What is behind ADHD / Attention & Focus
Attention-deficit/hyperactivity disorder — a developmental condition of inattention, hyperactivity and impulsivity with high heritability. Evidence A — Human trial evidence.
The chemistry of wanting, not of liking. Dopamine sets how much effort a goal feels worth — which is why its loss reads as apathy long before it reads as sadness. More is not better: the same system that drives pursuit drives compulsion. Evidence A — Human trial evidence.
Insulin-like growth factor-1 — the dermal-papilla growth factor that drives follicle proliferation and prolongs anagen (the active growth phase). Evidence A — Human trial evidence.
The cystine–glutamate exchange that supplies antioxidant building blocks while tuning excitatory neurotransmission. Evidence A — Human trial evidence.
Serotonin — the neurotransmitter of mood and satiety, and the precursor the body converts to melatonin for sleep. Evidence A — Human trial evidence.
GABA — the brain's principal inhibitory neurotransmitter, the source of calm and restful sleep. Evidence A — Human trial evidence.
The hypothalamic–pituitary–adrenal axis and its hormone cortisol — the body's central stress-and-recovery command. Evidence A — Human trial evidence.
Evidence on these pathways
Dopamine → Melatonin. “Through α1B-D4 and β1-D4 receptor heteromers dopamine inhibits adrenergic receptor signaling and blocks the synthesis of melatonin induced by adrenergic receptor ligands.” — Circadian-Related Heteromerization of Adrenergic and Dopamine D4 Receptors Modulates Melatonin Synthesis and Release in the Pineal Gland. PLoS Biology, 2012, volume 10, e1001347. doi:10.1371/journal.pbio.1001347
Dopamine → Mood (Positive Affect). “Boosting dopamine also increased happiness resulting from some rewards.” — Dopaminergic Modulation of Decision Making and Subjective Well-Being. Journal of Neuroscience, 2015, 35(27), 9811-9822. doi:10.1523/JNEUROSCI.0702-15.2015 | PMC4495239
GABA → Mood (Positive Affect). “In this review, we summarize clinical and preclinical evidence supporting a central and causal role of GABAergic deficits in the etiology of depressive disorders.” — The GABAergic deficit hypothesis of major depressive disorder. Molecular Psychiatry, 2011, vol 16, issue 4, pp 383-406. doi:10.1038/mp.2010.120
HPA Axis / Cortisol → Cognition. “Whereas treatments used in previous studies generally affect more than one memory phase and therefore cannot detect possible differential effects of glucocorticoids on the distinct phases of acquisition, consolidation and retrieval, here we show that treatment of healthy humans with cortisone at acute-stress levels specifically impaired retrieval of declarative long-term memory for a word list.” — Acute cortisone administration impairs retrieval of long-term declarative memory in humans. Nature Neuroscience, 2000, vol 3, pp 313-314. doi:10.1038/73873
Formulas that act on these pathways
Acts on 6 of these pathways: ADHD, Dopamine, Cystine–Glutamate Antiporter, Serotonin, GABA, HPA Axis / Cortisol.
Acts on 5 of these pathways: Dopamine, Cystine–Glutamate Antiporter, Serotonin, GABA, HPA Axis / Cortisol.
Acts on 5 of these pathways: Dopamine, Cystine–Glutamate Antiporter, Serotonin, GABA, HPA Axis / Cortisol.
Acts on 4 of these pathways: Cystine–Glutamate Antiporter, Serotonin, GABA, HPA Axis / Cortisol.
Acts on 4 of these pathways: Cystine–Glutamate Antiporter, Serotonin, GABA, HPA Axis / Cortisol.
Acts on 4 of these pathways: Dopamine, Cystine–Glutamate Antiporter, Serotonin, HPA Axis / Cortisol.
What this page does not claim
This page names the pathways involved and the published evidence on each. It does not claim that any formula treats, cures or prevents ADHD / Attention & Focus. A pathway opens here only on graded, published evidence, under a standard fixed before the evidence was gathered, and every figure above carries its grade.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.