> And, as with nearsightedness, it's readily apparent to those who use the prosthetic that they were impaired, because they now have access to experiences that they may have heard unimpaired people speaking of, but never previously got to experience for themselves.
The human body requires its internal chemicals to be maintained within certain ranges for various features to function. Each of these features is relevant to what would be called "the human experience"--things that are built into the generalized human utility-function to want, as terminal values.
When you have a neurotransmitter imbalance to a degree that it becomes an impairment, it is so because it disables some of these features, and therefore bars one's access to these terminal values.
In AD(H)D, the feature that gets impaired is the "sense of intrinsic motivation" generated by the dopamine system. The terminal values one loses access to are the feelings of striving, accomplishment, or pride in one's work; and, in more extreme cases, the feeling to hope that one will be able to improve one's lot in life by one's own hand. (When you know you can't motivate yourself to get a job, being jobless is a lot more depressing.)
When you apply the appropriate prosthetic to the impairment--combined dopamine agonist/reuptake inhibitors, in this case--you gain access to this feature, and through it, the terminal values you were barred from.
As with putting on glasses, if you have the impairment (everything is blurry), then it is very, very obvious that when everything comes into focus, that this is the way things were "meant" to be--not from some moral imperative, but just because the rest of your body was built to rely on this feature that was previously broken.
With glasses, this means you suddenly stop bumping into things, and don't find yourself moving closer to people to see them. With normalized dopamine levels, this means you suddenly feel able to make yourself accomplish things you've always wanted to accomplish.
If your dopamine is set to the correct range for your body, this doesn't "make you into a robot" or any of the things people talk about with various neuroaffective drugs. Inasmuch as that was ever true in clinical settings, it was from failure to identify the neurotransmitter which is in imbalance (i.e. treating a norepinephrine production deficiency with dopamine agonists).
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And now, a rant:
Inasmuch as AD(H)D treatment is made out to be a problem in pop-culture, though, it does indeed come from "overdiagnosis"--if you give a drug to boost a neurotransmitter into a reference range to someone who is not impaired, you will of course boost that neurotransmitter out of the reference range it was already in. People who can see fine already will find glasses quite harmful to their vision.
"Overdiagnosis" is a very strong word for what happens with AD(H)D, though. Population studies have been done, with random samples of adults brought in off the street given strict evaluations to test for AD(H)D--and as much as 3% of the population has scored far into the "impaired" range. (This is, coincidentally-enough, about the same percentage we see for all the other neurotransmitter-reference-range problems, e.g. clinical depression, giving merit to the genetic-drift hypothesis.) This number is far higher than the number of people actually diagnosed with AD(H)D. The stigma behind "overdiagnosis" has lead to underdiagnosis.
The real problem, of course, is parents wanting to treat their children for neurotransmitter imbalances at all. Children do not have stable neurotransmitter reference ranges. Their brains produce random spurts of neurotransmitters at random times, just like their bodies produce random spurts of growth in random body parts. (This is why children have such vivid nightmares and fantasies: random spurts of serotonin will induce visual and auditory hallucinations, much as are found during an LSD trip; coupled with random spurts of adrenaline, these hallucinations can be quite stressful. It is also why they may not "feel tired" after being awake for many hours: due to random spurts of acetylcholine, their bodies can be effectively self-caffeinating. You can surmise how this applies to each other neurotransmitter as well.)
AD(H)D is not a "childhood disease", any more than nearsightedness is. Both impairments tend to first reveal themselves, oddly-enough, when one is first asked in childhood to sit and stare at a blackboard--but this doesn't imply that the problem goes away when the blackboard does. In fact, it usually gets worse--but there is no longer a set of parents being sent report cards to indicate a problem which they might get it into their heads to "fix."
So, when I say "get checked for AD(H)D," I'm intending that advice for adults. Children might certainly have AD(H)D already--if you have a neurotransmitter imbalance, it's almost always present from a very young age--but the rampage of random neurotransmitter releases during development will moot any sort of prosthetic, just like (no, not glasses this time!) a bone- or skull-plate to fix a break would be inadvisable for a child: their bones haven't finished growing or forming, and the plate would soon harm instead of help.
Having said that, school systems must be designed around the fact that children will have various neurochemical imbalances--whether temporarily due to growth, or permanently, due to genetic problems--and around the fact that it is improper to expect the child to be treated for these before their neurology stabilizes. Grade-school must be an environment where a child is given the resources to succeed despite neurochemical imbalances. This calls for a radical restructuring, much moreso than the "radical" ideas one sees proffered on education around HN.
