Why do some people’s faces turn red?

Cause No. 1 of facial redness: rosacea.

The rosacea is a chronic skin condition that primarily presents as diffuse facial erythema, often localized on the cheeks, nose, forehead, and chin. This dermatosis frequently affects fair skin types and typically manifests in adulthood, around the age of thirty. Rosacea is characterized by a persistent or intermittent dilation of the superficial blood vessels, giving the face a red and sometimes warm appearance. Papules, pustules, and tingling sensations may also accompany these erythematous areas.

Good to know : There are several forms of rosacea. When it is limited to redness, it is called couperose. When papules and/or pustules appear, it is referred to as papulopustular rosacea.

Triggering factors for rosacea are numerous and can vary among individuals. Genetics, sun exposure, temperature fluctuations, certain spicy foods, alcohol, or even stress can provoke flare-ups. It should be noted that rosacea tends to progress over time and follows cyclical patterns. Thus, symptoms may persist for weeks or months before subsiding and then reappear more intensely. To date, medical treatments for rosacea (laser therapy, anti-inflammatory creams…) primarily serve to reduce symptoms and lengthen intervals between flare-ups, but cannot completely cure the condition.

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5.46%

Global prevalence of rosacea (a review that included 32 studies and 26,519,836 participants).

Cause No. 2 of facial redness: eczema.

Eczema, particularly atopic eczema, is a common cause of facial redness, affecting both children and adults. This chronic inflammatory condition presents as red patches, often accompanied by intense itching, significant dryness and sometimes small vesicles. On the face, these lesions most often appear on the cheeks, eyelids, or around the mouth. The skin then becomes more sensitive, more reactive, and more susceptible to tightness, making the daily management of redness quite challenging.

The eczema is linked to a profound impairment of the skin barrier, notably due to a lipid deficiency such as ceramides, which normally serve as intercellular cement in the stratum corneum and help limit water loss. This weakening of the skin barrier also leaves the skin highly exposed to irritants and allergens, perpetuating inflammation. The immune system also plays an important role in the pathogenesis of atopic dermatitis. Affected individuals often exhibit hyperactivity of immune cells that promotes inflammatory flares and redness. In addition to proper skin hydration, eczema is relieved by the topical application of corticosteroids, although these agents are more useful for controlling and spacing out flares than for truly curing the condition.

8.7% – 18.1%

Prevalence of eczema in children (study conducted in the United States with 102,353 children aged 17 years or younger).

10.2%

Prevalence of eczema in adults (study conducted in the United States with 27,157 adults aged 18 and older).

Cause No. 3 of facial redness: residual acne scarring.

The acne is an inflammatory disorder of the pilosebaceous follicles that affects many individuals, both during adolescence and adulthood. Its causes are multiple: excessive sebum production, thickening of the stratum corneum that obstructs pores, proliferation of Cutibacterium acnes and a more or less pronounced inflammatory response depending on the individual. On the face, the inflammatory lesions (papules, pustules, or nodules) are characterized in particular by a localized increase in redness, which reflects the intensity of the underlying inflammation. The stronger and deeper the inflammation, the greater the risk of residual marks after the lesion subsides.

80%

Adolescents are affected by acne.

20% – 30%

Young adults are affected by acne.

Inflammatory acne flare-ups can lead to persistent redness known as post-inflammatory erythema, even when the skin no longer shows active lesions.

This phenomenon is explained by the prolonged dilation of blood vessels beneath the skin and by the persistence of local inflammation, even in the absence of a pimple. Since the epidermis has been weakened by inflammation, it takes longer to restore its normal structure, making the redness more pronounced, especially in fair skin. These marks can last from several weeks up to several months, depending on the severity of the initial inflammation. The post-inflammatory erythema must not be confused with post-inflammatory hyperpigmentation, which affects darker skin phototypes : here, it is the dilation of blood vessels that is responsible, rather than a local overproduction of melanin.

Cause No. 4 of facial redness: an allergic or irritant reaction.

Facial redness can result from an allergic reaction, a mechanism involving the immune system that recognizes an allergen as a threat and triggers a excessive inflammatory response. This phenomenon, known as contact dermatitis, occurs after prior sensitization. The skin therefore reacts only upon the second contact with the allergen (nickel, fragrances, dyes, essential oils...). Various factors can cause contact dermatitis: costume jewelry, clothing, topical medications, perfumes, chemicals, cosmetics, hair care products... The redness then appears to varying extents, sometimes accompanied by itching, papules, or even mild edema, indicating that the inflammation is intensifying.

Contact eczema should be distinguished from atopic eczema: the former is acquired and can occur even without an atopic genetic background, unlike the latter.

Irritant reactions, on the other hand, do not involve the immune system: they occur when the skin is damaged by a substance that is too harsh or too concentrated. High concentrations of exfoliating agents (AHAs, BHAs…), retinoids, denatured alcohol or certain surfactants can disrupt the skin barrier and lead to redness and stinging. Irritant reactions are predominantly seen in sensitive skin, although any skin type may experience them at some point.

For allergic or irritant reactions, the resolution of redness depends on both discontinuing the offending product and on the soothing measures implemented.

Cause No. 5 of facial redness: certain emotions such as stress.

Facial flushing is sometimes simply linked to emotions. It arises from a very specific physiological mechanism. When someone experiences stress, discomfort, embarrassment, or some form of social exposure, the sympathetic nervous system activates immediately. This activation triggers rapid vasodilation of the facial blood vessels, increasing blood flow and causing redness. Brain regions involved in regulating social emotions, such as the dorsal hypothalamus and certain cerebellar areas, orchestrate this response by modulating autonomic neural activity. This involuntary mechanism can occur within seconds, independent of conscious control or reasoning: the skin responds before one is fully aware of the emotion.

Chronic stress or social anxiety significantly amplify this phenomenon. Excessive self-focused attention, fear of being judged, or negative anticipation of social interaction increase sympathetic nervous system activity, exacerbating facial vasodilation. In some cases, this flushing occurs so frequently that it shapes the emotional experience: it can intensify embarrassment and fuel a vicious cycle of anxiety, where, in addition to dreading social interaction, one also fears blushing.

Cause No. 6 of facial redness: a sunburn.

Also called actinic erythema, sunburn corresponds to a first-degree skin burn caused by erythemogenic UV rays (85% UVB and 15% UVA-II). It occurs after intense or prolonged unprotected sun exposure, although individuals with very fair (i.e., low-melanin) or sensitive skin may develop one after only a few minutes in the sun. Sunburn presents with diffuse redness, increased tenderness, sometimes itching, and, in more severe cases, blister formation.

On a biological level, actinic erythema results from an acute inflammatory reaction. Normally, during moderate sun exposure, the melanocytes produce melanin, a photoprotective pigment that migrates to the upper layers of the skin to absorb a portion of ultraviolet radiation: this is tanning. However, when the UV dose exceeds the skin’s defense capacity, this protection becomes insufficient. UVB rays then damage keratinocyte DNA and disrupt certain microRNAs which, once released, activate the production of pro-inflammatory cytokines. This inflammatory cascade causes vasodilation of the cutaneous blood vessels, accounting for the characteristic redness of sunburn.

Cause No. 7 of facial redness: cutaneous hypersensitivity.

Some individuals exhibit cutaneous hypersensitivity, that is, a reactive skin, which manifests as a tendency to flush in response to stimuli that are normally well tolerated. This skin type is characterized by a rapid and excessive activation of sensory nerve receptors. Consequently, a simple change in temperature, a slightly fragranced cosmetic product, or even the mere act of touching the face is enough to provoke a transient red patch. Hypersensitivity-related redness does not necessarily indicate a skin disorder but rather reflects excessive skin reactivity, which requires very gentle care.

38%

Prevalence of individuals with sensitive skin in the United States (a review including 26 studies and 51,783 participants).

44%

Prevalence of individuals with sensitive skin in Europe (review including 26 studies and 51,783 participants).

Cause No. 8 of facial redness: the consumption of alcoholic beverages.

In some individuals, the consumption of alcohol almost immediately triggers facial flushing, often accompanied by other symptoms such as headaches, nausea, or a general sense of discomfort. This phenomenon occurs with any alcoholic beverage, although it is more common with higher-proof drinks. It is in fact a form of ethanol intolerance, the active molecule in alcohol (C₂H₆O). Even in small amounts, ethanol can provoke this disproportionate reaction, making it a sign of metabolic hypersensitivity rather than a simple isolated skin response.

After ingestion, ethanol is primarily metabolized in the liver. The enzyme alcohol dehydrogenase (ADH) oxidizes it to acetaldehyde (C₂H₄O), a toxic compound capable of damaging cell membranes and disrupting mitochondrial function. When acetaldehyde accumulates, particularly in individuals with less efficient alcohol metabolism, it stimulates the release of histamine from mast cells. Histamine then binds to H1 receptors on endothelial cells and triggers rapid vasodilation of capillaries and an increase in blood flow in the skin. This appears visually as a sudden, pronounced facial flushing, with which the redness due to rosacea is frequently mistaken.