What is behind Alcohol Recovery
The repair state after ethanol exposure — hepatic, neurological and nutritional at once. Thiamine depletion and acetaldehyde clearance are separate problems on separate clocks. Evidence A — Human trial evidence.
Alcohol is broken down by the ADH and ALDH enzymes through a toxic intermediate, acetaldehyde. Supporting these enzymes and the liver eases the metabolic burden of alcohol. Evidence B — Preclinical.
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.
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
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
HPA Axis / Cortisol → Digestive Function. “Reports have consistently established that central administration of CRF acts in the brain to inhibit gastric emptying while stimulating colonic motor function through modulation of the vagal and sacral parasympathetic outflow in rodents.” — Corticotropin-Releasing Factor and the Brain-Gut Motor Response to Stress. Canadian Journal of Gastroenterology, 1999, vol 13, pp 18A-25A. doi:10.1155/1999/375916
HPA Axis / Cortisol → Prolactin. “Stress is also an important physiologic cause of hyperprolactinemia, and its clinical significance is still being explored.” — Stress-Induced Hyperprolactinemia: Pathophysiology and Clinical Approach. Obstetrics and Gynecology International, 2018, volume 2018, article ID 9253083. doi:10.1155/2018/9253083
HPA Axis / Cortisol → Muscle Recovery. “Glucocorticoids elicit the atrophy of muscle by increasing the rate of protein degradation by the ubiquitin-proteasome system and autophagy lysosome system.” — The Regulation of Muscle Mass by Endogenous Glucocorticoids. Frontiers in Physiology, 2015, 6, article 12. doi:10.3389/fphys.2015.00012
Formulas that act on these pathways
Acts on 4 of these pathways: Alcohol Recovery, Cystine–Glutamate Antiporter, Serotonin, HPA Axis / Cortisol.
Acts on 3 of these pathways: Cystine–Glutamate Antiporter, Serotonin, HPA Axis / Cortisol.
Acts on 3 of these pathways: Cystine–Glutamate Antiporter, Serotonin, HPA Axis / Cortisol.
Acts on 3 of these pathways: Cystine–Glutamate Antiporter, Serotonin, HPA Axis / Cortisol.
Acts on 3 of these pathways: Cystine–Glutamate Antiporter, Serotonin, HPA Axis / Cortisol.
Acts on 3 of these pathways: 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 Alcohol Recovery. 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.