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

Alcohol has a potent diuretic effect related to ethanol’s inhibition of the antidiuretic hormone (ADH). By blocking the action of this hormone, which is essential for water reabsorption by the kidneys, alcohol increases urine volume and speeds up fluid loss. Meanwhile, it promotes exudation and water loss through evaporation, further exacerbating the body’s overall dehydration. This does not spare the skin and compromises the skin barrier. Alcohol-induced dehydration particularly impacts the lips, which are highly sensitive as they lack sebaceous glands, the structures responsible for sebum production. The lips then tend to become chapped. As fluid losses intensify, the complexion may appear more uneven and discomfort may increase, especially in individuals already prone to dry skin or tightness.

Any advice on alleviating skin dehydration caused by excessive alcohol consumption?

To prevent your skin from becoming dehydrated following excessive alcohol intake, the best approach is, of course, to limit alcohol consumption. Otherwise, during an alcohol-fuelled evening, be 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 moisturising cream suited to your skin type. For example, you may choose to use our hydrating serum with hyaluronic acid, our plumping serum with polyglutamic acid, or even our biphasic repairing serum.

If skin ageing is primarily accelerated by UV rays, excessive alcohol consumption acts as an aggravating factor, much like an unbalanced diet. Indeed, alcohol provides calories devoid of nutrients, leading to significant metabolic stress in the body. Its breakdown by the liver consumes a vast amount of energy resources and generates reactive oxygen species, which cause oxidative stress that disrupts cellular regeneration. In the long term, this metabolic overload induces systemic fatigue and slows down keratinocyte turnover, rendering the skin duller, thinner and less resilient.

The connection between excessive alcohol intake and accelerated biological ageing was demonstrated in a study involving 308 men with alcohol-use disorders and 255 healthy controls. Telomere length, the repetitive DNA regions at the ends of chromosomes and regarded as a biomarker of ageing, was measured in a subgroup of 99 patients and 99 controls matched for age and smoking status. The results show that individuals suffering from alcoholism had significantly shorter telomeres than the controls. As telomeres naturally shorten with age, their accelerated reduction under the influence of alcohol promotes premature ageing of the entire body, 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 ageing. The participants assessed their facial ageing signs using photonumeric scales, enabling a standardised evaluation of various criteria: forehead wrinkles, crow’s feet, volume loss, dark circles, nasolabial folds… After adjusting for age, country, body mass and ethnic origin, the researchers showed that alcohol consumption exceeding eight drinks per week was significantly associated with a worsening of several visible signs : increased wrinkles in the upper face, accentuation of the labial commissures, more pronounced under-eye bags, cheek volume loss and a more frequent presence of visible blood vessels.

Note : It is not merely a matter of aesthetics. Telomere shortening also increases the risks of cardiovascular disease, diabetes and dementia, serving as a reminder that alcohol’s effects extend far beyond the dermatological sphere.

Regular alcohol consumption may exacerbate various dermatoses, particularly:

• Rosacea.

  Alcohol consumption is a recognised aggravating factor for rosacea. Indeed, it stimulates the release of catecholamines via bradykinin, leading to marked vasodilation. This dilation of blood vessels, combined with a local increase in skin temperature, favours the appearance of telangiectasias and redness on the face, two typical manifestations of rosacea. Simultaneously, alcohol increases the production of pro-inflammatory cytokines, creating a favourable environment for inflammatory flare-ups.

  This relationship was confirmed by a large epidemiological study of 82,737 women conducted between 1991 and 2005. Over the 14 years of follow-up, 4,945 cases of rosacea were diagnosed, establishing a strong link between alcohol consumption and an increased risk of developing the condition. Compared with women who had never consumed alcohol, those who drank regularly showed a higher risk. The analysis by type of alcohol also showed that white wine and spirits were particularly associated with rosacea.

It would, however, be unfair to systematically associate rosacea with alcohol consumption; although alcohol can exacerbate 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. A study conducted on 87 peri-ovulatory women notably showed that alcohol consumption (0.5 g/kg) significantly increased total and free testosterone levels at 45 and 90 minutes post-ingestion, regardless of oral contraceptive use. Researchers also observed an increased testosterone/androstenedione ratio, indicating enhanced hepatic conversion of androstenedione into testosterone, likely linked to a raised NADH/NAD⁺ ratio induced by ethanol oxidation. Theoretically, this mechanism could promote an excess of androgens, hormones that have a tendency to stimulate sebum production, a key factor in the pathogenesis of acne.

  Studies specifically examining the link between alcohol and acne do not, however, all point in the same direction. Some report no clear association, whereas others suggest a potential link. A cross-sectional study involving 3,888 participants aged 17 to 71 demonstrated that alcohol consumption was associated with more severe acne, with an almost 50% increase in risk. Although this association does not establish causality and the data remain heterogeneous, it underscores the need for further investigation into the impact of alcohol on hormonal balance and on the onset and exacerbation of acne.

• Eczema.

  The relationship between alcohol and eczema is fairly complex. Several studies have investigated 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 showed that maternal alcohol consumption was significantly associated with an increased risk of eczema in the infant. Some studies even observe a dose-dependent relationship.

  From a mechanistic standpoint, newborns naturally exhibit an immune response biased towards the Th2 axis during the first months of life, until the Th1/Th2 balance is restored. Maternal alcohol consumption may exacerbate this imbalance by further promoting Th2 polarisation, a mechanism known to increase susceptibility to atopic diseases. Another line of enquiry suggests alcohol-induced elevations in immunoglobulin E (IgE): studies have demonstrated a correlation between alcohol intake during pregnancy and higher IgE levels in cord blood, suggesting a potentiation of the allergic response at birth.

  Among 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 analysing eight observational studies. However, more recent data from a large cross-sectional study conducted in the Netherlands, involving 56,896 participants, show that consuming more than two alcoholic drinks per day is associated with moderate-to-severe atopic dermatitis, whereas lower levels of consumption do not appear to be related to the disease.

• Psoriasis.

  As a reminder, the psoriasis is an inflammatory autoimmune disease that causes thick, scaly plaques on the skin. Several studies have suggested that alcohol may be an environmental factor favouring the expression of this dermatosis. 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 Th1 and Th17 pathways, involved in psoriasis.

  A large prospective cohort comprising 82,869 women and 1,150 psoriasis cases confirms this association. Analysis by beverage type reveals a notable point: only beer consumption is significantly associated with psoriasis risk, whereas wine and distilled spirits do not increase the risk. This specificity suggests a potential role of non-alcoholic components of regular beer (gluten, polysaccharides, phytoestrogens, barley derivatives…) that may exacerbate the immune imbalance in predisposed individuals.

• Porphyria cutanea tarda.

  Alcohol consumption is the most frequent cause of porphyria cutanea tarda (PCT). This condition causes painful, blistering lesions on the skin after sun exposure. The disease arises from a decrease in uroporphyrinogen decarboxylase enzyme activity, leading to an accumulation of photosensitising porphyrins. PCT may be hereditary (20%) or acquired (80%), the latter being strongly associated with certain external factors, including alcohol intake. Alcohol increases the risk by impairing hepatic uroporphyrinogen decarboxylase activity and promotes a liver iron overload, an essential co-factor in the formation of toxic porphyrins.

Excessive alcohol consumption "marks" the skin visibly, due to its vascular, inflammatory and metabolic effects. As a potent vasodilator, alcohol induces rapid dilation of peripheral vessels, resulting in diffuse redness on the face, neck and hands. This repeated surge of blood progressively renders the vessels more visible at the surface, particularly on the sides of the nose and cheeks. Additionally, alcoholic beverages are high in sugars and lead to elevated circulating glucose levels, a phenomenon that disrupts cellular regeneration and can impair skin tone uniformity. The skin then appears more dull, with more pronounced dark circles , sometimes accompanied by swelling related to systemic inflammation.

Alcohol may also be implicated in pigmentary disorders, particularly when its consumption is associated with hepatic impairment. Some people with alcohol-related liver disease develop increased pigmentation, notably on the legs, around the eyes and mouth. The precise mechanisms are not fully elucidated, but appear linked to a increase in melanin within melanosomes. Moreover, alcohol enhances iron absorption and may contribute to acquired haemochromatosis, a condition in which excess iron induces a widespread brown-grey hyperpigmentation, particularly visible on sun-exposed areas. In these cases, the skin appears not only darker but also drier and scaly.

Excessive alcohol consumption is frequently associated with episodes of pruritus, particularly when cholestasis related to alcoholic liver disease occurs. These manifestations reflect the indirect yet profound impact of alcohol on the skin barrier and on the neural pathways involved in itch perception. The pathophysiology of pruritus in this context remains complex. The mechanism is thought to involve activation of unmyelinated C fibres specifically dedicated to conveying itch sensation. An accumulation of circulating ‘pruritogens’ appears to be responsible, although their exact nature remains unknown. Bile acids are among the most suspected molecules, as are certain cortisol metabolites and histamine.

Still poorly understood, alcohol-induced pruritus is also difficult to alleviate.

Finally, scientific literature shows that alcohol can contribute to an increased risk of skin cancers, particularly melanoma, the most severe form. When metabolised by the liver, ethanol is converted into acetaldehyde (AcAH), a compound capable of reacting with DNA and proteins and causing mutations likely to facilitate carcinogenesis. Some of this circulating ethanol and AcAH reaches the skin, where they are normally neutralised by enzymes. However, when these become less active – as observed in melanoma tissues, with a marked reduction in the expression of ADH1B, CYP2E1 and CAT – the skin becomes more susceptible to ethanol and AcAH toxicity. This alteration of cutaneous metabolism promotes oxidative stress, DNA damage and disruptions in the signalling pathways involved in melanocyte survival and transformation.

Epidemiological data confirm this association: nearly half of the available studies demonstrate a link between alcohol consumption and an increased risk of melanoma, and over 60% observe a dose-dependent effect.

Beyond tumour initiation, alcohol also appears to play a role in melanoma progression. Research using animal models demonstrates that ethanol and AcAH can promote metastasis by remodelling the tumour microenvironment. Alcohol notably reduces the number of CD8+ lymphocytes and NK cells, activates the inflammasome, stimulates HIF-1 expression and favours the degradation of the extracellular matrix via the increase in metalloproteinases. These mechanisms, combined with reduced expression of ethanol-metabolising enzymes in melanoma tissues, create a favourable environment for tumour progression.

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