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conséquences carence vitamine C

What are the consequences of a vitamin C deficiency?

Vital to the body, vitamin C contributes to bone health and the proper functioning of the immune system. It is important to consume it in sufficient quantities daily to stay in peak condition. Indeed, a deficiency in vitamin C can have numerous consequences on health.

Consequence #1: A deficiency in Vitamin C reduces the collagen in the skin.

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 fed a diet high in vitamin C.

Note: It's 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 catalyzed 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 levels (approximately 0.65 mmol/mm2 for both vitamin C-deficient and supplemented KO mice), while a vitamin C deficiency for 60 days decreased 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 exact mechanisms have not been identified.

Nevertheless, more studies are needed to clarify these results.

Consequence #2: A deficiency in Vitamin C impacts the keratinization process.

In the same study, researchers aimed to observe the effects of a vitamin C deficiency on keratinization, which is a process where living epidermal cells from the granular layer transform into dead cells. This is a synthesis of keratin, which is the main component of appendages (hair, nails...). A malfunction in keratinization can lead to diseases, 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 keratinization and thus an affected cellular state.

Studies have shown that in keratinocytes, vitamin C counteracts oxidative stress, which is responsible for the degradation of the dermis and various skin damages, such as skin aging, due 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, vitamin C deficiency intensifies the damage caused by free radicals to the keratinocytes of the epidermis, and increases the risk of skin diseases such as ichthyosis.

Consequence #3: A deficiency in Vitamin C disrupts the hair cycle.

Finally, in this same study, the researchers focused on the effect of vitamin C deficiency on the hair cycle. Colored 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.

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

Sources

  • 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).

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