Vitamin E: What benefits does this antioxidant offer for the skin?

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

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

By neutralizing free radicals, vitamin E thus limits the structural damage that gradually affects skin with age, an important benefit of tocopherols for the skin. Indeed, the oxidative stress in its chronic form contributes to the degradation of collagen and elastin, the two proteins of the dermal extracellular matrix responsible for the skin’s suppleness and elasticity. Free radical generation 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 to preserve its elasticity and to delay the onset of signs of aging.

An interesting study evaluated a serum combining vitamin C (20%), vitamin E and a raspberry leaf extract, applied for two months to one half of the face in 50 female participants. The results showed significant improvements in skin elasticity (parameter R2), radiance, and complexion uniformity (melanin index). However, it is important to remain cautious when attributing the observed effects to any single component, since the formula contained multiple actives recognized for their antioxidant properties; therefore, isolating the exact contribution of vitamin E to these outcomes is difficult.

Vitamin E is naturally present in sebum and protects its compounds from oxidation. It particularly preserves squalene, one of the main sebaceous lipids, from its conversion into squalene peroxide, an oxidized derivative recognized as comedogenic. This oxidation, promoted by exposure to UV rays and pollutants, compromises the quality of the hydrolipidic film, making it thicker, and contributes to comedone formation. By maintaining the stability of squalene and other lipid components, tocopherols benefit the skin by helping preserve sebum balance, thus limiting the risk of dysseborrhea. For reference, dysseborrhea is an imbalance caused by poor sebum quality that manifests as oxidative and inflammatory phenomena.

This protective role explains why the vitamin E is sometimes considered a biological marker of acne severity, an inflammatory skin disease closely linked to the amount and quality of sebum produced by the sebaceous glands. Several 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 colleagues illustrates this trend, as shown in the table below.

Beyond its antioxidant role, vitamin E also acts as modulator of the inflammatory response. It does so in particular by blocking certain intracellular signaling 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 for amplifying the allergic reactions.

Vitamin E thereby helps to reduce inflammatory processes and maintain a balance conducive to skin comfort.

A study 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 produces edema and marked hyperkeratosis. Six groups were established: 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 both 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-only 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 TNF-α levels, a proinflammatory cytokine, were significantly decreased.

The hyperpigmentation manifests as the appearance of brown spots, often found 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 these pigmented spots are not harmful per se, they are often regarded as a sign of skin aging and interfere with an even complexion, potentially causing self-consciousness.

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

However, certain studies in vitro have revealed a promising potential. For example, experiments conducted on B16 melanoma cells demonstrated that δ-tocotrienol, an isoform of the vitamin E, could 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, such as MC1R, MITF, TYRP-1, and TYRP-2, via activation of the MAPK/ERK pathway. Inhibition of this pathway nullified the effect of δ-tocotrienol, suggesting its role in regulating melanin production. The figure below notably shows a dose-dependent decrease in tyrosinase activity, an enzyme indispensable for proper melanogenesis.

These results suggest that, although clinical evidence is still lacking, certain isoforms of vitamin E may have a lightening effect and depigmenting action that warrant further scientific investigation.

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

This influence of vitamin E on blood circulation could have interesting implications for the skin. By enhancing blood flow and microcirculation, it could limit the onset of vascular dark circles, which stem from fluid accumulation around the eye contour. Similarly, smoother circulation in the extremities promotes venous return and may 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 administration, as shown in the table below. Additional clinical trials are needed to confirm these benefits in topical application.

• PANGANAMALA R. V. & al. Modulation of platelet thromboxane A2 and arterial prostacyclin by dietary vitamin E. Prostaglandins (1981).

• YASUE H. & al. Vitamin E administration improves impairment of endothelium-dependent vasodilation in patients with coronary spastic angina. Journal of the American College of Cardiology (1998).

• 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).

• HAJIBABAEI K. Antioxidant properties of vitamin E. Annals of Research in Antioxidants (2016).

• 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).