Facial redness: what are the causes?

The rosacea is a chronic skin condition that primarily presents as diffuse redness on the face, often concentrated on the cheeks, nose, forehead and chin. This dermatosis commonly affects fair skin and typically appears in adulthood, around the age of thirty. Rosacea is characterised by a permanent or intermittent dilation of superficial blood vessels, giving the face a red and sometimes warm appearance. Papules, pustules and tingling sensations may also accompany these flushes.

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.

The triggering factors of rosacea are multiple and can vary between individuals. Genetics, sun exposure, temperature fluctuations, certain spicy foods, alcohol or even stress may trigger flare-ups. Notably, the rosacea tends to evolve over time and follow cyclical patterns. Thus, symptoms manifest for weeks or months, then may subside before reappearing more intensely. To date, medical treatments for the rosacea (laser therapy, anti-inflammatory creams, etc.) primarily serve to reduce symptoms and prolong the intervals between flare-ups, but cannot completely cure it.

Eczema, in particular 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, marked dryness and sometimes small vesicles. On the face, these lesions most frequently appear on the cheeks, eyelids or around the mouth. The skin then becomes more sensitive, more reactive and more prone to tightness, which renders daily management of redness quite challenging.

Eczema is associated with a profound disruption 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 to 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 a crucial role in the pathogenesis of atopic dermatitis. Affected individuals often display immune cell hyperactivity, which promotes inflammatory flares and redness. In addition to adequate skin hydration, eczema is alleviated by the topical application of corticosteroids, although these primarily serve to control and prolong the intervals between flares rather than to truly cure the dermatosis.

The acne is an inflammatory disorder of the pilosebaceous follicles affecting many individuals, both during adolescence and adulthood. Its causes are diverse: excessive sebum production, a thickening of the stratum corneum that blocks the pores, a proliferation of Cutibacterium acnes and an inflammatory response that varies in intensity between individuals. On the face, the inflammatory lesions (papules, pustules or nodules) are characterised in particular by an increase in local redness, which reflects the intensity of the underlying inflammation. The stronger and deeper the inflammation, the higher the risk of residual marks after the lesion has healed.

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

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

Facial redness may result from an allergic reaction, a mechanism involving the immune system recognising an allergen as a threat and triggering an excessive inflammatory response. This phenomenon, known as contact dermatitis, occurs only after prior sensitisation. The skin therefore reacts only from the second exposure to the allergen (nickel, fragrances, dyes, essential oils…). Various factors can cause contact dermatitis: costume jewellery, clothing, topical medications, fragrances, chemicals, cosmetics, hair products… The redness then appears to varying degrees, sometimes accompanied by itching, papules or even slight swelling, 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 predisposition, unlike the latter.

Irritative reactions, meanwhile, do not involve the immune system: they occur when the skin is assaulted by a harsh or overly concentrated substance. High concentrations of exfoliating actives (AHAs, BHAs...), of retinoids, denatured alcohol or indeed certain surfactants can impair the skin barrier and lead to redness and stinging. Irritative reactions are predominantly found in sensitive skin, although all skin types may at some point experience them.

In allergic or irritant reactions, the resolution of redness depends both on discontinuing use of the responsible product and on adopting appropriate soothing measures.

Facial flushing is sometimes simply linked to emotions. It then results from a very specific physiological mechanism. When a person feels stress, discomfort, embarrassment or some form of social exposure, the sympathetic nervous system activates immediately. This activation triggers a rapid vasodilation of the facial blood vessels, increasing blood flow and causing the redness. Brain regions involved in the regulation of social emotions, such as the dorsal hypothalamus and certain areas of the cerebellum, orchestrate this response by modulating autonomic nerve activity. It is an involuntary mechanism that can occur within seconds, regardless of will or reasoning: the skin responds before one is even fully aware of one’s emotion.

Chronic stress or social anxiety markedly intensify this phenomenon. Excessive self-focus, fear of being judged or negative anticipation of a social interaction increase sympathetic nervous system activity, exacerbating facial vasodilation. In some cases, this blushing becomes so frequent that it shapes emotional experience: it can reinforce embarrassment and fuel a vicious cycle of anxiety, where, alongside dreading social interaction, one also fears blushing.

Also known as actinic erythema, sunburn corresponds to a first-degree cutaneous burn caused by erythemal UV rays (85% UVB and 15% UVA-II). It arises after intense or prolonged unprotected exposure to sunlight, although very fair-skinned or otherwise sensitive individuals with low melanin may develop it after just a few minutes in the sun. Sunburn presents with diffuse reddening, heightened sensitivity, occasional itching, and in more severe cases, blister formation.

From a biological standpoint, an 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 some ultraviolet light: this is tanning. However, when the UV dose exceeds the skin’s defence capabilities, this protection becomes insufficient. UVB rays then damage the DNA of keratinocytes and disrupt certain microRNAs which, once released, trigger the production of pro-inflammatory cytokines. This inflammatory cascade causes vasodilation of the cutaneous blood vessels, explaining the characteristic redness of sunburn.

Certain individuals display cutaneous hypersensitivity, in other words reactive skin, which presents as a tendency to redden in response to stimuli that are normally well tolerated. This skin type is characterised by a rapid and excessive activation of sensory nerve receptors. Consequently, a simple change in temperature, an overly fragranced cosmetic product, or even the mere act of touching one’s face can induce a transient red patch. Hypersensitivity redness does not necessarily signify a dermatosis but rather reflects excessive skin reactivity, which demands very gentle care.

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

After ingestion, ethanol is primarily metabolised in the liver. The enzyme alcohol dehydrogenase (ADH) oxidises it to acetaldehyde (C₂H₄O), a toxic compound capable of damaging cellular membranes and disrupting mitochondrial function. When acetaldehyde accumulates, particularly in individuals with a 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 the capillaries and an increase in blood flow to the skin. This manifests visually as a sudden and pronounced flushing of the face, which is often mistaken for the redness caused by the rosacea are frequently confused.

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