What is dysseborrhea?

Dysseborrhea is directly related to a qualitative alteration of sebum. On average, in an adult without skin concerns, sebum is normally composed of 57.5% triglycerides, 26% wax esters, 12% squalene, 3% cholesterol esters, 1.5% cholesterol, and a very small amount of vitamin E. Although present at low concentration, vitamin E plays a major role in preserving sebum balance. Indeed, vitamin E is an antioxidant that protects sebum lipids from oxidative stress, notably that induced by UV radiation, pollution, or certain internal metabolic reactions.

Individuals suffering from dysseborrhea exhibit sebum depleted in vitamin E.

This is also the reason why vitamin E is sometimes referred to as a marker of acne severity. Indeed, its plasma concentration is lower in individuals with this dermatosis, which is closely linked to seborrhea. A study conducted by Kalkan and colleagues in 2013 assessed plasma vitamin E levels in 94 acne patients and 46 healthy subjects. The mean concentration was 7.88 mg/L ± 3.00 in the former versus 11.06 mg/L ± 3.08 in the latter.

When vitamin E levels are low, sebum components are less protected against lipid peroxidation, particularly squalene. The latter is readily oxidized to squalene peroxide due to the numerous double bonds in its chemical structure. Moreover, when squalene is oxidized, it becomes squalene peroxide, a comedogenic compound primarily responsible for the greasy texture of sebum observed in cases of dyseborrhea.

Furthermore, squalene peroxide can induce an inflammatory response in keratinocytes by activating LOX, a lipoxygenase enzyme capable of producing conjugated hydroperoxides through the oxidation of polyunsaturated fatty acids. Squalene peroxide can also increase the production of the pro-inflammatory cytokine IL-6. This compound therefore plays an important role in the pathogenesis of acne by exerting a pro-inflammatory activity on the pilosebaceous unit.

We thus understand that dyseborrhea is not simply a qualitative alteration of sebum: it can initiate a vicious cycle and directly contribute to the development of inflammatory acne.

The vitamin E deficiency observed in skin prone to seborrhea can be explained by a combination of intrinsic and extrinsic factors, beginning with individual and genetic predispositions. Some individuals exhibit a reduced capacity to incorporate vitamin E into sebum, due to variations in the activity of lipid transporters or enzymes involved in tocopherol metabolism. Others may retain this antioxidant less effectively on the skin’s surface, which shortens the time during which it can exert its protective function.

Added to this are environmental factors. UV rays and air pollution are indeed generators of oxidative stress in skin cells, a phenomenon that results from the formation of free radicals or reactive oxygen species produced by excitation of skin molecules by UV photons or by the action of oxidants present in polluted air. These highly unstable free radicals seek stability by capturing electrons from surrounding lipids, proteins, or nucleic acids, initiating deleterious chain reactions. When their production exceeds the skin’s antioxidant defenses, particularly those of vitamin E, equilibrium is disrupted. Sebum components, especially squalene, are then no longer protected from oxidation, leading to dysseborrhea.

When faced with dyseborrhea, the goal is to restore sebum balance.

Dysseborrhea can be quite insidious because, unlike a visible excess of sebum on the face, it manifests as an alteration in sebum quality that can sometimes be difficult to detect. To restore sebum to a more balanced and fluid state, the first step is to incorporate antioxidant treatments into your routine. Indeed, the regular use of an antioxidant serum formulated with vitamin E, vitamin C, or astaxanthin can, for instance, help neutralize free radicals and protect sebum lipids from oxidation, thereby reducing the formation of squalene peroxide. At the same time, it is, of course, essential to apply a daily sunscreen, to prevent squalene oxidation by UV rays.

Note : Dysseborrhea is often accompanied by hyperseborrhea, so it may be relevant to use sebum-regulating active ingredients such as niacinamide, or mattifying agents, such as azelaic acid.

Furthermore, since dysseborrhea is linked to a vitamin E deficiency, a logical step would be to begin an oral vitamin E supplementation to make up for this shortfall. Some clinical studies, particularly in patients with acne, have shown a beneficial effect of this supplementation. For example, one conducted by KIMBERLY and her team involved 164 patients divided into two groups: the first received a daily capsule containing 11 IU of vitamin E, 100 mg of lactoferrin, and 5 mg of zinc gluconate, while the second group received a placebo. After three months, a significant reduction in the number of comedones, inflammatory lesions, and sebum production was observed in the first group. However, the precise role of vitamin E is impossible to evaluate since the supplements taken by the volunteers also contained lactoferrin and zinc gluconate. Thus, despite these encouraging results, further studies on this subject are still necessary.

If you suspect dysseborrhea or are experiencing acne, before you begin any supplementation, we strongly recommend that you consult a dermatologist so they can assess your needs and prescribe a treatment tailored to your situation.