What are the benefits of glycerine for the skin?

Being one of the most effective and widely used humectant polyols (hygroscopic) as moisturising ingredients in the cosmetic industry, the glycerine is known to increase skin hydration and decrease uncontrolled evaporation of water from the epidermis, thus preventing dehydration and the resulting physical damage.

In comparison to hyaluronic acid, urea, sorbitol, or even propylene glycol, glycerin is themost effective humectant available according to a 2016 study.

Various mechanisms of action of the glycerol have been reported to understand its moisturising properties:

• Enhancing epidermal hydration: to assist the skin in retaining its moisture, glycerol is able to permeate the stratum corneum and draw water towards the epidermis from the dermis and/or the environment under humid conditions. This is due to its three hydrophilic hydroxyl groups (-OH) that bind and retain water.

  In fact, glycerol will create a "reservoir" in the deep layers of the stratum corneum within the lipid bilayers. Furthermore, glycerine has excellent water solubility. According to a study, the higher the solubility of a polyol, the greater its ability to absorb water.

  Note : Pure glycerol (92 g/mol) can absorb its own weight in water in 3 days.

• Enhancing the protective barrier function of the skin: glycerol plasticises the stratum corneum by forming a "pseudo-occlusive" film, which helps to maintain the transepidermal water flow and improve the smoothness of the skin surface.

• Inhibiting the crystallisation of lipids in the stratum corneum: FRIBERG S. E. & co. have demonstrated with in vitro models that glycerol is capable of influencing the crystalline arrangement of lipids in the stratum corneum, by inhibiting the transformation of lipids from the liquid crystalline form to the solid crystalline form, thus preventing water loss and improving the properties of the skin barrier.

  Note : In dry skin, the proportion of lipids in a solid state can be high.

• Optimising Desmosomal Degradation: The desmolytic effect of glycerol, demonstrated by SABIN R. & al., can induce a decrease in intra-epidermal pressure on intercellular lipids and, consequently, indirectly cause an increase in lipids in the liquid crystalline state.

In over-the-counter skincare products, the glycerine is often combined with various other types of compounds to optimise its moisturising effects (hyaluronic acid, urea, xylitol, sorbitol, etc.).

It is important to understand that the degradation of corneodesmosomes, structural proteins that hold together the dead cells of the corneal layer (corneocytes), is a phenomenon dependent on the water content in the corneal layer. Indeed, it is significantly reduced when the ambient humidity is low (44%) compared to high humidity (80%), thus leading to a defective desquamation associated with a thickening of the stratum corneum.

Indeed, SABIN R. and his colleagues have demonstrated in a study in vitro the ability of glycerol (5%) to increase the degradation of these protein bonds. Measurements of the mechanical resistance of the corneal layer lamellae indicated a reduction in intercorneocyte forces after the use of glycerol.

According to initial data, glycerol appears to influence the activity of enzymes responsible for the breakdown of intercorneocyte attachments ("Stratum Corneum Tryptic Enzyme" and "Stratum Corneum Chymotryptic Enzyme"), which are desquamating proteases significantly influenced by the activity of water within the stratum corneum.

Furthermore, additional studies have shown that glycerine would modulate the behaviour of intercellular lipids in the stratum corneum and prevent the crystallisation of their lamellar structures in vitro at low humidity. Thus, based on the results obtained, glycerine would have allowed to "normalise" the enzymatic digestion of corneodesmosomes thanks to its humectant properties, thereby restoring the mechanisms of corneocyte elimination on the skin surface.

A study conducted on mice reported that the topical application of glycerine (5 or 10%) helped to soothe inflammation following an acute irritation induced by sodium lauryl sulphate (SLS). An explanation for the beneficial effects of glycerol could come from its ability to maintain the intercellular lipids of the stratum corneum in a liquid crystalline state, which is necessary for optimal barrier function, thus preventing an increase in water loss.

The study also demonstrated that glycerol (10%) significantly reduced the expression level of IL-1β and TNF-α, the primary mediators of the inflammatory response to irritation, in addition to decreasing the number of immune cells (lymphocytes, neutrophils, macrophages, etc.) at the site of irritation. However, the exact mechanism by which glycerol affects the expression of these inflammatory molecules requires further in-depth study.

Besides increasing water loss in the stratum corneum, skin exposure to SLS also results in an increase in dermal blood flow. However, this increase was reduced after treatment with 10% glycerol. It has been reported that 100% anhydrous glycerol reduces the speed of blood flow and the diameter of micro-vessels. Thus, according to the literature, glycerol, contributing to skin hydration and the maintenance of its homeostasis, proves to be a effective anti-irritant and anti-inflammatory.

In vivo studies have shown that mice deficient in aquaporin-3 (AQP3), an aquaglyceroporin highly localised in keratinocytes, resulted, among other things, in a delay in the healing of skin wounds in the animals. This alteration in the healing process was attributed to a decrease in the proliferation and migration of epidermal cells, alongside a significant reduction in the glycerol content in the stratum corneum and the epidermis. However, oral supplementation with glycerol was able to rectify this impaired healing and defective cell proliferation.

In 2013, SPARR E. and his colleagues explored theinfluence of glycerol on the permeability in vitro of skin membranes under various hydration conditions. They described that the addition of glycerol led to an increase in the flux of metronidazole across excised pig skin membranes under dehydration conditions, which would otherwise alter the transport characteristics.

These results suggest that glycerol impacts the state and molecular organisation of the lipid and protein components of the stratum corneum. Indeed, studies have shown that this effect could be explained by the interaction of glycerol with intercellular lipids, its inhibition on lipid crystallisation, its desmolytic effect and its hydrating effect. Glycerin would thus act as a "penetration enhancer".

Du Pont J. S. and his colleagues have studied the effect of various concentrations of glycerol (85 and 98%) at three different temperatures (4, 20 and 37°C) against the herpes simplex virus (HSV) and the poliovirus, which is responsible for poliomyelitis. Depending on the concentration and temperature, the results of the experiments showed that glycerol has a strong virucidal action at high concentrations (98%). It is believed to inactivate the viruses by influencing the enzymatic processes of nucleic acid degradation, but further studies are needed to confirm this effect and better understand its mechanism of action.

It has been reported that glycerol protects bacterial cells and transforming DNA against X-rays and ultraviolet light at a wavelength of 365 nm. However, this observation requires further study to determine whether these results can be extrapolated to human skin, in addition to an action mechanism of glycerol that remains unknown.

• PEAK J. G. & co. Protection offered by glycerol against the biological effects of near-ultraviolet light. Radiation Research (1980).

• FRIBERG S. E. & al. Prevention of stratum corneum lipid phase transition by glycerol - an alternative mechanism for skin moisturisation. Journal of the Society of Cosmetic Chemists (1990).

• DU PONT J. S. & al. Virucidal effect of glycerol as utilised in donor skin preservation. Burns (1994).

• SABIN R. & al. The impact of glycerol and humidity on desmosome degradation in the stratum corneum. Archives of Dermatological Research (1995).

• VERKMAN A. S. & co. The selective reduction of glycerol in the skin of aquaporin-3-deficient mice may explain the impaired skin hydration, elasticity, and barrier recovery. Journal of Biological Chemistry (2002).

• SURBER C. & al. Glycerol and the skin: a comprehensive approach to its origin and functions. British Journal of Dermatology (2008).

• VERKMAN A. S. & co. Aquaporin-3 aids in the migration and proliferation of epidermal cells during wound healing. Journal of Molecular Medicine (2008).

• SPARR E. & al. Glycerol and urea can be utilised to enhance skin permeability under conditions of diminished hydration. European Journal of Pharmaceutical Sciences (2013).

• ERÕS G. & al. Anti-irritant and anti-inflammatory effects of glycerol and xylitol in sodium lauryl sulphate-induced acute irritation. Journal of the European Academy of Dermatology and Venereology (2015).

• GAMBHIR M. L. & al. Moisturisers: The Slippery Road. Indian Journal of Dermatology (2016).