Severe deficiencies of thiamine contribute to Wernecke’s encephalopathy, Korsakoff psychosis, polyneuropathy, and myopathy. Numerous studies have shown that thiamine supplementation can ameliorate some of the neurological sequelae of chronic alcoholism. In addition, animal studies indicate that thiamine deficiency may increase alcohol consumption Zimatkin & Zimatkina, 1996. Thiamine supplementation is a well-established complementary treatment for alcoholism. Magnesium Acute alcohol administration can cause sudden severe vasoconstriction and decreased cerebral blood flow. Alcohol use, particularly binge drinking is associated with headaches, strokes, sudden death, and worse outcomes in patients with brain injury. Low levels of intracellular and extracellular magnesium modulate a cascade of events involved in cerebrovascular constriction. In rat studies, infusion of magnesium was found to attenuate alcohol-induced vasoconstriction.
In humans, intravenous magnesium sulfate relieved alcohol-associated headaches Altura, & Altura, 1999; Barbour, Gebrewold, Altura, & Altura, 2002. Although animal studies suggest that magnesium may improve alcohol-associated brain injury, clinical studies in nonalcohol related brain injury have not shown benefits Schouten, 2007; Temkin, Anderson, Winn, Ellenbogen, Britz, Schuster et al. Winn, Temkin, Anderson, & Dikmen, 2007. Taurine and Acamprosate Taurine, an amino acid and antioxidant, prevented toxic damage to the liver during alcohol withdrawal in rats by reducing acetaldehyde levels Watanabe, Hobara, & Nagashima, 1985. Supplementation with taurine 1-4 gm/day reduced alcohol withdrawal symptoms better than placebo in a RCT study of 60 patients Ikeda, 1977. Taurine has also been used to reduce alcohol craving. Acamprosate, a medication derived from taurine, is more effective than taurine for reducing alcohol craving in clinical practice. For this reason, and because medical insurance will cover the cost of acamprosate, few patients will require taurine.
Acetyl-L-Carnitine Alcar Alcohol abuse is associated with low serum carnitine levels. Abstinent alcoholics treated with acetyl-L-carnitine Alcar 2,000 mg/day for three months showed better performance on neuropsychological testing than control subjects Tempesta, Troncon, Janiri, Colusso, Riscica et al., 1990. Several rat studies have shown that Alcar protects against alcohol induced metabolic abnormalities, including glutathione major antioxidant depletion Calabrese, Scapagnini, Catalano, Dinotta, Bates et al. Calabrese, Scapagnini, Latteri, Colombrita, Ravagna et al. Acetyl-L-carnitine may have a role in the prevention and treatment of cognitive deficits associated with alcohol abuse. One rodent study found that Alcar protected against tremor during alcohol withdrawal and reduced alcohol consumption Mangano, Clementi, Costantino, Calvani, & Matera, 2000. N-acetylcysteine Animal studies have indicated that N-acetylcysteine NAC inhibits cocaine-seeking behavior.
In a DBRPC crossover trial, 15 hospitalized nontreatment-seeking patients with cocaine dependence were given four doses of either NAC 600 mg or placebo. In rating their responses to watching slides depicting cocaine and cocaine use, subjects reported less interest and less desire to use cocaine while they were taking NAC. This study suggests that NAC may reduce cocaine cue reactivity LaRowe, Myrick, Hedden, Mardikian, Saladin et al., 2007. A four-week open pilot study in 23 treatment-seeking cocaine-dependent patients tested NAC in doses of 1200 mg/day, 2,400 mg/day or 3,600 mg/day. The two higher doses of NAC were associated with better retention rates. A majority of the 16 subjects who completed the study either terminated cocaine use completely or significantly reduced their cocaine use during NAC treatment. All three doses were well-tolerated.
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