What are the effects of excessive alcohol consumption on the skin?

Alcohol has a potent diuretic effect linked to the inhibition of antidiuretic hormone (ADH) by ethanol. By blocking this hormone’s action, which is essential for water reabsorption in the kidneys, alcohol increases urine volume and accelerates fluid loss. At the same time, it stimulates exudation and water loss through evaporation, further exacerbating the body’s overall dehydration. This dehydration does not spare the skin and weakens the skin barrier. Alcohol-induced dehydration particularly affects the lips, which are highly sensitive because they lack sebaceous glands, the organs that produce sebum. The lips then tend to chap. As fluid losses intensify, the complexion may appear more uneven and the sensation of discomfort can increase, especially in individuals already prone to dry or tight-feeling skin.

What recommendations can help mitigate skin dehydration caused by excessive alcohol consumption?

To prevent your skin from becoming dehydrated due to excessive alcohol consumption, the most effective strategy is obviously to limit your intake. Otherwise, during a night of heavy drinking, make sure to drink a glass of water between each alcoholic beverage to reduce the risk of dehydration. Before going to bed, remember to thoroughly hydrate your skin with a serum paired with a moisturizing cream adapted to your skin type. For example, you can use our hydrating serum with hyaluronic acid, our plumping serum with polyglutamic acid, or our bi-phase repairing serum.

If skin aging is primarily accelerated by UV rays, excessive alcohol consumption serves as an aggravating factor, much like an imbalanced diet. Indeed, alcohol delivers calories devoid of nutrients, which leads to a significant metabolic stress in the body. Its breakdown by the liver consumes a great deal of energy resources and generates reactive oxygen species, responsible for oxidative stress that disrupts cellular regeneration. Over the long term, this metabolic overload induces systemic fatigue and slows the turnover of keratinocytes, leaving the skin duller, thinner, and less resilient.

The link between excessive alcohol consumption and accelerated biological aging has been demonstrated in a study of 308 men with alcohol‐related disorders and 255 healthy controls. Telomere length, the repetitive DNA regions at the ends of chromosomes and considered a biomarker of aging, was measured in a subgroup of 99 patients and 99 age- and smoking-status-matched controls. The results show that individuals with alcoholism exhibited significantly shorter telomeres than the controls. Because telomeres naturally shorten with age, their accelerated shortening due to alcohol contributes to premature aging of the entire organism, including the skin.

Another large-scale study, this time conducted with 3,267 women aged 18 to 75, also confirms the direct impact of excessive alcohol consumption on facial aging. Participants assessed their facial aging signs using photonumeric scales, allowing for a standardized evaluation of various criteria: forehead wrinkles, crow’s feet, volume loss, dark circles, and nasolabial folds. After adjusting for age, country, body mass index, and ethnicity, the researchers showed that consuming more than eight drinks per week was significantly associated with a worsening of several visible signs : increased upper-face wrinkles, accentuated mouth corners, more pronounced under-eye bags, cheek volume loss, and an increased occurrence of visible blood vessels.

Note : It’s not just about aesthetics. Telomere shortening also increases the risk of cardiovascular disease, diabetes, and dementia, underscoring that alcohol’s effects extend far beyond the dermatological sphere.

Regular alcohol consumption can be an exacerbating factor in various dermatoses, including:

• Rosacea.

  Alcohol consumption is a recognized aggravating factor for rosacea. Indeed, it stimulates the release of catecholamines via bradykinin, leading to pronounced vasodilation. This vascular dilation, combined with a local rise in skin temperature, promotes the appearance of telangiectasias and facial redness, two hallmark manifestations of rosacea. At the same time, alcohol increases the production of pro-inflammatory cytokines, creating a favorable environment for inflammatory flare-ups.

  This relationship was confirmed by a large epidemiological study conducted among 82,737 women between 1991 and 2005. Over a 14-year follow-up period, 4,945 cases of rosacea were diagnosed, establishing a strong link between alcohol consumption and an increased risk of developing the disease. Compared with women who had never consumed alcohol, regular drinkers showed a higher risk. Analysis by alcohol type also revealed that white wine and spirits were particularly associated with rosacea.

However, it would be unfair to automatically link rosacea to alcohol consumption: although alcohol can exacerbate the symptoms, the vast majority of rosacea cases arise independently of any alcohol intake.

• Acne.

  The acne is the most common skin disease worldwide, affecting both adolescents and adults. Several studies suggest that alcohol may influence certain hormonal mechanisms involved in its onset or exacerbation. Notably, a study in 87 periovulatory women showed that alcohol consumption (0.5 g/kg) significantly increased total and free testosterone levels at 45 and 90 minutes post-ingestion, whether or not they were using oral contraception. Researchers also observed an increased testosterone/androstenedione ratio, suggesting enhanced hepatic conversion of androstenedione to testosterone, likely linked to an ethanol-oxidation–induced rise in the NADH/NAD⁺ ratio. This mechanism could theoretically promote excess androgens, hormones that tend to stimulate sebum production, a key element in the pathogenesis of acne.

  Studies specifically focused on the link between alcohol and acne do not all point in the same direction. Some find no clear association, while others suggest a potential connection. A cross-sectional study involving 3,888 participants aged 17 to 71 showed that alcohol consumption was associated with more severe acne, with nearly a 50% increased risk. Although this relationship does not establish causality and the data remain heterogeneous, it underscores the importance of further exploring alcohol’s impact on hormonal balance and on the onset and exacerbation of acne.

• Eczema.

  The relationship between alcohol and eczema is fairly complex. Several studies have examined the impact of alcohol consumption during pregnancy on the risk of atopic dermatitis in the child. A meta-analysis combining three neonatal cohorts and a cross-sectional study found that maternal alcohol consumption was significantly associated with an increased risk of eczema in the infant. Some studies even observe a dose-dependent relationship.

  Mechanistically, newborns naturally exhibit an immune response biased toward the Th2 axis during the first months of life, until the Th1/Th2 balance is restored. Maternal alcohol intake may exacerbate this imbalance by further promoting Th2 polarization, a mechanism known to increase susceptibility to atopic diseases. Another proposed pathway involves alcohol-induced increases in immunoglobulin E (IgE): studies have found a correlation between alcohol consumption during pregnancy and higher IgE levels in cord blood, suggesting a potentiation of the allergic response at birth.

  In adolescents and adults, the findings are less consistent. A review concluded that there was no clear association between the atopic dermatitis and alcohol consumption after analyzing eight observational studies. However, more recent data from a large cross-sectional study conducted in the Netherlands, including 56,896 participants, indicate that consuming more than two alcoholic drinks per day is associated with moderate-to-severe forms of atopic dermatitis, whereas lower consumption levels do not appear to be linked to the disease.

• Psoriasis.

  As a reminder, psoriasis is an autoimmune inflammatory disease that causes thick, scaly plaques on the skin. Several studies have suggested that alcohol could act as an environmental factor promoting the expression of this skin disorder. Indeed, ethanol disrupts innate and adaptive immunity: its metabolite, acetaldehyde, stimulates the production of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) by monocytes, macrophages, and dendritic cells, which maintains the activation of the Th1 and Th17 pathways, involved in psoriasis.

  A large prospective cohort of 82,869 women, including 1,150 psoriasis cases, confirms this association. Beverage-specific analysis reveals a key finding: only beer consumption is significantly associated with psoriasis risk, while wine and distilled spirits show no increased risk. This specificity suggests a potential role of non-alcoholic components in conventional beer (gluten, polysaccharides, phytoestrogens, barley derivatives...) that may exacerbate immune imbalance in predisposed individuals.

• Porphyria cutanea tarda.

  Alcohol consumption is the most common cause of porphyria cutanea tarda (PCT). This condition produces painful, blistering lesions on the skin after sun exposure. The disease results from a decrease in the activity of the enzyme uroporphyrinogen decarboxylase, leading to an accumulation of photosensitizing porphyrins. PCT may be hereditary (20%) or acquired (80%), the latter being strongly linked to certain external factors, including alcohol intake. Alcohol raises the risk because it lowers hepatic uroporphyrinogen decarboxylase activity and promotes a iron overload in the liver, an essential cofactor in the formation of toxic porphyrins.

Excessive alcohol consumption leaves a visible “mark” on the skin due to its vascular, inflammatory, and metabolic effects. As a potent vasodilator, alcohol induces a rapid dilation of peripheral blood vessels, leading to diffuse redness on the face, neck, and even the hands. This repeated blood surge gradually makes the vessels more visible at the surface, especially along the sides of the nose and the cheeks. Moreover, alcoholic beverages are high in sugars and cause an increase in circulating glucose levels, a phenomenon that disrupts cellular regeneration and can compromise skin tone uniformity. The skin then appears more dull, with dark circles more pronounced, sometimes accompanied by swelling due to systemic inflammation.

Alcohol can also be involved in pigmentary disorders, especially when its consumption is associated with liver damage. Some individuals with alcohol‐related liver disease develop increased pigmentation, notably on the legs, around the eyes, and around the mouth. The precise mechanisms are not fully understood but appear linked to a increase in melanin within melanosomes. In addition, alcohol enhances iron absorption and can contribute to acquired hemochromatosis, a condition in which excess iron induces diffuse brown‐gray hyperpigmentation, particularly noticeable on sun‐exposed areas. In these cases, the skin appears not only darker but also drier and scaly.

Excessive alcohol consumption is often associated with episodes of pruritus, especially when cholestasis due to alcoholic liver disease develops. These manifestations reflect the indirect but profound impact of alcohol on the skin barrier and on the neural pathways involved in itch perception. The pathophysiology of pruritus in this setting remains complex. The mechanism is thought to involve activation of unmyelinated C fibers specifically dedicated to itch sensation. An accumulation of circulating "pruritogens" is implicated, although their exact identity is not known. Bile acids are among the most suspected molecules, along with certain cortisol metabolites and histamine.

Still poorly understood, pruritus associated with alcohol consumption is also difficult to alleviate.

Finally, the scientific literature shows that alcohol can contribute to increasing the risk of skin cancers, particularly melanoma, the most severe form. When metabolized by the liver, ethanol is converted into acetaldehyde (AcAH), a compound that can react with DNA and proteins and cause mutations that may promote carcinogenesis. A portion of this circulating ethanol and AcAH reaches the skin, where they are normally neutralized by enzymes. However, when these become less active, as observed in melanoma tissues—with a notable reduction in the expression of ADH1B, CYP2E1, and CAT—the skin becomes more vulnerable to the toxicity of ethanol and AcAH. This altered cutaneous metabolism promotes oxidative stress, DNA damage, and disruptions in the signaling pathways involved in melanocyte survival and transformation.

Epidemiological data confirm this association: almost half of the available studies show a link between alcohol consumption and an increased risk of melanoma, and more than 60% of the research observes a dose-dependent effect.

Beyond tumor initiation, alcohol also appears to contribute to melanoma progression. Animal model studies show that ethanol and AcAH can promote metastasis by remodeling the tumor microenvironment. Alcohol notably reduces the number of CD8+ lymphocytes and NK cells, activates the inflammasome, stimulates HIF-1 expression, and promotes extracellular matrix degradation via increased metalloproteinase activity. These mechanisms, combined with reduced expression of ethanol-metabolizing enzymes in melanoma tissues, create a conducive environment for tumor progression.

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