How can we explain the appearance of the first grey hairs?

The first grey hairs generally become visible between the ages of 35 and 40. This unavoidable and natural phenomenon is called "canities". It corresponds to a loss of hair pigmentation, with the hair gradually turning white over time. We are not all equal when it comes to the onset of grey hair. Numerous factors influence the age at which hair turns grey, and some people may see their hair whitening as early as their twenties, while others still have naturally pigmented hair well into their fifties.

The pigmentation of our hair results from the cooperation between two types of cells within the hair bulb: melanocytes and keratinocytes. Melanocytes, located at the base of the follicle, synthesise melanin. This pigment is then packaged into vesicles called melanosomes and transferred to keratinocytes, the cells that form the solid structure of the developing hair fibre. It is the nature and concentration of this melanin delivered into the core of the hair shaft that determine the final shade of the hair.

The whitening of hair, or canities, occurs when this transfer of pigments comes to a halt.

Over time, we observe a progressive reduction in the number of active melanocytes as well as a depletion of the reservoir of melanocyte stem cells located in the outer sheath of the hair. When these cells disappear or cease to function, the hair follicle continues to produce a hair shaft composed of keratin, but without any supply of melanin. The hair fibre then grows devoid of colour. It appears white to us due to an optical effect, although it is in fact translucent.

Another mechanism occurs at the biochemical level: the redox cycle of the follicle. During hair growth, cellular metabolism naturally produces hydrogen peroxide, H2O2 , as a by-product. Under normal conditions, this highly reactive substance is neutralised by a protective enzyme, catalase, which converts it into water and oxygen. However, when catalase activity decreases, hydrogen peroxide accumulates and directly attacks tyrosinase, a key enzyme in melanin synthesis. This blocks pigment production and turns the hair white.

2H2O2 → 2H2O + O2 (degradation reaction of hydrogen peroxide by catalase)

The appearance of white hair is therefore caused by a decrease in melanin synthesis and a reduced distribution of this pigment within the hair fibres. The most common cause is ageing. As with most cells in the body, melanocytes have a limited lifespan. Once these cells disappear, the hair is no longer pigmented and becomes white. Several factors can nevertheless accelerate or slow down this process.

Genetics, a predominant factor in hair greying.

The age at which the first grey hairs appear is above all a matter of heredity. Genetics largely determines the longevity of our melanocytes and our body’s ability to maintain hair pigmentation. Demographic observations have also made it possible to establish average values according to ethnic origin. As a general rule, so‑called “Caucasian” individuals see their first grey hairs appear in their early thirties, while this phenomenon tends to occur towards the late thirties in so‑called “Asian” individuals, and during the forties in so‑called “African” individuals.

At the heart of this mechanism is in particular the MC1R gene (MelanoCortin 1 Receptor), located on chromosome 16. This gene encodes a receptor protein on the surface of melanocytes which, when activated by the hormone α-MSH, triggers the production of melanin. Certain mutations or variants of this gene not only determine the natural colour of the hair, but may also influence how early greying occurs. Studies have shown that certain MC1R alleles are more common in individuals whose hair starts to turn grey before the age of 30, suggesting an increased vulnerability of melanocytes.

Another gene that may influence the appearance of white hair is the IRF4 gene, located on chromosome 6. This gene encodes a protein that regulates transcription, that is, the way in which genetic information is read by the cell to produce proteins. In the hair bulb, IRF4 appears to act on the differentiation and survival of melanocytes. Specific variants of this gene have been directly correlated with the premature onset of white hair.

Although researchers are still attempting to decipher the mechanisms involved, it appears that the combination of these genetic variants partly determines our hair-clock and explains why, for an equivalent lifestyle, two individuals do not develop grey hair at the same rate.

Oxidative stress contributes to the appearance of the first grey hairs.

While hair greying is a natural age-related process, it can be significantly accelerated by oxidative stress. This phenomenon occurs when free radicals, generated by external factors such as sunlight, pollution or smoking, exceed the body’s antioxidant capacity. A study carried out on more than 600 volunteers also demonstrated a direct link between smoking and canities (premature greying of the hair).

Free radicals target the melanocytes in the hair bulb and specifically attack the DNA of their mitochondria. These assaults cause mutations and losses of genetic material which impair mitochondrial function, thereby paralysing melanin synthesis. Normally, protective molecules such as those of the Bcl-2 family safeguard mitochondria from oxidation-induced apoptosis. 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 leads to a drop in 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 are prematurely converted 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 grey hair.

Autoimmune diseases are sometimes involved in canities.

Vitiligo is an acquired autoimmune disease that illustrates how a dysregulated immune system can affect pigmentation. It manifests as the appearance of white patches on the skin (leucoderma) 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 aggressors, mistakenly identify melanocytes as target cells to be eliminated. The melanocytes then lose their ability to synthesise melanin, which leads to white hair.

Even though vitiligo is the most direct example, other autoimmune disorders, particularly those affecting the thyroid, can disrupt the hormonal signals that regulate melanin production and hasten the onset of the first grey hairs.

Stress, a factor that accelerates hair greying.

The link between stress and hair greying, often illustrated by the legend of Marie Antoinette, whose hair is said to have turned white on the night before her execution, was long regarded as a mere myth. However, science has confirmed that psychological stress can indeed accelerate canities. This phenomenon results from an intense activation of the sympathetic nervous system, which governs our response to danger.

Under normal conditions, melanocyte stem cells remain in a resting state and only transform into melanocytes when required to pigment a new hair. However, in the event of acute stress, the sympathetic nervous system releases large amounts of noradrenaline. This sudden release of neurotransmitters saturates the receptors on the stem cells, triggering their immediate and dysregulated activation. This overstimulation leads to a massive and irreversible differentiation of the entire pool of stem cells into active melanocytes. Once these cells have differentiated, no stem cells remain in the follicle to ensure pigmentation during subsequent hair cycles. The hair that grows back is therefore white.

Nutritional deficiencies may promote the development of white hair.

Although ageing and genetics are the predominant causes of canities, the role of diet should not be underestimated. The hair follicle is one of the most metabolically active tissues in the body, and its ability to produce a strong, pigmented hair shaft depends on a continuous supply of vitamins and nutrients. Caution is nevertheless required, as studies on this topic remain scarce and are generally conducted with a limited number of participants. That said, the following compounds could be associated with the occurrence of white hair in situations of deficiency.

The whitening of hair is an unavoidable biological process, governed both by our genetic clock and by environmental factors.

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