Stopping alcohol consumption: benefits for the skin.

The consumption of alcohol affects the skin indirectly by disrupting the function of several organs, particularly the liver, which handles over 80% of its metabolism. Ethanol is converted there into acetaldehyde, a highly toxic molecule, then into less harmful compounds through successive enzymatic reactions. This process is especially energy-intensive and uses up many micronutrients, including minerals and antioxidants. These then become less available to protect the skin from oxidative stress and from photoageing. As a result, cutaneous cell turnover is slowed, dead cells accumulate, the complexion becomes duller and signs of ageing, such as wrinkles and fine lines, may appear prematurely.

Moreover, alcohol has a diuretic effect that promotes dehydration of the body, and therefore of the skin. This can result in a loss of suppleness and elasticity, with the onset of tightness and dry patches. The alcohol is also a potent vasodilator: when consumed repeatedly, it can induce a sustained dilation of the facial blood vessels, leading to redness or exacerbating that caused by rosacea. Finally, alcohol can alter hormonal balance by raising estradiol and testosterone levels, which stimulates sebum production by the sebaceous glands. Excessive sebum secretion then promotes pore blockage and the appearance of blemishes.

The link between excessive alcohol consumption and skin disorders should not be overlooked.

Stopping alcohol consumption is generally accompanied by a gradual improvement in skin condition, largely due to decreased oxidative stress. During its metabolism, alcohol generates excess free radicals, which exceed the body's antioxidant defences and weaken the skin barrier. This oxidative assault contributes to dryness, redness, chronic inflammation and the premature appearance of wrinkles. By stopping alcohol consumption, this oxidative burden gradually decreases, allowing the skin to return to a more favourable environment for its renewal and repair.

Some skin changes associated with alcohol appear to be at least partially reversible. In a murine model, ethanol consumption–induced cutaneous hyperpigmentation was observed in mice with reduced activity of the ALDH2 enzyme, which is responsible for acetaldehyde elimination. This pigmentation, linked to deposits of melanin in the epidermis, increased with the amount of alcohol consumed but regressed after ethanol withdrawal. These findings suggest that some alcohol-associated pigmentary alterations may fade when exposure ceases, even though this phenomenon has not been clearly documented in humans.

However, skin improvement after ceasing alcohol consumption is far from immediate. Studies in rats show that several cutaneous parameters altered by chronic alcohol intake, such as increased transepidermal water loss, changes in blood circulation, impairment of the skin barrier or lipid peroxidation, can persist for several weeks after cessation. These data suggest that alcohol induces profound structural and functional changes in the skin, the normalisation of which requires time.

Thus, while stopping alcohol consumption represents a first step towards improving skin quality, visible benefits appear progressively, at the pace of skin regeneration and the rebalancing of physiological functions.

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