Dihydromyricetin (DHM) is a natural flavonoid compound. This bioactive molecule, also known as ampelopsin, is a type of flavanonol found in several plant species. It is most commonly extracted from the bark and fruit of the Hovenia dulcis, known as the Japanese raisin tree, and Ampelopsis grossedentata, or Chinese vine tea. DHM has a long history of use in traditional Asian medicine, often as a purported remedy for hangovers. Its rising popularity stems from scientific investigation into its potential to modulate the body’s response to ethanol.
How Dihydromyricetin Modulates Alcohol Metabolism
Dihydromyricetin’s influence on the body’s processing of alcohol involves a dual mechanism, acting both on the central nervous system (CNS) and the liver. Alcohol exerts its intoxicating effects by potentiating Gamma-Aminobutyric Acid-A (\(\text{GABA}_\text{A}\)) receptors in the brain, which are the primary inhibitory neurotransmitter receptors. This potentiation leads to the sedative, anxiolytic, and motor-impairing effects of intoxication.
DHM is thought to counteract this by interacting with the benzodiazepine (BZ) binding site on the \(\text{GABA}_\text{A}\) receptor complex. This interaction appears to antagonize the way alcohol affects the receptor, essentially blocking the excessive inhibitory signaling that causes intoxication. By modulating this neural pathway, DHM may reduce the level of CNS depression and the behavioral signs of intoxication.
The second proposed mechanism involves enhancing the liver’s ability to clear alcohol and its toxic byproducts. Ethanol is metabolized in the liver first by the enzyme Alcohol Dehydrogenase (ADH) into acetaldehyde, a highly toxic compound responsible for many negative effects of drinking. Acetaldehyde is then rapidly broken down by Aldehyde Dehydrogenase (ALDH) into harmless acetate.
Research suggests that DHM may trigger the liver to increase the expression and activity of both ADH and ALDH enzymes. This enhancement in enzymatic function is thought to accelerate the clearance of both ethanol and the poisonous acetaldehyde from the bloodstream. However, some studies present conflicting data, indicating that DHM’s effects on ADH and ALDH activity in vivo may be negligible. The consensus points to DHM’s ability to reduce alcohol-induced liver injury, even if the exact mechanism of enzyme induction remains debated.
Mitigating Alcohol Intoxication and Hangovers
The practical consequence of DHM’s interaction with the \(\text{GABA}_\text{A}\) receptor is its reported ability to reduce symptoms of acute intoxication. In animal models, DHM has been shown to significantly shorten the duration of severe motor impairment and sedation. This suggests that DHM may help preserve motor coordination and cognitive function to a greater extent than would be expected based on blood alcohol concentration alone. This neurological modulation occurs independently of the rate of ethanol elimination.
In the context of a hangover, DHM is proposed to reduce the severity and duration of symptoms. Hangover symptoms such as headache, nausea, and fatigue are largely linked to the accumulation of acetaldehyde and the inflammatory response following alcohol consumption. By potentially boosting the efficiency of ALDH, DHM may help to metabolize the harmful acetaldehyde more quickly, thus reducing the duration of its toxic presence.
DHM’s broader anti-inflammatory and antioxidant properties also contribute to mitigating hangover severity. Alcohol consumption induces significant oxidative stress and inflammation. By reducing these inflammatory markers and scavenging free radicals, DHM assists the body in recovering from the metabolic stress caused by ethanol. This combined action forms the basis of DHM’s reputation as a compound that lessens the negative effects of alcohol.
Broader Health Implications
Beyond its effects on alcohol metabolism, dihydromyricetin is recognized for its general properties as a flavonoid compound. A significant benefit is its potent antioxidant capacity, which involves directly scavenging free radicals to reduce cellular damage and oxidative stress. DHM also demonstrates anti-inflammatory effects by modulating various inflammatory pathways and inhibiting the production of certain inflammatory mediators. This reduction in systemic inflammation has implications for numerous health conditions.
The compound has shown promise in hepatoprotection, or liver protection, even in contexts unrelated to immediate alcohol consumption. Research indicates that DHM may improve metabolic function in models of non-alcoholic fatty liver disease (NAFLD). In clinical studies, DHM administration has been associated with a reduction in serum levels of liver enzymes, such as ALT and AST, and improvements in lipid and glucose metabolism. These effects are attributed to DHM’s ability to reduce fat accumulation and suppress inflammation in the liver tissue.
Dosage, Safety Profile, and Sourcing
Dihydromyricetin is widely available as an over-the-counter dietary supplement, with the extract typically derived from the Japanese raisin tree or Chinese vine tea. Standard commercial and research dosages often fall within a range of 150 mg to 1000 mg per day. For example, some human studies investigating metabolic effects have used 150 mg administered twice daily.
The safety profile of DHM is generally considered favorable, and it has been well-tolerated in short-term human trials without reported adverse events. This relative safety may be partly due to its poor oral bioavailability, meaning only a small fraction of the ingested compound enters the bloodstream. However, there is a lack of extensive data from long-term human trials to fully confirm its safety over prolonged periods.
A consideration for individuals taking other medications is DHM’s potential for drug interactions. In vitro studies suggest that DHM may inhibit certain cytochrome P450 (CYP) enzymes, including CYP3A4, CYP2E1, and CYP2D6, which are responsible for metabolizing many common prescription drugs. Individuals should consult a healthcare provider before taking DHM, especially if they are on chronic medication, to evaluate any potential for altered drug metabolism.