Gray hair in children

, medical expert
Last reviewed: 28.09.2022

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Can a child have gray hair? Yes they can.

Why do they appear and what does it mean? This means that in the hair follicles the level of melanin pigment, which colors the hair, is reduced or completely absent.

Also in medicine there is the term "poliosis", which means areas of bleached hair on the line of their growth in the forehead, on the eyebrows and / or eyelashes, as well as blotches of gray hair in other places of the scalp. Poliosis can be observed even in newborns.

Reasons why a child has gray hair

The causes of a symptom such as gray hair in a child are focal or diffuse hypopigmentation (depigmentation) of the hair or  hypomelanosis .

This condition may be due to:

  • vitiligo ; [1]
  • albinism in children  or piebaldism (incomplete albinism); [2]
  • Ito hypomelanosis, a rare neurodermatological disease associated with X-chromosomal abnormalities, which manifests itself in skeletal deformities, ophthalmic disorders (nystagmus, strabismus, cataracts) and deviations from the central nervous system (intelligence and motor retardation); [3]
  • Recklinghausen's disease or hereditary  neurofibromatosis type  I; [4], [5]
  • tuberous sclerosis  - a genetic disease with an autosomal dominant type of inheritance, in which a child has a strand of gray hair and hypopigmented spots on the skin at birth; [6]
  • Chediak-Higashi syndrome  (Chedyak-Higashi); [7]
  • Vogt-Koyanagi syndrome (or Vogt-Koyanagi-Harada disease) with inflammation of the iris and choroid, hearing problems and severe neurological symptoms; [8]
  • associated with hereditary gene mutations Grizzelli syndrome, which has three forms and various non-pigmentary, neurological and immune symptoms; [9]
  • Graves' disease or  hyperthyroidism in children ,  [10] as well as Hashimoto's disease or  autoimmune thyroiditis .

With Waardenburg syndrome, gray hair in a newborn child (along the forehead) is not the only sign of pathology, and children may have iris heterochromia (eyes of different colors); hypertelorism (broad bridge of the nose) and synophrysis (united eyebrows); sensorineural hearing loss, convulsions, tumor formations. The prevalence of this syndrome in the population is estimated at one case per 42-50 thousand people, and in schools for the deaf, according to some reports, one child out of 30 has Waardenburg syndrome. [11]At the same time, if a newborn has intestinal obstruction or constipation from birth (congenital agangliosis of the large intestine or Hirschsprung's disease), then Waardenburg-Shah syndrome is diagnosed. [12]And when combined with hypoplasia of the muscles of the limbs and articular contractures - Kline-Waardenburg syndrome. [13]

Risk factors

Among the risk factors for impaired melanin synthesis, experts note:

  • malnutrition and / or protein-energy malnutrition;
  • lack of cyanocobalamin - vitamin B12 - with the development of pernicious anemia (quite common with veganism), as well as deficiency of this vitamin and folic acid (vitamin B9) during pregnancy in the mother, leading to megaloblastic anemia in the child;
  • copper deficiency in the body;
  • problems with the thyroid gland;
  • adrenal insufficiency;
  • chronic exposure to heavy metals (lead).


Melanin-producing cells - melanocytes - are formed from cells of the neuroectoderm of the neural crest of the embryo (melanoblasts), which spread in tissues and are further transformed. Melanocytes are present not only in the skin and hair follicles, but also in other tissues of the body (in the lining of the brain and in the heart, in the choroid of the eyes and the inner ear).

The production of melanin in the hair shaft (follicular melanogenesis) by oxidizing L-tyrosine does not occur constantly, as in the epidermis, but cyclically, depending on the  phase of hair growth . At the beginning of anagen, melanocytes multiply, mature by the end of this stage, and then, during the catagen period, they undergo apoptosis (they die). And this whole process depends on a number of factors and is regulated by many enzymes, structural and regulatory proteins, etc.

The production of melanin and its transfer from melanocytes to keratinocytes of hair follicles depend not only on the presence of its precursors (5,6-dihydroxyindoles, L-dopaquinone, DOPA-chromium), but also on many auto- and endocrine factors. The researchers concluded that follicular melanocytes - compared to skin melanocytes - are more sensitive to the effects of peroxides and free radicals, that is, they are more easily damaged by oxidative stress.

Thus, mutations in the tyrosinase (TYR) gene, a copper-containing enzyme-catalyst for the synthesis of melanin from the amino acid tyrosine, lead to the minimal formation of melanin or its absence in all forms of albinism. As well as mutations in the genes of the TYRP1 and TYRP2 enzymes, which are important participants in melanogenesis that regulate the activity of tyrosinase, the proliferation of melanocytes, and the stability of the structure of their melanosomes.

In tuberous sclerosis (which occurs in one child in 6 thousand children), the pathogenesis is associated with a hereditary or sporadic mutation of the genes for the proteins hamartin and tuberin (TSC1 and TSC2), which regulate the growth and proliferation of cells (including melanocytes).

Multisystem Vogt-Koyanagi syndrome is believed to be the result of an abnormal autoimmune response to melanin-containing cells in any body tissue.

And in such an organ disease as Waardenburg syndrome, the mechanism for the development of the pathological condition is rooted in mutations in the EDN3, EDNRB, MITF, PAX3, SNAI2 and SOX10 genes, which are directly related to the formation of melanocytes.

See also:  Anatomical and physiological features of the skin and its appendages .

Consequences and complications

By itself, gray hair in children cannot cause complications or cause negative health effects.

However, the appearance of such a symptom as bleached hair in a child can be combined with other signs of certain diseases and pathological conditions (listed above) that pose a serious risk.


To determine the cause of hair depigmentation, a complete history (including family history) is required.

A general blood test and thyroid hormones are taken.

An examination of a skin area with depigmented hair is carried out using a Wood's lamp, as well as by  dermatoscopy .

Based on the assessment and comparison of all clinical signs, differential diagnosis is carried out.

What to do, treatment

If PUVA therapy is used in the treatment of vitiligo, then Ito's hypomelanosis is tried to be treated with injections of glucocorticosteroids, since there are simply no etiotropic agents for the treatment of pathologies of this type or albinism.

In syndromes with ophthalmic or neurological lesions, appropriate symptomatic agents are used. But what to do in case of violation of melanin synthesis?

If a lack of vitamin B12 is identified, supplements with this vitamin are prescribed. With a copper deficiency, it is recommended to introduce whole grains, legumes, beef liver, sea fish, eggs, tomatoes, bananas, apricots, walnuts, sunflower seeds and pumpkins into the child's diet.

Doctors also recommend taking ginkgo biloba preparations for two to three months, which are said to promote repigmentation.

You can use a hair tonic consisting of carrot juice, sesame oil and fenugreek seed powder; make aloe vera gel hair masks (which contain antioxidants, vitamins B12 and B9, zinc and copper).


Specific ways to regulate melanogenesis have not yet been found, therefore, there are no measures to prevent congenital pathologies of melanin synthesis in hair follicles.

Although researchers claim that antioxidants contribute to the increase in melanin synthesis: vitamins A, C and E, as well as biologically active compounds contained in greens, dark-colored berries and fruits and brightly colored vegetables.


Most likely, a child’s gray hair will be his “mark” for life: this is the medical prognosis for genetically determined focal or diffuse pigmentation disorders and orphan syndromes.

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