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DTOX - Research

Alcohol Impairs Metabolism and Cognitive Function

The ingestion of alcohol and its subsequent metabolism disrupts the body’s digestion, storage, utilization, and excretion of nutrients. [1]

Specifically…

Alcohol interferes with digestion by inhibiting the breakdown of nutrients into usable molecules by decreasing secretion of digestive enzymes from the pancreas. [2]

Alcohol further impairs nutrient absorption by causing damage to the cells lining the stomach and intestines and disables transport of some nutrients into the blood. [3]

Even if these crucial nutrients are digested and absorbed, alcohol can prevent them from being properly utilized by altering their transport, and storage.[4]

Two critical nutrients depleted by alcohol are Thiamine (Vitamin B1) and Lipoic Acid. 

Thiamine deficiency is actually one of the hallmarks of “Alcoholic Brain Disease”. [5]

Like most B vitamins, Thiamine (B1) plays a role in converting the food we eat into fuel. As noted above, alcohols depletion of these B vitamins impair our ability to assimilate nutrients we eat into food for fuel.

Thiamine also plays a role in critical several cognitive functions, including motor control, but also perceptual – motor tasks, executive functions, and learning and memory, all of which are impaired in alcoholics [6]

Amino Acid Cysteine Blocks “Hangover” Effects Of Alcohol

When consumes alcohol is broken down by the body in a multi-step process. ONe of the by products of the breakdown is aldehyde.

Aldehyde is the compound responsible that blocks normal molecular function, damages our liver, suppresses the immune system, causes accelerates wrinkling of the skin, and leads to the dreaded hangover. [7]

Blocking these toxic effects of aldehyde could reduce both the short and long-term negative impacts of alcohol.

Fortunately for us, the amino acid cysteine has been shown to prevent or block the toxic impact of aldehyde by binding to these molecules before they can interfere with normal biological functions. [8]

“A combination of l-ascorbic acid [Vitamin C] with l-cysteine, and thiamin·HCl [Vitamin B1] at reduced dose levels (2.0, 1.0 and 0.3 mM/kg, respectively) gave virtually complete protection.” [9]

Vitamin C is a well known antioxidant. [10]

It does not always have to exhibit its antioxidant properties on humans. It can direct those properties toward other molecules as it does when it prevents L-cysteine from being oxidized. [11] By keep L-cysteine in its unoxidized state, Cysteine is more available to block aldehyde’s toxic impact.

This same study also concluded that taking Vitamin C and Cysteine “along with ethanol (alcohol) attenuated the amount of oxidation which suggested that cysteine-methionine and vitamin C could play a protective role in the stomach against oxidative damage resulting from chronic alcohol ingestion.

The combination of cysteine, Vitamin C, R-Lipoic Acid, and Vitamin B1 has been found to reduce feelings of alcohol-induced irritability, brain fog, sleep disruption, and generally increases functional capacity the day after alcohol consumption when consumed before each alcoholic beverage. [12]

N-Acetyl-Cysteine (NAC) and Lipoic Acid Effective For Removing Toxins From Body

A meta-analysis on heavy metal toxicity concluded that adjunctive therapies with the antioxidants N-acetyl-cysteine (NAC) and lipoic acid have shown considerable promise in improving clinical recoveries in animal models.”  [13,14,15]

Resources:

  1.  Gordis, E. M.D. Alcohol and Nutrition. National Institute of Alcohol Abuse and Alcoholism.
  2.   Korsten, M.A. Alcoholism and pancreatitis: Does nutrition play a role? Alcohol Health & Research World 13(3):232-237, 1989
  3.  Feinman, L. Absorption and utilization of nutrients in alcoholism. Alcohol Health & Research World 13(3):207-210, 1989.
  4. Thomson, A.D., and Pratt, O.E. Interaction of nutrients and alcohol: Absorption, transport, utilization, and metabolism. In: Watson, R.R., and Watzl, B., eds. Nutrition and Alcohol. Boca Raton, FL: CRC Press, 1992. pp. 75-99.  
  5. Peter R. Martin, M.D, et al. The Role of Thiamine Deficiency in Alcoholic Brain Disease. National Institute of Alcohol Abuse and Alcoholism.  
  6. PARKS, M.H.; DAWANT, B.M.; RIDDLE, W.R.; et al. Longitudinal brain metabolic characterization of chronic alcoholics with proton magnetic resonance spectroscopy. Alcoholism: Clinical and Experimental Research 26(9):1368–1380, 2002.    
  7. Koppaka V, Thompson DC, Chen Y, et al. Aldehyde Dehydrogenase Inhibitors: a Comprehensive Review of the Pharmacology, Mechanism of Action, Substrate Specificity, and Clinical Application. Sibley DR, ed. Pharmacological Reviews. 2012;64(3):520-539. doi:10.1124/pr.111.005538.   
  8. Alessandra T. Peana, et al. Reduction of Ethanol-Derived Acetaldehyde Induced Motivational Properties by L-Cysteine. Alcoholism: Clinical and Experimental Research. Vol. 33, No. 1 January 2009. 
  9. Sprince H, Parker CM, Smith GG, Gonzales LJ (1974) Protection against acetaldehyde toxicity in the rat by L-cysteine, thiamin and L-2-methylthiazolidine-4-carboxylic acid. Inflamm Res 4:125–130.  
  10. Padayatty SJ, et al. Vitamin C as an antioxidant: evaluation of its role in disease prevention. J Am Coll Nutr. 2003 Feb;22(1):18-35.
  11. Amanvermez R. Protective effects of cysteine, methionine and vitamin C on the stomach in chronically alcohol treated rats. J Appl Toxicol. 2008 Jul;28(5):591-8.
  12. Fowkes, S. Living With Alcohol. Cognitive Enhancement Research Institute. Smart Drug News [v5n5]. Copyright (c) 1996, 1997
  13. Flora SJS, Pachauri V. Chelation in Metal Intoxication. International Journal of Environmental Research and Public Health. 2010;7(7):2745-2788. doi:10.3390/ijerph7072745.
  14. Flora SJS, Pande M, Kannan GM, Mehta A. Lead induced oxidative stress and its recovery following co-administration of melatonin or n-acetylcysteine during chelation with succimer in male rats. Cell. Mol. Biol. 2004;50:543–551.
  15. Pande M, Flora SJS. Lead induced oxidative damage and its response to combined administration of α-Lipoic acid and succimers in rats. Toxicology. 2002;177:187–196.

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