Vitamin E: what are its benefits for the skin?

That's why the vitamin E is considered a major defense against oxidative stress, a key factor in the loss of skin firmness and radiance.

By neutralizing free radicals, vitamin E thus limits the structural damage that progressively affects the skin with age. Indeed, 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 fibers and weakens the extracellular matrix as a whole, promoting the appearance of wrinkles. By strengthening the skin’s natural antioxidant defenses, vitamin E therefore helps preserve its elasticity and delay the appearance of signs of aging.

This protective role explains why vitamin E is sometimes considered a biological marker of acne severity, an inflammatory skin disease intimately linked to the quantity and quality of sebum produced by the sebaceous glands. Multiple studies have shown that people with acne have, on average, lower plasma concentrations of vitamin E than individuals without acne. The study conducted by KALKAN and his team illustrates this trend, as shown in the table below.

Beyond its role as an antioxidant, vitamin E also acts as an inflammatory response modulator. It does so in part by blocking certain intracellular signaling factors, such as NF-κB and JAK-STAT6, which control the expression of numerous proinflammatory cytokines and chemokines. By limiting their activation, vitamin E reduces the production of mediators responsible for skin redness, itching, or swelling. Tocopherols also inhibit the production of prostaglandin E2 by cyclooxygenase-2, as well as that of leukotrienes via arachidonate 5-lipoxygenase, two pathways especially known for amplifying the allergic reactions.

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

In a study on 24 mice, the anti-inflammatory effect of a topical microemulsion enriched with 0.1% vitamin E and 0.05% vitamin A was evaluated. Inflammation was induced by TPA (12-O-tetradecanoylphorbol-13-acetate), which causes marked edema and hyperkeratosis. Six groups were formed: control without TPA or treatment (A), TPA alone (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 presented a notable reduction in erythema and histological lesions compared to the TPA or emulsion-only groups. The combination of vitamins A and E had an even more pronounced effect: the epidermis regained a thickness close to that of the control mice, and levels of TNF-α, a pro-inflammatory cytokine, were significantly reduced.

The hyperpigmentation manifests as the appearance of brown spots, often localized 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 pigmented spots are not harmful per se, they are often perceived as a sign of skin aging and disrupt the uniformity of the complexion, potentially causing self-consciousness.

To date, no clinical trial in humans has demonstrated that vitamin E alone exerts 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, could significantly inhibit melanin formation and free radical production at a concentration of 20 μM. This treatment also inhibited the expression of proteins essential for proper melanogenesis, such as 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. These results suggest that, although clinical evidence is still lacking, certain vitamin E isoforms may have a whitening effect and depigmenting action that warrant further scientific exploration.

The vitamin E plays an important role in blood circulation thanks to several complementary mechanisms. It has vasodilatory properties by promoting nitric oxide (NO) production by endothelial cells, which relaxes vascular smooth muscle and enhances blood perfusion. Tocopherols also inhibit LDL cholesterol oxidation, limiting the formation of atheromatous plaques responsible for atherosclerosis. Moreover, vitamin E improves red blood cell membrane fluidity, facilitating their passage through capillaries, and reduces the release of thromboxane A2 (TXA2) from 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 promising implications for the skin. By improving blood flow and microcirculation, it could help prevent the appearance of vascular dark circles, resulting from fluid accumulation around the eye contour. Similarly, smoother circulation in the extremities promotes venous return and can reduce the sensation of heavy legs.

However, it is important to note that the effects of vitamin E on blood circulation have, to date, only been demonstrated through oral intake. Additional clinical trials are needed to confirm these benefits when applied topically.