FAQ – Supernine

In 2018, Professor Ketan Patel's team from Cambridge, UK, published in the top academic journal Nature, found that after knocking out the ALDH2 gene in mice, the DNA became unstable because alcohol and its metabolite (acetaldehyde) failed to degrade in time. This, in turn, can lead to a marked decrease in the activity of hematopoietic stem cells and even increase the risk of cancer.

It's worth noting that the ALDH2 gene that was knocked out in the study, in 540 million people around the world, already carries a mutation that does not clear acetaldehyde. Also, Asians make up a large portion of the population.

Therapy

Test the metabolic capacity of the liver

我们喝下去的酒，会被口腔、胃、小肠快速吸收，通过呼吸和排尿大概可以排出10%，其余会通过血液循环到达肝脏。所以，“解酒”最重要的就是考验肝脏的代谢能力。肝脏对酒精（乙醇）的代谢会经过一系列复杂的转化—

1. Alcohol (ethanol) converts to acetaldehyde under the action of ADH (ethanol dehydrogenase) and NAD+ (nicotinamide adenine dinucleotide);

2. Acetaldehyde is converted to acetic acid by ALDH2 (acetaldehyde dehydrogenase 2) and NAD+;

3. Acetic acid enters the tricarboxylic acid cycle and, after a series of reactions, is converted to carbon dioxide and water.

Among these, the most harmful to health is the toxic acetaldehyde, ALDH2 deletion or mutation, will make the liver to acetaldehyde metabolism pathway blocked. As a result, excess acetaldehyde is present in the liver, and when it encounters a protein, it binds forcibly to form an acetaldehyde protein adduct.

Acetaldehyde robbed apolipoprotein, will block the transport of fat, resulting in fat backlog in the liver cells, the formation of alcoholic fatty liver;

Acetaldehyde harms the proteins on the liver cell membrane, which is easy to induce inflammation, leading to alcoholic hepatitis;

Acetaldehyde protein adducts also speed up the process of liver fibrosis, which, if allowed to progress, can lead to the dreaded cirrhosis of the liver.

In fact, even for those who are heavy drinkers, long-term or excessive drinking that exceeds the liver's metabolic capacity will inevitably lead to liver damage over time. Alcohol reduces NAD+ levels in the liver We already know that NAD+ is required in the liver to metabolize alcohol. NAD+ is also known as coenzyme 1. As the "number one coenzyme", it is involved in a number of important biochemical reactions in the human body, including REDOX reaction, metabolism and DNA repair mechanism. The Sirtuins family, known as longevity proteins, are also highly dependent on NAD+. The decline in NAD+ levels in our bodies is thought to be one of the key causes of aging in humans. If the liver is always busy metabolizing alcohol, lower levels of NAD+ in the liver are thought to be important factors in inducing steatosis, oxidative stress, fatty liver, insulin resistance and gluconeogenesis inhibition. It seems that the wine drunk not only hurt liver, but also "urge people old".

Supplementary NMN

Helps "cure alcohol and protect liver"

In this case, is NAD+ useful? The researchers believe that taking NMN (nicotinamide mononucleotide), a precursor of NAD+, can rapidly increase the level of NAD+ in the liver and accelerate the catabolism of alcohol, thus playing a role in rapid hangover. However, more important than "cure" is "protect the liver". In 2019, Kristofer S. Fritz et al. from the University of Colorado, USA, found that NMN can increase the level of NAD+ in the liver of experimental mice, and has a protective effect on the liver.

When mice with alcoholic liver disease were fed 500mg/kg of NMN every other day, levels of NAD+ and a range of precursor substances returned to control levels. In addition, NMN prevented the elevation of ALT and AST, two biomarkers of liver injury in plasma, suggesting that NMN had a protective effect on alcohol-induced liver injury. Using RNA sequence analysis, they also found that ethanol significantly altered the expression of 1,778 genes, of which NMN treatment reduced the effect of ethanol on 25% (437 genes). These results suggest that NMN is of great significance in the treatment of alcoholic fatty liver disease.