And another one from CFC.
Personally, I think these are just general metabolic benefit, not specifically for meth use, and I'm skeptical of more than a few, but the question comes up a lot. I know that vitamin D has been shown to specifically protect brain cells from specifically meth-induced damage.
FROM CFC, who was referring to methamphetamine users:
supplements that may or may not (depending on how you interpret a hundred different in vivo, in vitro, rodent, primate, human or cell culture studies) be of benefit, besides vitamin D, in some sort of descending order of usefulness off the top of my head might include:
Taurine (cheap, helps cells everywhere by stabilising their membranes, tenuous potential GABAa agonism)
Vitamin E (the principle lipophilic antioxidant)
Vitamin C (the principle hydrophilic antioxidant, synergises with E somewhat)
Aspirin (COX inhibitor to reduce inflammatory harms including potentially MPTP, lessen risk of clots, strokes and heart attacks; sometimes NSAIDs aggravate heart though)
Selenium (comes up in several studies)
Acetyl-l-carnitine (to aid energy metabolism)
N-acetylcysteine (important glutathione precursor, especially helpful for liver, also potentially stymie development of arterial fibrosis from stimulants)
Creatine monohydrate (energy metabolism/helps myocytes in the heart particularly, but may raise BP/HR in consequence)
Alpha-lipoic acid (also aids energy metabolism)
Coenzyme Q10 (energy metabolism)
Nicotinamide (not niacin, but niacinamide; energy metabolism)
The list could go on, but one of the key points here is about energy metabolism. Ultimately all this oxidative damage from excess catecholamines is harmful because it prevents your mitochondria (the little cellular factories that produce the energy your other cells need to function) producing ATP, and that eventually leads to a cascade of cellular death all across the body.
Therefore getting frequent and sufficient food during any binge is probably more important than any of those supplements. Especially carbohydrates (eg fructose from fruits plus some slower digesting carbs) to deliver a relatively stable blood glucose level and limit the need for what's called beta-oxidation, which is the less efficient burning of fats and ketones for energy that becomes a part of that terminal cascade at the mitochondria.