Protecting Against Hangover and Cellular Damage
Nutrients that neutralize alcohol byproducts and protect cells against the damaging effects of alcohol include vitamin C, vitamin B1, S-allyl-cysteine (antioxidant found in garlic), glutathione, vitamin E, and selenium (Sprince 1975; Hell 1976; Loguercio 1993; van Zandwijk 1995; Marotta 2001). These nutrients can be taken at the time the alcohol is consumed or before bedtime to help prevent a hangover.
Vitamin C. Vitamin C is one of the essential nutrients depleted by alcohol consumption (Hancock 2005). Because it is the body's primary water-soluble dietary antioxidant, this depletion results in severe oxidative stress in daily drinkers (Masalkar 2005). Vitamin C is also an essential co-factor for many enzymes, and its depletion lowers levels of internally produced antioxidant enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase (Zhou 2001). Low levels of these antioxidants may be associated with increased rates of cancers in humans, whether or not they consume alcohol (Devasagayam 2004).
Vitamin B1. Thiamine (vitamin B1) is an essential water-soluble vitamin. Thiamine deficiency can cause lethargy, fatigue, apathy, impaired awareness, loss of equilibrium, disorientation, memory loss, anorexia, muscular weakness, and eventually death (Martin 2003). Alcohol consumption depletes thiamine and produces the same symptoms as non-alcoholic thiamine deficiency (Betrosian 2004). Thiamine deficiency damages brain cells and other nerve cells throughout the body. Thiamine deficiency—rather than the toxic effects of ethanol—has been proposed as the primary cause of cerebellar degeneration in alcoholics (Maschke 2005).
Garlic extract (S-allyl-cysteine). Because the heavy consumption of alcohol produces many deleterious effects within the body, including an increased risk of cancer, liver disease, and neurological disease, it is suggested that hangover-prevention ingredients such as garlic be taken any time alcohol is consumed. Garlic contains S-allyl-cysteine, a neutralizer of acetaldehyde.
S-allyl-cysteine scavenges free radicals and reduces oxidative stress (Perez-Severiano 2004; Maldonado 2003). In experimental animal models, S-allyl-cysteine helped protect the nervous system from neurotoxins and the kidneys against damage from reactive oxygen species (Perez-Severiano 2004; Maldonado 2003).
Vitamin E. Brain and liver cells contain the lion's share of lipids among the body's organs, and lipid peroxidation rates are highest in the brain and liver due to their fat content. Accordingly, vitamin E content is also highest in these organs.
Nature has tailored vitamin E to block the peroxidation process, thus explaining its concentration in these two organs and its depletion by alcoholism and cirrhosis (Zhou 2001; Prakash 2004; Gutteridge 1978). Vitamin E is an essential nutrient that may prevent damage caused by alcohol in the brain and liver (Waluga 2003; Mansouri 2001). As such, it is a supplement that should always be taken by those who consume alcohol.
Selenium. In humans, low selenium status is associated with increased risk of colon cancer (Ferguson 2004a). Selenium levels tend to be reduced in people who drink alcohol regularly (Dey Sarkar 2007). That is especially concerning because selenium deficiency is a major risk factor for liver cancer; conversely, people with the highest levels of selenium in their tissues have a 50% reduction in their risk of this cancer (Sakoda 2005).
Glutathione. Oxidative stress combined with acetaldehyde causes a profound impairment of the body's natural antioxidant systems, by depleting stores of a compound called glutathione (McKillop 2005). Restoring cellular healthy glutathione levels, therefore, seems to be a natural strategy to prevent alcohol-related cancers.
Glutathione, one of the body's most important natural antioxidants, plays a key role in alcohol detoxification. In the liver, glutathione binds to toxins and transforms them into compounds that can be excreted in the bile or urine. The liver's supply of glutathione may be exhausted by binding to carcinogens produced during alcohol detoxification by the liver. The direct conjugation of acetaldehyde and glutathione has been observed in acute models of alcohol ingestion. When depleted by chronic alcohol ingestion, glutathione becomes unavailable for ordinary regulatory processes.
These findings should not surprise anyone who understands that the ingestion of alcohol inflicts massive free-radical damage throughout the body. When a person is exposed to a known toxic substance (such as alcohol), it makes sense to take an antidote (antioxidants) to provide at least partial protection against the short-term (hangover) and long-term (degenerative disease) effects.
N-acetyl cysteine. N-acetyl cysteine (NAC) powerfully replenishes glutathione levels in tissues, helping to fend off the consequences of acute oxidative stress (Pascale 1989; Novitskiy 2006). Rats supplemented with NAC prior to treatment with acetaldehyde are potently protected against toxicity and death; the effect is even more powerful when combined with vitamin C and thiamine (Novitskiy 2006). Independently, NAC binds acetaldehyde directly, further preventing its damaging effects (Vasdev 1995).
Chlorophyllin. Chlorophyllin is a water-soluble form of the green plant pigment chlorophyll (Egner 2003; Egner 2001). It has been evaluated as a chemopreventive agent in populations at high risk for liver cancer, one of the most common tumors known, and one that is frequently caused by ingested toxins (Egner 2003; Egner 2001; Kensler 2004). Chlorophyllin is a large molecule thought to bind to many carcinogens and toxins, enhancing their excretion from the body before they damage DNA (Kensler 2004; Ferguson 2004b). Binding to toxins in the intestine prevents their uptake, further reducing their cancer-producing effects (Kensler 2004). Chlorophyllin also induces important enzymes that protect against oxidants arising from toxins such as acetaldehyde, while also reducing expression of inflammatory mediators (Fahey 2005; Yun 2005).
Grape Seed extract. Extracts of grape seeds are known to be powerful antioxidants with health benefits for many tissues. In both animal and human studies, these extracts reduce markers of oxidative damage and enhance natural antioxidant mechanisms to protect cells and DNA from injury (Simonetti 2002; Fan 2004; Llopiz 2004; Lu 2004; Busserolles 2006). Grape seed extracts have been shown to prevent alcohol-induced oxidative damage in all tissues examined in animal studies (El-Ashmawy 2007; Guo 2007). These extracts are highly bioavailable in humans, making them especially appealing in combating the cancer-causing effects of alcohol (Sano 2003; Ward 2004).
L-theanine. L-theanine is a non-protein amino acid found exclusively in green tea (Vuong 2011; Nathan 2006). It contributes significantly to the favorable taste of green tea and has numerous health-promoting benefits (Vuong 2011). Research from Japan shows that theanine is a powerful antidote to the effects of alcohol. If theanine is given to mice before or after they drink alcohol, it significantly lowers blood levels of alcohol (Sadzuka 2005). It works by modulating alcohol chemistry.
Theanine accelerates the breakdown of acetaldehyde and blocks toxic radicals (Sadzuka 2005). The remarkable powers of theanine to intercept free radicals were demonstrated in the same study. It blocked radicals caused by alcohol and suppressed levels to below normal for five hours. Theanine also helps to counteract the alcohol-induced loss of glutathione (Sadzuka 2005).
S-Adenosylmethionine (SAMe). As has already been discussed, supplementing with the right antioxidants while consuming ethanol significantly reduces consequences of these free radicals throughout the body. SAMe has additional value because, like NAC, it helps restore depleted glutathione in alcohol-damaged cells, providing additional antioxidant protection (Holguin 1998; Powell 2010).
Ethanol also depresses an enzyme required to convert methionine into S-adenosylmethionine (SAMe) (Mato 1994), resulting in a deficiency of SAMe. Alcohol-induced depletion of SAMe can be overcome by SAMe supplementation which restores hepatic SAMe levels (Lieber 1997; 2000a; 2000b; 2000c).
Supplementation with SAMe may help support healthy liver function. For those who cannot afford SAMe, supplementation with trimethylglycine (TMG, also known as glycine betaine), folic acid, and vitamin B12 could help the liver to synthesize SAMe.
Probiotics. One reason that 30% of alcoholics develop cirrhosis may be a leaky gastrointestinal system. According to research (Keshavarzian 1999), another factor might be a gut-derived endotoxin. This would suggest that the use of probiotic substances might aid in the prevention of cirrhosis or other liver damage. Probiotics are beneficial bacteria that help to recolonize the intestinal tract. Intestinal flora (bacteria) help our digestive system absorb nutrients and act as a protective barrier in keeping toxins out. Along with taking a probiotic formula, a supplement to nourish intestinal flora such as fructo-oligosaccharides (FOS) is suggested. FOS helps reduce the formation of toxic liver metabolites and therefore is beneficial to people with chronic liver problems.
Magnesium. Chronic alcohol consumption can constrict arteries in the brain and lead to neurological deficit (Thomson 1988). Daily supplementation could help keep cerebral blood vessels open by blocking excess infiltration of calcium into endothelial cells.
Milk thistle extracts: Silymarin and Silibinin. Silymarin is a compound extracted from the milk thistle plant. It has long been used to improve liver health and enhance excretion of toxins, particularly those that are related to alcohol toxicity. Silymarin is a powerful antioxidant and protects DNA from cancer-inducing damage, especially in alcohol-induced liver disease (Ha 2010; Feher 2008). It inhibits conversion of ethanol to acetaldehyde and reduces cell proliferation in laboratory models of liver cancer (Brandon-Warner 2010).
Those who drink routinely might consider taking a special milk thistle extract called silibinin, which may have a protective effect on the liver (Flora 1998). Clinical evidence supports silibinin for alcohol-induced cirrhosis (Saller 2008; Ferenci 1989). Silibinin is the most active constituent of silymarin. In Germany, silibinin is sold as a drug to treat liver diseases.
Picrorhiza. Picrorhiza kurroa is a member of the figwort family, with a long history of use in traditional south Asian medical systems ((Rajkumar 2011). Picrorhiza extracts given to laboratory animals following chronic alcohol ingestion reverse most of the deleterious biochemical changes induced by alcohol (Rastogi 1996; Saraswat 1999). A powerful antioxidant (Rajkumar 2011), picrorhiza also has specific anti-cancer effects, inhibiting toxin-induced cancer generation and increasing life span of tumor-afflicted animals (Rajeshkumar 2000; Rajeshkumar 2001).
Polyenylphosphatidylcholine (PPC). PPC, also referred to as polyenylphosphatidylcholine, is a fat-soluble nutrient with many health-promoting benefits. These include protecting the liver, sustaining cardiovascular health, and supporting nervous system and gastrointestinal function. Dietary sources of PPC include soybeans, liver, oatmeal, cabbage, cauliflower, egg yolk, meat, and vegetables.
For those who consume large amounts of alcohol (i.e., binge drinkers), PPC supplementation is recommended prior to alcohol consumption. The administration of PPC has been shown to provide significant protection against certain forms of alcohol-induced liver injury in animals via several unique mechanisms (Aleynik 1999; Lieber 1997; 2000a; 2000b; 2000c). PPC also reduces gastric irritation (Anand 1999).
In a study in mice, alcohol administration induced numerous changes, depleting the liver-supportive nutrients S-adenosylmethionine (SAMe) and glutathione, as well as increasing lipid peroxidation. PPC protected against these effects, restoring levels of SAMe and glutathione, and relieving oxidative stress in the liver (Aleynik 2003).
In a study of baboons, PPC helped to prevent alcohol-induced cirrhosis. PPC also helped to prevent two common detrimental effects of alcohol: the formation of fatty liver and the elevation of blood lipid levels (Navder 1997). In a human study, investigators examined the effects of PPC on heavy alcohol drinkers. While PPC treatment for two years did not affect the progression of liver fibrosis, it did promote favorable changes in blood levels of bilirubin (a liver-produced waste product) and liver transaminases (enzymes that are elevated by liver damage) (Lieber 2003).
European Medications. European medications such as Picamilon (50 mg, three times a day) and Pyritinol (200 mg, three times a day) could help prevent and restore neurological function lost due to chronic ethanol intake. An expensive prescription drug called Nimotop® (nimodipine), at the dose of 30 mg 3-4 times a day, can slowly repair central nervous system damage caused by excess alcohol intake.