ADHS-Medikamente im Kindesalter können das Psychoserisiko verringern. Bei Kindern, die vor dem 13. Lebensjahr mit Methylphenidat behandelt wurden, war die Wahrscheinlichkeit geringer, dass sie im Erwachsenenalter Erkrankungen wie Schizophrenie entwickelten. Die Ergebnisse widerlegen langjährige Bedenken, dass Stimulanzien das Risiko einer Psychose erhöhen könnten.
https://www.ed.ac.uk/news/childhood-adhd-medication-may-reduce-psychosis-risk
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Childhood ADHD medication may reduce psychosis risk
Commonly prescribed medication for attention deficit hyperactivity disorder (ADHD) could lower the risk of developing serious psychotic disorders later in life, new research suggests.
Experts found that children treated with methylphenidate before the age of 13 were less likely to go on to develop conditions such as schizophrenia in adulthood.
The findings challenge long-standing concerns that stimulant medications may increase the risk of psychosis, experts say
For those interested, here’s the link to the peer reviewed journal article:
https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2846833
Very interesting. I wonder how much could be related to mediating substance use in adolescence and early adulthood particularly cannabis and stimulants.
This is kinda funny to me because when I was a kid they put me on dexedrine (a different ADHD med) and it made me stay up to 3 AM plotting world domination with space lasers. I still have the notebooks, it reads like something out of seven meets pepe silva.
My mom immediately took me off of it.
Be warned, what I’m about to say is entirely anecdotal and not to be taken as evidence to substantiate any true claim. The point of saying it is just to express a personal experience.
A big part of ADHD, for me, is constantly forgetting things. Important things, unimportant things – a myriad and unknowable mixture of the two. When I forget a major thing, it really harps on my consideration of my own mental competence. “Did I just go on a red light? Did I leave a space heater on? Did I remember to add X reagent to my reaction?” This constant second-guessing creates a feedback loop of panic. Unless I am itemizing and crossing out lists, I will forget. I will make small and large mistakes. When I take Vyvanse, I have a bit of a trade-off. I’m less inventive with my synthesis reaction mechanisms in my organic chemistry class, but I do not make small and large mistakes in lab settings. The lack of mistakes makes lab work a breeze, which helps restore my consideration of my mental acuity.
I think that there may be epigenetic causality to schizophrenia, though I’m unfamiliar with the research and only propose this as a hypothesis (among submitting to a myriad of other circumstance). I think what stimulants do is reduce certain epigenetic agents, which in my opinion would be being reflexively uncertain of one’s prior actions, which I believe ADHD patients often experience.
As someone with bipolar disorder and ADHD I really find present models of how to manage the condition through medications to be really reductionist. (Hold your horses, this is not an antipsychiatry take)
I feel that the underlying internal process really needs a dynamical systems kind of approach. Problem is that you can’t really measure any of the neurotransmitters and the resulting activation and reuptake in the long run time series way needed for this data collection. We’d need a brain equivalent of a holter monitor.
For what it’s worth, here’s another sample: I exited my worst SI crisis after being put on a small dose of methylphenidate(apart from my usual industrial strength stabilizers). What was expected was the requisite elevation of mood to baseline. Unexpected — I am way more stable since then. This runs contrary to the idea that stimulants as a whole are destabilizing at all doses.
My hypothesis: let’s call „A“ the latent variable which when excessively high corresponds to mania/psychosis and when excessively low corresponds to depression.
If „A“ is just right, both healthy and dyregulated brains are fine.
If „A“ is too low, dysregulated brains may struggle to control it. There may be both lag and overshoot — the level of „A“ going too high, precisely because it was too low, and the underlying system has too much inertia and cannot easily compensate.
The small dose of methylphenidate brings the baseline value of „A“ closer to optimum, reducing the need for the system to push aggressively on A.
PS: Please tell me if the above sounds a little „out there“ or worse, unhinged.