What is behind Addiction & Recovery Support
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.
CREB-mediated synaptic plasticity and gene transcription; learning, memory and addiction remodeling. ΔFosB needs CREB and SRF together — either alone leaves it intact (Vialou 2012), so this is one required factor, not the switch. Evidence A — Human trial evidence.
Blood-sugar handling and insulin sensitivity. Evidence A — Human trial evidence.
The cystine–glutamate exchange that supplies antioxidant building blocks while tuning excitatory neurotransmission. Evidence A — Human trial evidence.
GABA — the brain's principal inhibitory neurotransmitter, the source of calm and restful sleep. 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.
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
Serotonin → Hot Flushes & Night Sweats. “Most studies have indicated the efficacy and safety of some antidepressants, such as SSRIs and SNRIs, in decreasing the frequency and severity of HF.” — The Efficacy and Safety of Selective Serotonin Reuptake Inhibitors and Serotonin-Norepinephrine Reuptake Inhibitors in the Treatment of Menopausal Hot Flashes: A Systematic Review of Clinical Trials. Iranian Journal of Medical Sciences, 2022, vol 47, no 3, pages 173-193. doi:10.30476/ijms.2020.87687.1817
Formulas that act on these pathways
Acts on 4 of these pathways: Dopamine, Cystine–Glutamate Antiporter, GABA, Serotonin.
Acts on 4 of these pathways: Dopamine, Cystine–Glutamate Antiporter, GABA, Serotonin.
Acts on 4 of these pathways: Dopamine, Cystine–Glutamate Antiporter, GABA, Serotonin.
Acts on 3 of these pathways: Cystine–Glutamate Antiporter, GABA, Serotonin.
Acts on 3 of these pathways: Cystine–Glutamate Antiporter, GABA, Serotonin.
Acts on 3 of these pathways: Dopamine, Cystine–Glutamate Antiporter, Serotonin.
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 Addiction & Recovery Support. 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.