What are the consequences of a vitamin C deficiency?

Indeed, not having enough vitamin C in the body can cause adverse effects. A study conducted by Toshio NISHIYAMA and his colleagues sought to examine the effects of vitamin C deficiency on the collagen in the skin of mice using SMP30 knock-out (KO) mice. The Senescence Marker Protein 30 (SMP30) is necessary for the synthesis of vitamin C. Some KO mice were fed a diet low in vitamin C, while others were given a diet high in vitamin C.

Note: It is important to understand that the process of collagen formation includes the hydroxylation reaction of pro-collagen. This leads to the production of hydroxyproline, and this reaction is catalysed by ascorbic acid-dependent hydroxylases: the resulting hydroxyproline residues contribute to the rigidity and structural integrity of collagen.

A deficiency in vitamin C for 36 days did not affect the skin's hydroxyproline content (approximately 0.65 mmol/mm2 for both vitamin C deficient and supplemented KO mice), whereas a vitamin C deficiency for 60 days reduced hydroxyproline levels (0.4 mmol/mm2 for vitamin C deficient KO mice) and the decrease was slowed in vitamin C supplemented KO mice (0.6 mmol/mm2).

These results reveal that a deficiency in Vitamin C could impair collagen synthesis, through an effect on the hydroxyproline reaction. However, the precise mechanisms have not yet been identified.

Nevertheless, more studies are required to clarify these results.

In this same study, the researchers aimed to observe the effects of a vitamin C deficiency on keratinisation, which is a process by which living epidermal cells from the granular layer transform into dead cells. This is a synthesis of the keratin, which is the main component of appendages (hair, nails...). A malfunction in keratinisation can lead to pathologies, such as psoriasis for example.

High magnification views of the epidermis from skin sections showed that 36 days after weaning, the keratinocytes of all animal groups were normal. However, 60 days after weaning, the keratinocytes of the vitamin C deficient KO mice exhibited flat shapes and numerous cornified layers remained on the skin surface of these animals, indicating poor keratinisation and thus an affected cellular state.

Studies have shown that in keratinocytes, vitamin C counteracts the oxidative stress responsible for the degradation of the dermis and various skin damages, such as skin ageing, thanks to its antioxidant capacity against free radicals. It is possible that epidermal keratinocytes may be exposed to higher oxidative stress and be more sensitive to vitamin C deficiency than cells from other tissues, due to the skin's greater exposure to oxygen compared to other organs. Ultimately, a deficiency in vitamin C intensifies the damage caused by free radicals to the keratinocytes of the epidermis, and increases the risk of skin diseases such as ichthyosis.

Finally, in this same study, the researchers focused on the effect of vitamin C deficiency on the hair cycle. Coloured skin sections show that 36 days after weaning, the majority of vitamin C deficient KO mice contained anagen hair follicles, meaning the hair was still in the growth stage. However, the mice were 10 weeks old, and at this age their hair should be in the telogen stage under normal conditions, that is, the hair shedding phase after its complete growth.

A deficiency in Vitamin C thus affects the hair cycles. However, the mechanisms behind these changes are still unknown.

• NISHIYAMA T. & al. Effects of vitamin C deficiency on the skin of the senescence marker protein-30 (SMP30) knockout mouse. Biochemical and Biophysical Research Communications (2009).