Free radicals target the melanocytes in the hair bulb and attack in particular the DNA of their mitochondria. These assaults cause mutations and losses of genetic material that impair mitochondrial function, thereby blocking melanin synthesis. Normally, protective molecules such as those in the Bcl-2 family shield mitochondria from apoptosis induced by oxidation. However, oxidative stress eventually degrades these same protective molecules, making melanocytes increasingly vulnerable. At the same time, the body’s natural antioxidant enzymes, such as catalase and superoxide dismutase, are also damaged, which affects tyrosinase and sharply reduces its activity.
Finally, oxidative stress targets melanoblasts, the stem cells that are precursors of melanocytes. In response to oxidative damage, researchers have observed an ectopic differentiation of these cells. Instead of remaining in reserve to ensure future renewal, the stem cells prematurely transform into active melanocytes in an attempt to compensate for the losses. This process depletes the pool of stem cells in the hair follicle. Once this reservoir is exhausted, the renewal of pigment-producing cells can no longer occur, which marks the onset of white hair.
Autoimmune diseases are sometimes involved in canities.
Vitiligo is an acquired autoimmune disease that illustrates how a dysfunction of the immune system can affect pigmentation. It is characterized by the appearance of white patches on the skin (leukoderma) and is frequently accompanied by depigmentation of body hair and scalp hair. This phenomenon occurs when T lymphocytes of the immune system, which are supposed to protect the body against external threats, mistakenly identify melanocytes as target cells to be destroyed. As a result, melanocytes lose their ability to synthesize melanin, which leads to white hair.
Even though vitiligo is the most direct example, other autoimmune disorders, especially those affecting the thyroid, can disrupt the hormonal signals that regulate melanin production and speed up the appearance of the first gray hairs.
Stress, a factor that speeds up hair graying.
The link between stress and hair whitening, often illustrated by the legend of Marie Antoinette, whose hair is said to have turned white the night before her execution, was long regarded as a mere myth. Yet science now confirms that psychological stress can indeed accelerate canities (the graying or whitening of hair). This phenomenon is due to an intense activation of the sympathetic nervous system, which regulates our response to danger.
Under normal conditions, melanocyte stem cells remain in a resting state and only transform into melanocytes when needed to pigment a new hair. However, in cases of acute stress, the sympathetic nervous system releases large amounts of noradrenaline. This sudden surge of neurotransmitters overwhelms the receptors on the stem cells, triggering their immediate and disordered activation. This overstimulation leads to a massive and irreversible differentiation of the entire reserve of stem cells into active melanocytes. Once these cells have differentiated, no stem cells remain in the follicle to provide pigmentation for subsequent hair growth cycles. The hair that grows back is therefore white.