I’ve stacked a lot of this info as it’s top notch
Not me- credits to Allyl
* very low-dose pregnenolone (1-30mg, regenerative via multiple mechanisms) — Note: for benzodiazepine recovery omit pregnenolone
* very low-dose thiamine (10-50mg, metabolic repair, w/carbs or honey)
* very low-dose riboflavin (1-10mg, metabolic repair, w/carbs or honey)
* very low-dose nicotinamide (10-50mg, metabolic repair, w/carbs or honey)
* very low-dose biotin (1-5mg, metabolic repair, w/carbs or honey)
* very low-dose aspirin (5-30mg, metabolic repair, TLR4, boosts dopamine synthesis)
* theanine (calms adrenals, regenerates dopamine system, neuroprotective)
* magnesium (anti-glutamate, protects from excitotoxicity, not the 'glycinate' form: 'malate' seems appropriate)
* agmatine (multiple mechanisms, +TLR4) — Note: for some people agmatine can be too sedating. If you choose to try it please introduce it at a very low dose.
Optional but very* helpful:
* *palmitoylethanolamine (reduces histamine, metabolic support)
* *linalool (GABAergic sedative, others)
* *myrcene (potent sedative)
* *beta-caryophyllene (sedative, neuroprotective, TLR4, others)
* *essential minerals necessary for proper cellular function, outlined here
* phytol (pro-GABA sedative)
* bisabolol (GABAergic sedative)
* nerolidol (GABAergic sedative)
* borneol (GABAergic sedative)
Specific for opioid recovery (the first 5 items are helpful for other drugs also):
* CBG (α2A adrenergic agonist, TLR4, others)
* L-phenylalanine (dopamine precursor, not the DL- form)
* sodium ascorbate (outlined here)
* low-dose creatine (multiple mechanisms)
* beta-caryophyllene (sedative, neuroprotective, opioidergic, others)
* agmatine (detailed above)
* pregnenolone (detailed above)
* thymoquinone (multiple mechanisms)
* curcumin (multiple mechanisms, +TLR4)
* myrrh oil/extract (opioidergic)
This presentation synthesizes peer-reviewed research demonstrating how specific myrrhessential oil constituents directly interact with central nervous system opioid receptors. Furanoeudesma-1,3-diene acts as a specific δ-opioid receptor agonist with naloxone-reversible analgesic effects.
β-Caryophyllene stimulates endogenous β-endorphin release, producing opioid-mediated antinociception without direct receptor agonism. Clinical trials demonstrate efficacy at 8-16 mg bioactive furanodienes daily.
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These findings suggest that β-Caryophyllenemay have certain therapeutic effects against opioid use disorders with fewer unwanted side-effects by itself.
Moreover, we found that the behavioral effects of curcumin on opioid tolerance and dependence correlated with its inhibition of morphine-induced CaMKIIα activation in the brain. These results suggest that curcumin may attenuate opioid tolerance and dependence by suppressing CaMKIIα activity.
This specific combo has similar qualities to drugs like clonidine, guanfacine and tizanidine (alpha-2 adrenergic agonists):
* agmatine (endogenous α2-adrenergic agonist, TLR4)
* CBG (α2-adrenergic agonist)
* myrcene (α2-adrenergic agonist)
* linalool (GABAergic sedative, others)
* beta-caryophyllene (sedative, neuroprotective, TLR4, others)
Alpha-2 adrenergic agonists are able to produce sedation, analgesia, euphoric effects and partially block acute withdrawal symptoms in chronic opioid users.
Adding an α2-adrenergic to a sedation regimen reduces opioid requirement by 50–75% and benzodiazepine requirement by upwards of 80%.
Anesthesia Progress is the official publication of the American Dental Society of Anesthesiology. The journal invites submissions of review articles, reports on clinical techniques, case reports, conference summaries, and articles of opinion pertinent to the control of pain and anxiety in dentistry.
doi.org
— Clarification on the avoidance of Magnesium glycinate:
For some people glycine can have unpleasant stimulating effects as it's a "co-activator" (co-agonist) of the glutamate NMDA receptor. For someone going through drug recovery who is already dealing with excess excitatory noise (eg glutamate), taking Magnesium glycinate can aggravate this. Magnesium 'malate' is usually well tolerated.
Quote — "Glycine is deeply involved in regulating the glutamatergic transmission, acting as a co-agonist of NMDAR, allowing for its activation and enhancing excitatory glutamatergic tone ."
— On aspirin:
FYI aspirin does a lot more than what it's known for, specifically metabolic & mitochondrial repair. It has unique theraputic properties which make it a valuable addition for drug recovery. A very low dose ranges from 5-30mg. If using aspirin over a long period of time it's recommended to combine it with a small amount of vitamin K2.
Quote — "Because aspirin has been abused by pharmaceutical companies that have competing products to sell, people can easily find reasons why they shouldn’t take it.
