| > https://www.frontiersin.org/articles/10.3389/fsoc.2022.81476... Written by an elementary education specialist and an unknown lecturer. No medical value. > https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626918/ A very nice summarization paper on ADHD. You do not seem to have read the summary at the end, as it does not support your points of argument. It primarily suggests a wider approach using additional medication, as well as DNA based diagnosis and treatment. The latter does not seem to be available yet. > https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2011.1... This suggests the brain adapts to long-term medication with methylphenidate, but does not go as far as establishing a causal relationship, or show that the dopamine transporter alterations are to the detriment of the patient. In fact, this meta-study seems to be a contribution to the field of establishing the origins of ADHD; its argument is that these dopamine transporter changes may not be useful in understanding ADHD as they are caused by the treatment. However, there's this: "It is, however, also possible that lower dopamine transporter density and lower dopamine release in medication-naive ADHD patients reflect prefrontal pathology, well demonstrated in neuroimaging results for ADHD (5), since frontostriatal glutamatergic circuits regulate striatal dopamine release." It's hinting at a possibility that, in reverse, the unmedicated state without the long-term effects may be a key contributor to ADHD itself. > https://pubmed.ncbi.nlm.nih.gov/25066615/ This discusses distinctions between ADHD diagnostic criteria in DSM-IV vs. DSM-5. The ones in DSM-5 cast a wider net than DSM-IV. The study comes to the conclusion that the net is still not wide enough, particularly in adults. I don't know why you believe this paper supports any of your points. |
Assistant professor, lecturer, reviewed by post doc. It's an article that summarizes stuff nicely referencing papers.
> but does not go as far as establishing a causal relationship
I love how the attitude is: here is a drug that you would think would cause side-effects and tolerance...which is does...and then the onus is on everyone to conclusively prove that it's bad. Smoke until we realize it causes cancer. Take opiates until we realize they are extremely addictive in certain packaging.
It's very much carefree experimentation on the world, rather than being risk-averse and acknowledging what we don't know.
It is common sense that the body will seek homeostasis to deal with this artificially increased dopamine levels. Which this study seems to indicate.
But it comes down to risk-appetite.
> DSM-IV vs. DSM-5.
We changed the diagnosis criteria and got: surprise, 27% increase in expected prevalence. How convenient.
The diagnosis criteria are just made up. The cause is not proven at all. There is no biomarker or imagery that can diagnose the condition successfully.
So patients present with an impairment...then you look at who has the impairment and craft the criteria such that it explains the impairment. Its a circular definition and extremely broad.