The Science Behind the Formula
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Hair of the dog or hair of the dog that bit you is an expression used to refer to alcohol that is consumed within 24 hours of the last drink with the aim of lessening the effects of a hangover. Hangovers are often referred to as the first stage of alcohol withdrawal, which is then alleviated by further alcohol intake. In one study, low ethanol doses may effectively prevent alcohol withdrawal syndrome in surgical patients. This statement is questionable as the symptoms of hangover and alcohol withdrawal are very different.1
1. Wiese, Jeffrey G.; Shlipak, Michael G.; Browner, Warren S. (2000). “The Alcohol Hangover”. Annals of Internal Medicine. 132(11): 897–902. doi:10.7326/0003-4819-132-11-200006060-00008. PMID 10836917.
We think we have a better solution. Here is our Hair of the Dog:
Enzymes and P450’s in Alcohol Metabolism:
How does alcohol go through one’s body? It begins in the liver where ethanol is converted to acetaldehyde by an enzyme called alcohol dehydrogenase (ADH). After it is broken down to acetaldehyde, it is broken down to acetate by aldehyde dehydrogenase (ALDH2). Once converted to acetate it can be further broken down into carbon dioxide and water, and finally eliminated from the body.1
What causes a hangover?
There still is no known cause of what causes a hangover, but there are a couple culprits that have been researched. Dehydration has been seen in most people who consume large amounts of alcohol. This is because alcohol has a diuretic effect by decreasing the amount of anti-diuretic hormone and increasing urination. There are also products other than ethanol in alcoholic beverages. One that is believed to increase hangover severity is methanol, which is converted to toxic formaldehyde and formic acid by the same enzymes as ethanol. Alcohol also affects the concentration of inflammatory cytokines in the body. The cytokines increased by alcohol include IL-10, IL-12, and IFN-y which can increase hangover severity.2
Alcohol Dehydrogenase and Aldehyde Dehydrogenase
There are two major pathways that are responsible for the breakdown of alcohol. The most prominent pathway is the breakdown of ethanol into acetaldehyde by alcohol dehydrogenase and then to acetate by aldehyde dehydrogenase. Acetaldehyde is a highly reactive and toxic byproduct of ethanol and has been known to cause tissue damage, cancer, and may even be the reason for the addictive process of alcoholism.1,3 Elevated levels of acetaldehyde have been shown to condense with dopamine in the
brain to form tetrahydro-papoveroline, a morphine-like substance, which has been postulated to cause alcohol addiction.4
Acetaldehyde is also believed to be why people experience hangover symptoms. When ethanol is converted to acetaldehyde, intermediate carrier electrons become involved. These electrons, nicotinamide adenine dinucleotide (NAD), are reduced by two electrons to form NADH. NADH is then used in multiple areas of the body to generate energy.1,3
Once acetaldehyde is produced, it is rapidly metabolized to acetate by aldehyde dehydrogenase found in the mitochondria. Once again, NAD is involved in the reaction and produces NADH as a byproduct. This NADH is then oxidized through a series of oxidative reactions in the mitochondria and produces energy for the body to use. After acetate is made, it is oxidized into carbon dioxide (CO2) and water. Most of the CO2 is used in the heart, skeletal muscle, and brain cells.1,3
Cytochrome P450 and Catalase
Along with ADH and ALDH enzymes breaking down ethanol, there are other pathways that are involved in alcohol metabolism. The isozymes CYP2E1, CYP1A2, and CYP3A4 contribute to alcohol oxidation in the liver. CYP2E1 is induced by chronic alcohol consumption and plays an important role in ethanol to acetaldehyde metabolism. CYP2E1-dependant ethanol oxidation may also occur in other tissues where ADH has low activity. This process produces reactive oxygen species (ROS), which can also increase the risk of tissue damage. The enzyme catalase located in cell bodies called peroxisomes has the ability to oxidize ethanol when there is a hydrogen peroxide generating system available. Chronic alcohol consumption in rats has been shown to result in increased hydrogen peroxide production and increased catalase activity.1,3
Along with the oxidative pathways as stated above, there are also a couple of nonoxidative pathways that may have pathological and diagnostic relevance. One pathway leads to the formation of molecules of fatty acid ethyl esters. This results in the formation of fat molecule which contain phosphorous. They are detected in serum and other tissues after consuming alcohol and remain long after. These fatty acids may lead to tissue damage, but more information is needed to adequately determine this
Another pathway that is involved is an enzyme called phospholipase D, which is responsible for the breakdown of phospholipids to produce phosphatidic acid. This pathway is an imprtant component in cellular communication. The product of this reaction, phosphatidyl ethanol, is poorly metabolized in the body, which can lead to accumulation. This accumulation inhibits phosphatidyl ethanol and disrupts cell signaling.1,3
- Alcohol Metabolism: An Update [Internet]. National Institute on Alcohol Abuse and Alcoholism. U.S. Department of Health and Human Services; https://pubs.niaaa.nih.gov/publications/aa72/aa72.htm. Published July 2007. Accessed July 18, 2019.
- The Chemistry of a Hangover [Internet]. Compound Interest. Andy Brunning/Compound Interest. https://www.compoundchem.com/2016/01/01/hangover/. Published January 1, 2016. Accessed July 18, 2019.
- Zakhari S. (2006). Overview: how is alcohol metabolized by the body? Alcohol research & health: The Journal of the National Institute on Alcohol Abuse and Alcoholism, 29(4), 245–254. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6527027/. Accessed July 18, 2019.
- Davis BE, Walsh MJ. Alcohol, amines and alkaloids: A possible biochemical basis for alcohol addiction. Science 167:1005-7, 1970
Ascorbic Acid (Vitamin C):
Ascorbic acid (Vitamin C) is a vitamin that plays a role in many biological reactions throughout the body1. The human body cannot make its own Vitamin C and must rely on an adequate dietary intake for its requirement2.
There is an association between ascorbic acid concentration and alcohol plasma concentration levels. Studies have shown an association between excessive alcohol intake and ascorbic acid defecincy3. Alcohol can damage the cells that line the gut (gastrointestinal enterocytes). This can lead to intestinal malabsorption of many nutrients including vitamin C5. This might impact the restoration of Vitamin C levels by the oral route of administering Vitamin C. One such study examined the effect of short term (five consecutive days) intravenous Vitamin C on alcoholics who are Vitamin C deficient4. Even after the duration of this therapy, many patients still remained deficient. Oral intake of Vitamin C would likely produce less desirable levels. Likewise, chronic alcohol ingestion induces liver toxicity, which can negatively impact the transformation of many vitamins to their active form. When Vitamin C is taken before or during alcohol ingestion, supplementation may prevent fatty infiltration of the liver7.
Study results also showed that vitamin C can possibly protect against the formation of acetaldehyde, which would reduce liver toxicity and possible influence on the biochemical reactions of many other vitamins. A study in guinea-pigs that were given alcohol showed that the ones with the highest tissue concentration of Vitamin C proved to have significantly decreased residual levels of ethanol and acetaldehyde in the liver and the brain. Vitamin C appears to accelerate ethanol and acetaldehyde metabolism and reduce some of their adverse health effects6. Additionally, pretreatment with Vitamin C significantly enhanced the clearance of plasma alcohol. Supplementation may reduce the effects of ethanol toxicity by improving ethanol clearance8.
- Englard S , Seifter S . The biochemical functions of ascorbic acid. Annu Rev Nutr 1986;6:365–406.doi:10.1146/annurev.nu.06.070186.002053
- Bonjour, J. P.: Internat. J. Vit. Nutr. Res. 49, 434 (1979).
- Fain O , Pariés J , Jacquart B , et al. Hypovitaminosis C in hospitalized patients. Eur J Intern Med 2003;14:419–25.doi:10.1016/j.ejim.2003.08.006
- Majumdar SK , Patel S , Shaw GK , et al . Vitamin C utilization status in chronic alcoholic patients after short-term intravenous therapy. Int J Vitam Nutr Res 1981;51:274–8.
- Thomson, A. D., Majumdar, S. K.: Clinics Gastroenterol. 10, 263 (1981).
- Ginter E, Zloch Z, Ondreicka R. Influence of vitamin C status on ethanol metabolism in guinea-pigs. Physiol Res. 1998;47(2):137-41.
- DiLuzio NR. A mechanism of the acute ethanol induced fatty liver and the modification of liver injury by antioxidants. Lab Invest 15:50-61, 1966.
- Chen MF et al. Effect of ascorbic acid on plasma alcohol clearance. J Am Coll Nutr 9(3):185-9, 1990
Thiamine (Vitamin B-1):
Also known as Vitamin B1, thiamine is one of the essential vitamins required by all tissues, including the brain. The body does not produce thiamine but absorbs it from the diet. Thiamine is used to aid specific enzymes that protect the body from harmful molecules and create new brain chemicals and building blocks for your body.1
Function in the Liver
Glucose molecules, also known as carbohydrates, undergo metabolism by many enzymes (three of which use thiamine).2 The enzymes transketolase, pyruvate dehydrogenase (PDH), and alpha–ketoglutarate dehydrogenase (α–KGDH) [1, 2 and 3 respectively shown in the diagram below depicted in blue] require thiamine to assemble the various parts that create them.
Transketolase is an enzyme used to form glucose-6-phosphate from glucose molecules4. Glucose-6-phosphate is very important for the creation of ribose-5-phosphate (needed for DNA) and NADPH (also known as NADP)4. NADPH provides hydrogen ions for biochemical reactions that are needed for many functions, including the production of neurotransmitters, amino acids, fatty acids, and steroids4. Also, NADPH is needed for fighting against oxidative stress3. As you can see, many important products for life are made from these enzymes by the indirect action of thiamine.3
Thiamine and alcohol
In the cells, thiamine is converted to its active form thiamine diphosphate (ThDP) by an enzyme called thiamine phosphokinase (TPK). In one study, subjects with alcohol ingestion had 70% lower TPK activity than those who did not receive alcohol. This showed that not only is more thiamine lost to urination, but less thiamine is utilized and absorbed when alcohol is consumed. Thus, many complications ensue from thiamine deficiency due to alcohol consumption. However, when given high concentrations of thiamine, the amounts of the active vitamin were found to be unaffected by alcohol.4
Alcohol can impact thiamine absorption by alteration of the enterocytes (cells that line the gastrointestinal tract)5. Alcohol also impairs the utilization of thiamine inside all cells. Generally, when thiamine enters a cell and converts to ThDP and then binds to enzymes, this step requires magnesium5. Chronic alcoholics are usually magnesium deficient4. Therefore, when thiamine enters the cell, it cannot be used effectively4. When there is thiamine deficiency, the thiamine dependent enzyme alpha–ketoglutarate dehydrogenase (α–KGDH) will not be activated and will result in damage of the mitochondria and eventually cause cell death4. At that point, the cells of the nervous system and heart seem particularly sensitive to the effects of thiamine deficiency4.
- Suter PM, Russell RM. Vitamin and Trace Mineral Deficiency and Excess. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. Harrison’s Principles of Internal Medicine, 20e New York, NY: McGraw-Hill; . http://0-accessmedicine.mhmedical.com.carlson.utoledo.edu/content.aspx?bookid=2129§ionid=192283003. Accessed July 08, 2019.
- Yu-Shi Gong, Juan Guo, Kun Hu, Yong-Qing Gao, Fang-Li Hou, Feng-Lin Song, Cui-Yi Liang, Chronic Ethanol Consumption and Thiamine Deficiency Modulate β-Amyloid Peptide Level and Oxidative Stress in the Brain, Alcohol and Alcoholism, Volume 52, Issue 2, March 2017, Pages 159–164.
- Gangolf, Marjorie & Czerniecki, Jan & Radermecker, et al. (2010). Thiamine Status in Humans and Content of Phosphorylated Thiamine Derivatives in Biopsies and Cultured Cells. PloS one. 5. e13616. 10.1371/journal.pone.0013616.
- Peter R. Martin, M.D., Charles K. Singleton, Ph.D., and Susanne Hiller–Sturmhöfel, Ph.D., The Role of Thiamine Deficiency in Alcoholic Brain Disease, Alcohol Research & Health. 2003;27(2): 134-42.
- A M Hoyumpa, Mechanisms of thiamin deficiency in chronic alcoholism, The American Journal of Clinical Nutrition, Volume 33, Issue 12, December 1980, Pages 2750–2761, https://doi.org/10.1093/ajcn/33.12.2750
Riboflavin (Vitamin B-2):
Riboflavin converts in the gastrointestinal tract mostly to flavin adenine dinucleotide (FAD) and smaller amount will become flavin mononucleotide (FMN), or riboflavin-5-phosphate1. FAD and FMN is involved in several important enzymatic reactions in metabolism. For example, the production of the important form of active Vitamin B6, pyridoxyl-5-phophate is FMN dependent. FAD is involved in oxidation of pyruvate, fatty acid oxidation and conversion of Vitamin A to retinoic acid. FAD also is responsible for the synthesis of the active form of folic acid, methyltetrahydrofolate. FAD is required to convert the amino acid tryptophan to Vitamin B3 (Niacin). Disruption in this pathway may lead to a build up of quinolinic acid, which is thought to contribute to major depression and agitation. Quinolinic acid is an agonist of the N-methyl-D-aspartate (NMDA) receptor.
Since acute ethanol consumption and riboflavin deficiency each induces oxidative stress within tissues. Ethanol consumption together with riboflavin, or FAD deficiency depletes hepatic reduced glutathione (GSH), which is the major anti-oxidative stress system in the liver. This situation also blunts enzyme activities controlling GSH metabolism and may enhance alcohol-induced liver injury. Also affected are the activities of GSH peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase (G6PD). Glucose-6-phosphate is the form of sugar that our body metabolizes for energy.2
- Hilary J Powers, Riboflavin (vitamin B-2) and health, The American Journal of Clinical Nutrition, Volume 77, Issue 6, June 2003, Pages 1352–1360, https://doi.org/10.1093/ajcn/77.6.1352Causes of vitamin B12 and folate deficiency
- Dutta, P, et al. Acute ethanol exposure alters hepatic glutathione metabolism in riboflavin deficiency. Alcohol. Volume 12 Issue 1 pages 43-47
Niacin (Vitamin B-3; as Niacinamide):
Niacin is converted to its active form, (NAD) nicotinamide adenine dinucleotide. NAD is needed to catalyze over 400 enzymes. It is also converted to another active form (NADP) nicotinamide adenine dinucleotide phosphate. NAD is ‘reduced’ via oxidation/reduction reaction to NADH. NADH can be oxidized back to NAD. NADP to NADPH occurs similarly.
NAD is needed for catabolic reactions that convert carbs/fats/proteins to an energy source (ATP), or adenosine triphosphate. It is also needed for cellular functions such as control of gene expression and cellular communication. NADP is needed for anabolic reactions such as synthesis of cholesterol and fatty acids and maintaining cellular antioxidant function.1
Niacin is primarily absorbed in the small intestine, as well as small amounts in the stomach. Alcohol consumption can interfere with absorption of nutrients in the in the small intestines. Most niacin is consumed from the diet where the average amount consumed in animal sources is 5-10 mg and from plant-based diets 2-5mg.2
Tryptophan is an amino acid found in dairy and meats and can be converted to niacin. As tryptophan makes its journey to niacin, a by-product, quinolinic acid is produced. Quinolinic Acid is thought to contribute to major depression and agitation. Quinolinic acid is an agonist of the N-methyl-D-aspartate (NMDA) receptor.
Severe deficiency in niacin can result in disease called pellagra, which can result in diarrhea, dermatitis, dementia, and possibly even death. Pellagra is common in poor parts of world but has been essentially eliminated in the US. It can also result from existing medical conditions such as anorexia nervosa, chronic alcohol abuse, Crohn’s disease, carcinoid syndrome, vitamin B deficiencies and some medications.3
Niacin is needed to produce vital products for the metabolism of ethanol.4 So, a deficiency in niacin would decrease the metabolism of alcohol overall. Niacin, as NAD and NADP works in tangent with alcohol dehydrogenase to oxidize ethanol to acetaldehyde. Acetaldehyde is oxidized to acetate via aldehyde dehydrogenase and NAD, which is reduced to NADH. The acetate that is produced in the liver leaves and circulates to peripheral tissues where it is activated to acetyl Coenzyme A. Acetyl Coenzyme A is a key metabolite produced from all major nutrients (carbs, fats and excess proteins). The Coenzyme A component requires pantothenic acid (Vitamin B5) for its formation.
- Public Health Reports, June 26, 1914. The etiology of pellagra. The significance of certain epidemiological observations with respect thereto. Public Health Rep 1975; 90:373.
- Kim H, Jacobson EL, Jacobson MK. Position of cyclization in cyclic ADP-ribose. Biochem Biophys Res Commun 1993; 194:1143.
- Ashourian N, Mousdicas N. Images in clinical medicine. Pellagra-like dermatitis. N Engl J Med 2006; 354:1614.
- Abdulla A.-B. Badawy, Pellagra and Alcoholism: A Biochemical Perspective, Alcohol and Alcoholism, Volume 49, Issue 3, May/June 2014, Pages 238 250, https://doi.org/10.1093/alcalc/agu010
Pyridoxyl-5-Phosphate (active Vitamin B-6):
Pyridoxal-5-phosphate (P5P) is the active form of Vitamin B6, or pyridoxine. P5P acts as co-enzyme for a wide variety of metabolic transformations of amino acids, namely tryptophan, tyrosine, sulfur-containing amino acids and other hydroxy-amino acids. Other enzymes which require P5P for their function are important for the biosynthesis of dopamine, serotonin (5HT), gamma amino- n-butryric acid (GABA) and taurine. Deficiency of pyridoxal-5-phosphate could lead to a deficiency of all these neurotransmitters.1
A functional deficiency of P5P is common due to impaired creation from pyridoxine because of the effects of a build-up of acetaldehyde.2
- Thomson AD. Alcohol and nutrition. Clin Endocrinol Metab 7(2):405-28, 1978
- Lumeng L. The role of acetaldehyde in mediating the deleterious effect of ethanol on pyridoxal-5-phosphate metabolism. J Clin Invest 62:286-93, 1978
Pantothenic Acid (Vitamin B-5; as d-calcium pantothenate):
Pantothenic acid (Vitamin B5) forms Pantethine, which is two pantothenic acid molecules linked together with 2 sulfurs.
Image courtesy of Wikipedia
Pantethine is a precursor of Coenzyme A, which is involved in the metabolism of fats and oils.
Image courtesy of Dr. Jeffery Dach MD
Supplementation with pantethine may reduce the adverse effects of acetaldehyde by increasing the activity of aldehyde dehydrogenase. Pantethine increased aldehyde
dehydrogenase activity by as much as 71%4 Acetaldehyde, the primary metabolite of alcohol, may promote alcohol addiction by combining with monamine metabolites to form addicting morphine-like alkaloids1,2,3
Acetaldehyde has also been implicated in the pathogenesis of alcoholic liver disease and alcoholic cardiomyopathy and may play a role in the development of atherosclerosis as related to ethanol ingestion4,5
- Myer RD. Tetrahydro-isoquinolines in the brain: The basis of an animal model of addiction. Alcohol Clin Exp Res 2:145, 1978
- Cohen G, Collins MA. Alkaloids from catecholamines in adrenal tissue: Possible role in alcoholism. Science 167:1749-51, 1970
- Davis VE, Walsh MJ. Alcohol, amines, and alkaloids: a possible biochemical basis for alcohol addiction. Science 167:1005-7, 1970
- Watanabe A et al. Lowering of blood acetaldehyde but not ethanol concentrations by pantethine following alcohol ingestion: Different effects in flushing and non-flushing subjects. Alcohol Clin Exp Res 9:272, 1985
- Sprince H et al. Protection against acetaldehyde toxicity in the rat by L-cysteine, thiamin and L-2-methylthiazolidine-4-carboxylic acid. Agents Actions 4(2):125-30, 1974
Manganese (as manganese aminomin):
Manganese is involved in the metabolism of carbohydrates, of which ethanol is a simple carbohydrate1. In alcohol-induced liver damage, there is an increase in the production of the superoxide, reactive oxygen species (ROS). Superoxides are harmful to our cells but are rapidly broken down in a healthy functioning body2. Manganese superoxide dismutase is the main enzyme in the mitochondria responsible for breaking down superoxide radicals3. When ingesting alcohol, the liver is placed into a stressed environment and the mitochondria in the cells begin producing oxidative species which in turn damage the liver cells3. Without enough manganese in the body to maintain the activity of manganese superoxide dismutase, the balance between the production and breakdown of superoxide is compromised and the oxidants begin damaging cells in the liver. Ensuring an adequate supply of manganese in the body allows critical enzymes to effectively breakdown carbohydrates and protects the liver from oxidative stress damage induced by alcohol.
- Food and Nutrition Board, Institute of Medicine. Manganese. Dietary reference intakes for vitamin A, vitamin K, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:394-419.
- Higdon J. Manganese. Oregon State University, 2001.
- Wheeler MD, Nakagami M, Bradford BU, Uesugi T, Mason RP, Connor HD, Dikalova A, Kadiiska M, Thurman RG. Overexpression of Manganese Superoxide Dismutase Prevents Alcohol-induced Liver Injury in the Rat. J Biol Chem 276: 36664-36672, 2001.
Magnesium (as magnesium glycinate):
Magnesium is one of the most abundant minerals in the body and involved in over 500 biological reactions. It is a cofactor to enzymes that help move glucose across cell membranes when breaking down carbohydrates for energy, specifically in the liver.1 Magnesium deficiencies prevent the liver from processing carbohydrates and other glucose sources quickly and efficiently. At low alcohol concentrations the rate of conversion of glucose into energy in the body is decreased.2 This is partially due to cell damage caused by ethanol use, thereby leading to a leakage of minerals, including magnesium.3 Supplementing magnesium when drinking alcohol will prevent the loss of other minerals and allows optimal break down of carbohydrate and ethanol molecules in liver cells by helping activate the necessary enzymes.
- Guerrero-Romero F, Rodr´ıguez-Mor´an M. Complementary therapies for diabetes: the case for chromium, magnesium, and antioxidants. Arch Med Res 2005; 36: 250–257.
- Dombek KM, Ingram LO, 1986. Magnesium limitation and its role in apparent toxicity of ethanol during yeast fermentation. Applied Environ. Microbiol., 52: 975-981.
- Pornthap Thanonkeo, Pattana Laopaiboon, Kaewta Sootsuwan and Mamoru Yamada, 2007. Magnesium Ions Improve Growth and Ethanol Production of Zymomonas mobilis under Heat or Ethanol Stress. Biotechnology, 6: 112-119.
Zinc (as zinc aspartate):
Ethanol is broken down by three major pathways in the liver. Two of the main pathways are the enzyme alcohol dehydrogenase and the microsomal ethanol-oxidizing system.1 Liver damage resulting from alcohol occurs from the production of harmful reactive oxygen species (ROS) produced by these pathways. The microsomal ethanol-oxidizing system is especially important because it contains an enzyme called the cytochrome P450 2E1 (CYP2E1) that is the most significant when considering ethanol-induced oxidative stress in the liver. Studies have shown that alcohol causes an overexpression of the CYP2E1 enzyme, and inhibition of this enzyme significantly reduces liver damage caused by alcohol.2 Zinc supplementation inhibits the activity of the CYP2E1 enzyme while increasing the activity of the less harmful pathway using alcohol dehydrogenase. Alcohol dehydrogenase is a zinc-metalloenzyme therefore it is increased with zinc supplementation.3
Antioxidants are the enzymes responsible for removing reactive oxygen species from the body before they can cause harm. Glutathione is the body’s most important antioxidant and its concentration is decreased with ethanol ingestion. Zinc prevents alcohol from suppressing glutathione levels and increases glutathione reductase activity in the liver, the enzyme responsible for glutathione production.4 By promoting antioxidant activity and suppressing the production of reactive oxygen species, zinc supplementation can prevent ethanol-induced liver damage.
- Lieber CS: Alcohol metabolism, cirrhosis and alcoholism. Clin Chim Acta 1997, 257:59-84.
- Nanji AA, Zhao S, Sadrzadeh SM, Dannenberg AJ, Tahan SR, Waxman DJ: Markedly enhanced cytochrome P450 2E1 induction and lipid peroxidation is associated with severe liver injury in fish oil-ethanol-fed rats. Alcohol Clin Exp Res 1994, 18:1280-1285.
- Zhou Z, Wang L, Song Z, Saari JT, McClain CJ, Kang YJ. Zinc Supplementation Prevents Alcoholic Liver Injury in Mice through Attenuation of Oxidative Stress. Am JPathol 2005; 166: 1681–90.
- Parat MO, Richard MJ, Beani JC, Favier A: Involvement of zinc in intracellular oxidant/antioxidant balance. Biol Trace Elem Res 1997, 60:187-204.
L-Cysteine (an amino acid):
L-cysteine is an amino acid that can be found naturally in the body, in food, and in dietary supplements. L-cysteine plays a role in both alcohol and carbohydrate metabolism.
L-cysteine contributes to acetaldehyde’s break down into acetate but at a smaller level compared to aldehyde dehydrogenase.1 When alcohol is excessively consumed, aldehyde dehydrogenase and L-cysteine molecules become overwhelmed causing a build-up of acetaldehyde. Acetaldehyde is toxic to the human body and is a main reason why humans experience hangover symptoms the day after excessive alcohol consumption. It is hypothesized that increasing L-cysteine concentration in the body will augment acetaldehyde metabolism and will therefore decrease signs and symptoms associated with hangovers.
L-cysteine plays a role in carbohydrate metabolism by influencing blood sugar levels. It is hypothesized that L-cysteine increases insulin production by increasing tissue levels of H2S and PIP3 improving glucose metabolism.2 Increasing glucose metabolism signals the body to continue metabolizing carbohydrates to produce more sugar to create more energy for the body to use. Subsequently, this should lead to less fat production, decreasing weight gain within patients with higher levels of L-cysteine.
- A Supplement That May Block The Toxic Effects of Alcohol – Medscape – Sep 26, 2017.
- Jain SK. L-Cysteine supplementation as an adjuvant therapy for type-2 diabetes. Canadian Journal of Physiology and Pharmacology [Internet]. 2012 [cited 2019Jul2];90(8):1061–4. Available from: https://web-b-ebscohost-com.onu.ohionet.org/ehost/pdfviewer/pdfviewer?vid=4&sid=57921e5d-d625-4b17-b8de-835cbb8e1eb8@pdc-v-sessmgr01
- Alcohol Metabolism: An Update [Internet]. National Institute on Alcohol Abuse and Alcoholism. U.S. Department of Health and Human Services; [cited 2019Jul2]. Available from: https://pubs.niaaa.nih.gov/publications/aa72/aa72.htm
- Novak I. Purinergic receptors in the endocrine and exocrine pancreas. Purinergic Signalling [Internet]. 2007 [cited 2019Jul2];4(3):237–53. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2486345/
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