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It is obvious from this research that genetic polymorphysisms and developmental challenges with neurotransmitter function are critical factors in ADHD

[16] [18] Animal studies have not demonstrated teratogenicity, but high doses in pregnancy may theoretically increase the risk of fetal oxalate nephropathy or other metabolic disturbances

Makrantoni, V

The study was conducted on 32 male mice divided into four groups: a control (C) group receiving a standard diet with biotin, a biotin-deficient (BD) group on a biotin-free diet, a ketogenic control (KC) group on a ketogenic diet (low-carbohydrate and high-fat) with biotin, and a ketogenic biotin-deficient (KBD) group on a ketogenic diet without biotin