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.