t the brightest pencils in the drawer either.
Now fast-forward to my 23andme results, or more accurately to the SNPedia interpretation of them. I wasn’t expecting to pay too much attention to the individual genes but the effects of one particular stood out dramatically: rs4680(A;A) which, when one takes away the layers of media sensationalization and bullshit, basically means that my dopamine system is sensitive to overdoses which can significantly reduce cognitive functioning.
And this fits the above data way more strongly than would be expected by mere confirmation bias: XR methylphenidate doesn’t allow rapid adjustment of dosing based on immediate need which causes disastrous results with an inherently unstable neurochemistry, but IR can be dosed to avoid both over- and underdoses. The paradoxical effect of faster-acting anxiolytics matches the claims that A;A carriers are likely to be more suspectible to stress-related reduction in performance. Subjectively it seems to take the “edge” off larger doses of methylphenidate, removing the typical side effects of high doses while maintaining the benefits. Without sedatives I’m suspectible to a phenomenon where high levels of stress inevitably lead to a situation where the only choices I have are to be either comparably useless because I’m not taking stimulants, or comparably useless and also very jittery because I’m taking stimulants and environmental effects are turning any dose into an overdose.
So what I’d like to know is, is there any way to rapidly tune my brain “down” without excessive risks or side effects, in the same way methylphenidate tunes my brain “up”, to allow near-instant optimization of neurotransmitter levels etc. to match situational need because my brain emprically needs tuning on the fly, not every few months in the doctor’s office.
For legal reasons it’s okay to limit the advice to “you might want to talk about X to your doctor”, as I’m already planning to use my next appointment to discuss the need to do basic due diligence so I don’t have to do their job for them, such as “finding out before you prescribe drugs whether your patient is relatively likely to be immune to the things you’re throwing at them, or alternatively such a slow metabolizer that the things are going to stay in the system forever and ever”, and it would be convenient to have something that could be actually useful to point them towards; but I’d also like to hear about the interesting stuff if possible.
4 months ago · 1 note · .permalink
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