Updated on February 8, 2023
For a growing proportion of Americans, liver damage is a frightening prospect. The liver plays an important role in metabolism and detoxification, and patients with liver damage face debilitating symptoms and a significantly higher risk of death from liver failure. The increasing prevalence of liver damage is driven in part by lifestyle issues; the most common cause of liver damage in the United States is excessive alcohol intake, but a high-fat diet can also contribute to the condition, especially when it leads to obesity. Liver damage is also associated with inflammatory bowel diseases (IBDs) and some of the inflammation-related pathological processes underpinning IBDs, such as ulcerative colitis and Crohn’s disease, are linked to the development of liver disorders. Moreover, recent research indicates that the drugs used to treat IBDs, including immunosuppressants and biologics, can also lead to liver damage.
Regardless of the cause of the liver damage, the health risks are serious, spurring patients to look for ways to support normal functioning and protect against the development of cirrhosis. Unfortunately, depending on the cause of the liver damage, therapeutic options are limited, which has led to growing research interest in the field. Currently, one particular target of research interest is alcohol dehydrogenase, an enzyme found primarily in the liver.
Alcohol dehydrogenase is responsible for catalyzing the oxidation and reduction of various alcohols and aldehydes (organic molecules similar to alcohols, but with a slightly different molecular structure). That makes alcohol dehydrogenase a key player in the detoxifying processes that protect the liver from damage. More specifically, when high levels of toxins like alcohols, “unhealthy” dietary fats, and certain medications reach the liver, they can contribute to the production of free radicals that aggravate inflammation and directly damage hepatic tissue. The activities of alcohol dehydrogenase resist these effects and limit damage.
Emerging research suggests that curcumin, the active compound in turmeric, supports the activity of alcohol dehydrogenase in a way that helps maintain a healthy liver. Although clinical trials have yet to be conducted, there are several early studies in mice that offer key insight into the mechanisms through which all-natural curcumin supplements could provide protective benefits.
The first indication there might be a relationship between alcohol dehydrogenase and curcumin came in 2011 when a group of Japanese scientists published an article in the Proceedings of the Natural Academy of Sciences of the United States (PNAS) describing their discovery of the curcumin metabolic pathway in an intestinal microorganism. Intriguingly, the unique curcumin-metabolizing enzyme they found (which they called NADPH-dependent curcumin/dihydrocurcumin reductase, or CurA), bore a significant sequence similarity to well-known enzymes in the alcohol dehydrogenase family. This finding provided the first indication that it could be possible for curcumin to interact directly with the alcohol dehydrogenase enzymes in the human liver.
The strongest evidence for a direct relationship between curcumin and alcohol dehydrogenase, however, came in 2013, when a group of researchers from several universities in South Korea collaborated on an effort to investigate the protection that low doses of curcumin could provide against liver damage caused by chronic alcohol intake and a high-fat diet. To explore this question, they treated mouse models on high-alcohol, high-fat diets with two different doses of curcumin (0.02 percent and 0.05 percent body weight) for six weeks. At both levels, they observed significant effects. In addition to reducing the activity of the enzymes known to contribute to liver damage, the curcumin supplements restricted the alcohol-induced inhibition of alcohol dehydrogenase activity to a statistically significant degree. Notably, curcumin supplementation also led to significant declines in plasma levels of leptin, free fatty acids, and triglyceride levels, all of which contribute to inflammation and liver damage. These results serve as preliminary evidence that by modulating key enzymes like alcohol dehydrogenase, curcumin supplements can effectively support liver health.
The results of the 2013 study were later supported by a paper out of George Washington University, in which the researchers again reported a connection between supplementary curcumin intake and liver damage in mouse models. Like the Korean researchers, the research team from George Washington set out to explore this connection by treating mice on high-fat, high-alcohol diets with curcumin, this time with supplements of 150 mg/kg/day, daily for eight weeks. At the end of the intervention period, they found that the mice in the treatment group were protected from ethanol-induced hepatic steatosis (that is, the accumulation of fatty tissue in the liver) and displayed lower levels of oxidative stress and liver injury markers (as measured in blood samples) than those that did not take the supplements. Thus, like previous researchers, they concluded that curcumin supplements can offer protection from liver damage.
Like the research community, more patients and practitioners than ever are intrigued by the hepatoprotective benefits that curcumin can provide, partially through its mediation of the alcohol dehydrogenase enzymes in the liver. For patients who are seeking to avoid the health risks of liver damage—whether it is associated with alcohol intake, dietary fats, medications, or inflammatory bowel conditions—a curcumin supplement might offer therapeutic benefits. In the future, clinical research will likely shed more light on the effects in humans, but for now, the animal studies suggest that curcumin supplements are worth exploring.
As patients and practitioners work together to develop a curcumin supplementation strategy to support liver health, it is important to choose a curcumin supplement with high bioavailability. Even though the Korean researchers reported that the mice in the study were treated with “low-dose” curcumin supplements, curcumin is well-known for low bioavailability, meaning it is poorly absorbed in the GI tract. This means its impact on the body can be limited by its formulation, even when it is taken in higher amounts. To maximize the likelihood that a curcumin supplement will be absorbed, metabolized, and provide the desired protective benefits, patients and practitioners should therefore look for curcumin supplements that are specifically designed for optimal bioavailability.
The power of Tesseract supplements lies in enhancing palatability, maximizing bioavailability and absorption, and micro-dosing of multiple nutrients in a single, highly effective capsule. Visit our website for more information about how Tesseract’s products can help support your hepatic health.*
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