Dysseborrhoea: what is this sebum-related imbalance?

Dyseborrhoea: what does it refer to?

Definitions:
Hyperseborrhoea = excessive sebum production
Dysseborrhoea = production of poor-quality sebum

Dysseborrhoea refers to a qualitative alteration of sebum, the lipid substance produced by the sebaceous glands and essential for maintaining skin hydration and protection. Unlike mere overproduction or a sebum deficiency, dysseborrhoea primarily affects its composition: the proportions of triglycerides, wax esters, squalene and free fatty acids are unbalanced. This alters sebum fluidity, making it thicker and greasier. As with hyperseborrhoea, dysseborrhoea can lead to the appearance of blemishes, or even acne.

Indeed, a richer, thicker sebum circulates less easily on the skin’s surface, promoting its accumulation within the pores. This phenomenon can lead to pore obstruction, creating an environment conducive to the proliferation of certain bacteria, such as Cutibacterium acnes, involved in the development of comedones and inflammatory lesions. Dysseborrhoea can affect all skin types, although it is more frequently observed in oily skin. Unlike hyperseborrhoea, it is not necessarily accompanied by marked shine. It is more commonly recognised by pore dilation, a more irregular skin texture and a slight roughness to the touch.

What are the causes of dyseborrhoea?

Dysseborrhoea is directly linked to a qualitative alteration of sebum. On average, in an adult with healthy skin, sebum typically comprises 57.5% triglycerides, 26% wax esters, 12% squalene, 3% cholesterol esters, 1.5% cholesterol and a very small amount of vitamin E. However, despite its low concentration, the latter plays a key role in preserving sebum balance. Indeed, vitamin E is an antioxidant that protects sebum lipids from oxidative stress, notably that induced by UV rays, pollution or certain internal metabolic reactions.

Individuals suffering from dyseborrhoea exhibit sebum deficient in vitamin E.

This is precisely why the vitamin E is sometimes regarded as a marker of acne severity. Indeed, its plasma concentration is lower in individuals affected by this dermatosis, which is closely associated with seborrhoea. A study carried out by KALKAN and his team in 2013 assessed the plasma concentration of vitamin E in 94 acne patients and 46 healthy individuals. It averaged 7.88 mg/L ± 3.00 in the former, compared with 11.06 mg/L ± 3.08 in the latter.

When vitamin E levels are low, the components of sebum are less well protected against lipid peroxidation, particularly the squalene. The latter is readily oxidised into squalene peroxide due to the numerous double bonds present in its chemical structure. When squalene is oxidised, it is converted into squalene peroxide, a comedogenic compound primarily responsible for the oily texture of sebum observed in dyseborrhoea.

Structure chimique du squalène (a) et mécanisme de peroxydation lipidique (b). — Chemical structure of squalene (a) and mechanism of lipid peroxidation (b).
Source: Perugini P. et al. Squalene peroxidation and biophysical parameters in acne-prone skin: A pilot ‘in vivo’ study. Pharmaceuticals (2023).

Moreover, squalene peroxide can induce an inflammatory response in keratinocytes through the activation of LOX, a lipoxygenase enzyme capable of producing conjugated hydroperoxides by oxidising polyunsaturated fatty acids. Squalene peroxide may also enhance the production of the pro-inflammatory cytokine IL-6. Therefore, this compound plays an important role in the pathogenesis of acne by exerting a pro-inflammatory activity on the pilosebaceous unit.

It is therefore understood that dysseborrhoea is not merely a qualitative alteration of sebum: it can initiate a vicious circle and directly contribute to the development of inflammatory acne.

The vitamin E deficiency observed in skin prone to dyseborrhoea can be explained by a combination of intrinsic and extrinsic factors, beginning with individual and genetic predispositions. Some individuals exhibit a reduced ability to incorporate vitamin E into sebum, linked to variations in the activity of lipid transporters or of enzymes involved in tocopherol metabolism. Others may have less efficient retention of this antioxidant on the skin’s surface, which shortens the period during which it carries out its protective function.

Environmental factors also contribute: UV rays and air pollution are indeed generators of oxidative stress in skin cells, a phenomenon resulting from the formation of free radicals or reactive oxygen species produced by the excitation of skin molecules under UV photons or by the action of oxidants present in polluted air. These free radicals, which are highly unstable, strive to stabilise themselves by capturing electrons from surrounding lipids, proteins or nucleic acids, initiating damaging chain reactions. When their production exceeds the skin’s antioxidant capacity, particularly that of vitamin E, balance is disrupted. The constituents of sebum, especially squalene, are then no longer shielded from oxidation, leading to the onset of dyseborrhoea.

What should be done in the event of dyseborrhoea?

When faced with seborrhoea imbalance, the aim is to restore sebum equilibrium.

Dysseborrhoea can be quite insidious because, unlike an obvious excess of sebum on the face, it manifests as an alteration in its quality, which can sometimes be hard to perceive. To restore more balanced and fluid sebum, the first step is to incorporate antioxidant treatments into your routine. Indeed, the regular use of an antioxidant serum containing vitamin E, vitamin C or astaxanthin for example it can help neutralise free radicals and protect sebum lipids from oxidation, thereby reducing squalene peroxide formation. At the same time, it is, of course, essential to apply a daily sunscreen, to prevent squalene oxidation by UV rays.

Note : Dyseborrhoea, which is often accompanied by hyperseborrhoea, may warrant the use of sebum-regulating actives, such as niacinamide, or mattifying agents such as azelaic acid.

Furthermore, since dysseborrhoea is linked to a vitamin E deficiency, a logical course of action would be to begin a oral vitamin E supplementation to counteract this shortfall. Some clinical studies, particularly in patients with acne, have shown a beneficial effect of this supplementation. One example is the trial conducted by Kimberley and her team. This 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, the patients in the first group exhibited a significant reduction in the number of comedones, inflammatory lesions and sebum production. However, the precise role of vitamin E cannot be determined, as the supplements given to the volunteers also contained lactoferrin and zinc gluconate. Therefore, despite these encouraging results, further studies are still required.

If you suspect dyseborrhoea or are affected by acne, before commencing any supplementation, we strongly encourage you to consult a dermatologist so that they can assess your needs and prescribe a treatment tailored to your situation.