Vitamin E: what are the benefits of this antioxidant for the skin?

Vitamin E, and in particular its most active form α-tocopherol, is regarded as the primary fat-soluble antioxidant in the body. It protects cell membranes rich in polyunsaturated fatty acids, which are particularly susceptible to oxidation. When a free radical attacks a lipid, it initiates a chain reaction known as lipid peroxidation, leading to the formation of new radicals and by-products that impair membrane structure and function, thereby accelerating skin ageing. α-Tocopherol can prevent this process: by donating a hydrogen atom it neutralises peroxyl radicals (LOO•) before they can propagate the reaction. The tocopheryl radical thus formed is sufficiently stable not to reinitiate the oxidative cycle, thereby interrupting the cascade of damage.

This is why vitamin E is considered a major defence against oxidative stress, contributing to the loss of skin firmness and radiance.

By neutralising free radicals, vitamin E thus limits the structural damage that progressively affects the skin with age, a significant benefit of tocopherols for the skin. Indeed, the chronic oxidative stress contributes to the degradation of collagen and elastin, the two proteins of the dermal extracellular matrix responsible for the skin’s suppleness and elasticity. The generation of free radicals also disrupts the synthesis of new fibres and compromises the extracellular matrix as a whole, promoting the appearance of wrinkles. By strengthening the skin’s natural antioxidant defences, vitamin E therefore helps to preserve its elasticity and to delay the appearance of signs of ageing.

An intriguing study assessed a serum combining vitamin C (20%) with vitamin E and red raspberry leaf extract, applied for two months to one side of the face in 50 female participants. The results demonstrated significant improvements in skin elasticity (R2 parameter), radiance and evenness of skin tone (melanin index). However, it is important to exercise caution when attributing the observed effects specifically to vitamin E, as the formula contained several ingredients known for their antioxidant activity, making it difficult to isolate the exact contribution of vitamin E in these outcomes.

Vitamin E is naturally present in sebum and protects its components from oxidation. It particularly preserves squalene, one of the main sebum lipids, from conversion into squalene peroxide, an oxidised derivative known to be comedogenic. This oxidation, promoted by exposure to UV radiation and pollutants, alters the quality of the hydrolipidic film, making it thicker, and contributes to the formation of comedones. By maintaining the stability of squalene and other lipid components, tocopherols benefit the skin as they help preserve sebaceous balance, thereby limiting the risk of dysseborrhoea. For reference, dysseborrhoea is an imbalance due to poor sebum quality, manifesting as oxidative and inflammatory phenomena.

This protective role explains why vitamin E is sometimes considered a biological marker of acne severity, an inflammatory skin condition closely linked to the quantity and quality of sebum produced by the sebaceous glands. Several studies have shown that individuals with acne have, on average, lower plasma concentrations of vitamin E than those without acne. The study carried out by KALKAN and colleagues illustrates this trend, as shown in the table below.

Beyond its role as an antioxidant, vitamin E also acts as a modulator of the inflammatory response. It notably functions by blocking certain intracellular signalling factors, such as NF-κB and JAK-STAT6, which regulate the expression of numerous pro-inflammatory cytokines and chemokines. By limiting their activation, vitamin E reduces the production of mediators responsible for redness, itching or swelling of the skin. Tocopherols also inhibit the production of prostaglandin E2 by cyclooxygenase-2, as well as that of leukotrienes via arachidonate 5-lipoxygenase, two pathways notably known to amplify allergic reactions.

Vitamin E thus contributes to mitigating inflammatory processes and maintaining a favourable balance conducive to skin comfort.

An investigation conducted on 24 mice evaluated the anti-inflammatory effect of a topical microemulsion enriched with vitamin E (0.1 %) and vitamin A (0.05 %). Inflammation was induced by TPA (12-O-tetradecanoylphorbol-13-acetate), which provokes marked oedema and hyperkeratosis. Six groups were formed: control without TPA or treatment (A), TPA only (B), microemulsion without vitamins (C), microemulsion with vitamin E (D), microemulsion with vitamin A (E), and microemulsion with vitamins A and E (F). The results showed that mice treated with the microemulsion containing vitamin E exhibited a notable reduction in erythema and histological lesions compared with the TPA or microemulsion-only groups. The combination of vitamins A and E produced an even more pronounced effect: the epidermis regained a thickness close to that of control mice, and levels of TNF-α, a pro-inflammatory cytokine, were significantly decreased.

The hyperpigmentation manifests as the appearance of brown spots, often localised on the face, hands or areas frequently exposed to sunlight. It results from an excessive production of melanin by melanocytes, which can be triggered by UV rays, inflammation or hormonal imbalances. Although pigment spots are not harmful in themselves, they are often perceived as a sign of skin ageing and disrupt the evenness of the complexion, potentially leading to self-consciousness.

To date, no clinical trial in humans has shown that vitamin E alone has a depigmenting effect.

However, some studies in vitro suggest a promising potential. For example, work conducted on B16 melanoma cells has shown that δ-tocotrienol, an isoform of the vitamin E, was able to significantly inhibit melanin formation and free radical production at a concentration of 10 μM. This treatment also inhibited the expression of proteins essential for proper melanogenesis, namely MC1R, MITF, TYRP-1 and TYRP-2, via activation of the MAPK/ERK pathway. Inhibition of this pathway abolished the effect of δ-tocotrienol, highlighting its role in regulating melanin production. The figure below notably shows a dose-dependent decrease in tyrosinase activity, an enzyme crucial for proper melanogenesis.

These findings suggest that, although clinical evidence is still lacking, certain isoforms of vitamin E may have a lightening effect and depigmenting action that merit more in-depth scientific investigation.

The vitamin E also plays an important role in blood circulation through several complementary mechanisms. It has vasodilatory properties by promoting the production of nitric oxide (NO) by endothelial cells, which relaxes the smooth muscle of blood vessels and improves blood flow. Tocopherols also inhibit the oxidation of LDL cholesterol, limiting the formation of atheromatous plaques that cause atherosclerosis. Moreover, vitamin E enhances the membrane fluidity of red blood cells, facilitating their passage through capillaries, and reduces the release of thromboxane A2 (TXA2) by platelets, decreasing clot formation and ensuring better overall blood fluidity. These effects contribute to cardiovascular protection and the maintenance of efficient blood circulation.

This influence of vitamin E on blood circulation could have interesting benefits for the skin. By improving blood flow and microcirculation, it could limit the appearance of vascular dark circles, resulting from fluid accumulation around the eye contour. Likewise, smoother circulation in the extremities enhances venous return and can lessen the sensation of heavy legs.

However, it is important to note that so far the effects of vitamin E on blood circulation have only been demonstrated through oral administration, as shown in the table below. Further clinical trials are required to confirm these benefits for topical application.

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• NESTEL P. & al. Vitamin E improves arterial compliance in middle-aged men and women. Artherosclerosis (1999).

• MEREDITH I. T. & al. Vitamin E supplementation improves endothelial function in type I diabetes mellitus: A randomized, placebo-controlled study. Journal of the American College of Cardiology (2000).

• NIKBIN MEYDANI S. & al. Vitamin E increases production of vasodilator prostanoids in human aortic endothelial cells through opposing effects on cyclooxygenase-2 and phospholipase A2. The Journal of Nutrition (2005).

• JIALAL I. & al. Vitamin E, oxydative stress and inflammation. Annual Review of Nutrition (2005).

• TSUJI H. & al. Delta-tocotrienol causes decrease of melanin content in mouse melanoma cells. Journal of Health Science (2009).

• KALKAN G. & al. Evaluation of serum vitamins A and E and zinc levels according to the severity of acne vulgaris. Cutaneous and Ocular Toxicology (2013).

• LIN C. C. & al. Anti-melanogenic effects of δ-tocotrienol are associated with tyrosinase-related proteins and MAPK signaling pathway in B16 melanoma cells. Phytomedicine (2014).

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• BENTLEY M. V. & al. Microemulsion co-delivering vitamin A and vitamin E as a new platform for topical treatment of acute skin inflammation. Materials Science and Engineering (2020).

• MAIPRASERT M. & al. Anti-aging and brightening effects of a topical treatment containing vitamin C, vitamin E, and raspberry leaf cell culture extract: A split-face, randomized controlled trial. Journal of Cosmetic Dermatology (2020).

• BARRADAS T. N. & al. Vitamin E and derivatives in skin health promotion. Interactions, Diseases and Health Aspects (2021).

• PERUGINI P. & al. Squalene peroxidation and biophysical parameters in acne-prone skin: A pilot “in vivo” study. Pharmaceuticals (2023).