Articles about ADHD drugs are fine talking about success, work, competition, and advancement, but try finding one that calls the drug by its name: Speed.
There is a reason front groups like CHADD and ADDA focus on “the science of ADHD,” which is not hard science, and ignore the science of the drugs used to treat it, which is hard science.
A cheap and limitless supply of pharma-grade amphetamine, signed off by a friendly medical professional, struck me as an incredibly unwise pursuit. That’s how you become a heavy or daily user.
But it’s been a long time since I bought the stuff [meth/adderall]. I now stick to the weak classical highs of coffee and tea, which can honestly and without obfuscation be described as harmless stimulants.
Don't kid yourself, if you're taking ADD meds, you're using speed. Probably using it responsibly, but you're still taking speed. There's nothing magical about your brain that makes it affect you differently from everyone else.
It's Different for Girls with ADHD
Past research has suggested that children with ADHD are at higher risk of obesity than those without the disorder. Now, new research from the Johns Hopkins Bloomberg School of Public Health in Baltimore, MD, suggests that this increased risk may be a result of ADHD treatment, rather that the disorder itself.
Stimulant use 'leads to rapid BMI growth later in adolescence'
Both amphetamine and methamphetamine are potent CNS stimulants with a few biomolecular targets and affected transporters in common; however, there are important pharmacodynamic differences between the two compounds.[Refnote 2] Both compounds are potent trace amine-associated receptor 1 (TAAR1) agonists (causing non-competitive inhibition of DAT, NET, and SERT) and inhibitors of VMAT2, SLC22A3, and SLC22A5.[Refnote 3] However, methamphetamine appears to bind at a different site at VMAT2 than amphetamine. Methamphetamine also inhibits VMAT1, has agonist activity at all alpha-2 adrenergic receptor and sigma receptor subtypes, and is directly toxic to dopamine neurons in humans, whereas there is no evidence of acute amphetamine toxicity in humans. Sigma receptor activity is known to potentiate the stimulant and neurotoxic effects of methamphetamine.
When taken orally, 30–54% of the dose is excreted in urine as methamphetamine and 10–23% as amphetamine. Following IV doses, about 45% is excreted as methamphetamine and 7% as amphetamine. The half-life of methamphetamine is variable with a mean value of between 5–12 hours.
Unlike amphetamine, methamphetamine is neurotoxic to humans, damaging both dopamine and serotonin neurons in the CNS.[i] Contrary to the long-term use of amphetamine,[iii] there is evidence that methamphetamine causes brain damage from long-term use in humans;[ii] this damage includes adverse changes in brain structure and function, such as reductions in gray matter volume in several brain regions and adverse changes in markers of metabolic integrity.[ii]
At normal urine pH, the half-lives of dextroamphetamine and levoamphetamine are 9–11 hours and 11–14 hours, respectively
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