How does alcohol affect men's health?

Chronic alcohol use wreaks havoc on metabolism and male fertility: Explore the hidden mechanisms that link liver damage, hormonal imbalances, and reproductive health, and understand why it's time to rethink your relationship with alcohol.

In a recent review published in the journal Metabolites, researchers from Italy examined how alcohol consumption affects metabolism and male reproductive health, focusing on its role in liver function, lipid metabolism, and testosterone production. They highlighted the risks associated with chronic alcohol use and the need for further research to address existing inconsistencies, particularly with regard to individual variability, genetic predisposition, and the influence of other factors.

Moderate Alcohol Consumption and Antioxidant Effects: Although heavy alcohol consumption has been shown to negatively impact sperm quality and testosterone production, moderate consumption may have antioxidant benefits due to compounds such as polyphenols in wine and beer. However, this potential effect remains controversial and requires further study.

Alcohol dependence is a global health problem associated with 5-8% of deaths worldwide and an increased risk of metabolic disorders. Long-term alcohol abuse contributes to more than 200 diseases, including various types of cancer. It impairs the functioning of many organs, including the brain, endocrine system, liver, heart, and digestive system, and interferes with nutrient metabolism.

In this review, researchers examined the impact of alcohol on male reproductive health and the gonadal axis, focusing on the complex physiological and pathological mechanisms of alcohol metabolism and its interactions with other lifestyle factors such as diet and physical activity.

Alcohol and Metabolic Health

Alcohol metabolism begins with absorption in the stomach and small intestine and is then processed in the liver via oxidative and non-oxidative pathways. In oxidative metabolism, enzymes such as alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) convert alcohol into acetaldehyde and acetate, generating reactive oxygen species (ROS) and contributing to oxidative stress and inflammation.

Nonoxidative pathways generate metabolites such as fatty acid ethyl esters and phosphatidylethanol. Individual metabolic efficiency depends on factors such as genetics, diet, comorbidities, and frequency and volume of alcohol consumption.

Chronic alcohol consumption is associated with a variety of diseases, including metabolic syndrome, type 2 diabetes, fatty liver disease, and alcoholic liver disease (ALD). ALD can progress from reversible fatty liver disease to severe conditions such as alcoholic hepatitis, cirrhosis, and hepatocellular carcinoma.

Alcohol worsens insulin resistance, mitochondrial dysfunction, and oxidative stress by disrupting lipid metabolism and promoting inflammation. Some studies suggest that light to moderate alcohol consumption may reduce the risk of type 2 diabetes, but excessive consumption causes liver damage and metabolic dysfunction through impaired insulin signaling, oxidative stress, and dysregulation of cellular pathways.

Chronic alcohol consumption causes significant liver dysfunction through excess acetaldehyde formation, oxidative stress, lipid metabolism disorders and apoptosis.

Alcohol abuse also disrupts the balance of gut microbiota and increases intestinal permeability, leading to increased levels of lipopolysaccharides (LPS), which activate immune cells and induce liver cell apoptosis, contributing to the development of severe alcoholic hepatitis.

Recent evidence also suggests that alcohol-induced mitochondrial dysfunction exacerbates apoptosis and impairs liver regeneration.

In addition, alcohol disrupts lipid and carbohydrate metabolism, impairing fatty acid oxidation, gluconeogenesis, and mitochondrial homeostasis, leading to liver fat accumulation and glucose intolerance. This metabolic disruption contributes to inflammatory cascades, oxidative damage, and epigenetic changes that may underlie alcohol-induced metabolic syndrome.

The Effect of Alcohol on Testosterone Production

Impact on adolescent reproductive health: The effects of alcohol on testosterone production and male fertility during adolescence, an important developmental period, remain poorly understood, indicating a significant research gap.

Alcohol consumption affects testosterone production through complex mechanisms. Acute alcohol consumption can reduce testosterone levels by depleting NAD+, suppressing gonadotropins and disrupting steroidogenesis, and altering the hypothalamic-pituitary-gonadal (HPG) axis.

Chronic alcohol use tends to lower testosterone levels, with liver damage and hormonal imbalances (such as elevated estrogen) making matters worse. A meta-analysis found that chronic alcohol use reduced serum testosterone levels by an average of 4.86 nmol/L compared to abstainers.

Alcohol abuse, especially binge drinking, often results in feminization symptoms due to hyperestrogenism and oxidative damage to Leydig cells. These effects depend on the dose of alcohol, liver function, and individual factors. It is important to note that the effects of alcohol on testosterone production during adolescence require further study.

The Effect of Alcohol on the Male Reproductive System

Alcohol consumption negatively impacts male fertility, particularly through its effects on spermatogenesis. Acute alcohol consumption may impair sperm production by increasing oxidative stress and impairing Sertoli cell function, although results from human studies are inconsistent. Chronic alcohol consumption is more clearly associated with decreased sperm quality, including decreased sperm volume, concentration, and morphology.

Some evidence suggests possible antioxidant benefits of moderate alcohol consumption, but these results remain inconclusive and context-dependent. Heavy alcohol consumption causes significant testicular damage, including spermatogenesis arrest and Sertoli cell-only syndrome. However, the damage may be reversible upon cessation of alcohol consumption.

A major limitation of the studies is the failure to account for factors such as smoking, drug use, and comorbidities, making it difficult to draw conclusions about the effects of alcohol on fertility.

In conclusion, the review highlights the negative impact of chronic alcohol consumption on testicular metabolism and function, including hormonal disturbances, impaired spermatogenesis and deterioration of sperm quality.

In addition, alcohol abuse increases intestinal permeability and causes inflammation by activating LPS and acetaldehyde-induced inflammation, mitochondrial dysfunction and oxidative stress, which contribute to the development of alcoholic fatty liver disease.

These data may inform public health strategies by highlighting the importance of distinguishing between moderate, acute and chronic alcohol consumption, and the need for further research to develop clinical guidelines and preventive measures.