How is Thyroid connected to hair loss?

The thyroid is a butterfly-shaped endocrine gland present in the base of the neck. The gland is responsible for the production of three essential hormones: the two thyroid hormones, triiodothyronine (T3), thyroxine (T4), and a peptide hormone, calcitonin. The thyroid hormones play a crucial role in influencing the metabolic rate, protein synthesis, and the generalized growth and development of the body cells. The functional disorders of the gland are classified based on thyroid hormone levels into hyper (excessive) or hypo (deficient) thyroidism.

Hair loss and thyroid disorders

How is Thyroid connected to hair loss?Similar to its anabolic effect in other parts of the body, thyroid hormones also play an essential role in the development and maintenance of the hair follicles. Therefore, hormonal dysregulation can affect the hair growth cycle and impair the hair quality resulting in premature hair loss. Both hyper and hypothyroidism are known to, directly and indirectly, impact the health of hair follicles and are associated with hair fall. These disturbances are also known to exacerbate the pre-existing pathologies that cause hair loss, such as androgenetic alopecia and diffuse alopecia.

A descriptive study published in 2013 accessed the association of alopecia with thyroid disorders by following 1200 subjects over 25 months. They classified different types of hair fall based on their clinical diagnosis. The main types of hair loss conditions recorded were diffuse alopecia (71%), alopecia areata (11.%), and androgenetic alopecia (14%). All the subjects were then tested for thyroid-stimulating hormone (TSH) and autoantibodies to thyroid receptors. It was found that there was a significant difference in thyroid dysfunction with respect to gender and age. With age group 21-40 age group showing the highest thyroid level abnormalities along with a high incidence of diffuse alopecia (44.64%) followed by androgenetic alopecia. In the age groups of 0-20 years and 21-40 years, alopecia areata and diffuse alopecia were seen to be equally prevalent with dysfunction. Lastly, the subjects above 40 years of age demonstrated an equal incidence of alopecia areata and androgenetic alopecia (50%) with thyroid dysregulation.

Hair loss associated with autoimmune thyroid disease

Hypo-hyperthyroidism is also known to trigger autoimmune conditions such as alopecia areata and telogen effluvium. Alopecia areata causes nonscarring, patchy hair loss, and is often transient. On the other hand, telogen effluvium is a type of premature diffuse hair loss that usually occurs in the crown region. Early graying of hair is also linked with autoimmune thyroid diseases, and multiple studies show the administration of thyroid hormone to reverse this condition.

Clinical features of thyroid-related hair loss

The hair loss related to thyroid disorders type is not patterned or associated with bald spots, rather a diffuse thinning of hair is apparent over time. The hair fall is not limited to the scalp and may involve eyebrows, eyelashes, and body hair as well. Hypothyroidism is known to be associated with dry, brittle, and dull hair shafts that are highly prone to easy shedding. Hyperthyroidism, on the other hand, is known to substantially reduce the tensile strength of the hair shaft leading to easy breakage.

Treatment options

To tackle thyroid-related hair loss, treatment of the underlying thyroid disorder is the primary approach. Fortunately, in most cases, hair loss related to thyroid diseases is reversible and transient.


For patients suffering from a hyperactive thyroid, antithyroid medications are the first line of drugs in management. These include methimazole (Tapazole) and propylthiouracil (PTU). They work by inhibiting the production and peripheral activation of thyroid hormone. For resistance to treat hyperthyroidism, patients may also be offered radioactive iodine that destroys the glandular cells inducing hypothyroidism. A significant population of patients also undergo surgical removal of some or all parts of the gland, especially in cases of enlarged glands.


Hypothyroidism is rather simpler to manage and requires the consumption of synthetic hormone preparation called levothyroxine sodium (Levothroid, Levoxyl, Synthroid, or Unithroid) to replenish the deficient hormone.

Lifestyle changes

Symptoms related to mild or moderate thyroid hair disorders can also be managed with simple lifestyle and diet changes. These include:

  • Increased consumption of fish oil that contains omega-3 fatty acid which provides nourishment to the scalp preventing dry scalp.
  • Incorporating dark green leafy vegetables in meals such as spinach that are rich in vitamins A and C.
  • Adding protein-rich foods to the diet can prevent weak and brittle hair. These include dairy products, legumes, nuts, and lean meats, etc.
  • Biotin or vitamin B7 deficiency is known to cause brittle hair and increased hair loss mimicking thyroid-related hair loss. Sources of biotin include whole grains, egg yolks, liver, salmon, avocados, sweet potatoes, soy flour, and yeast. However, taking biotin supplements can produce false thyroid hormone levels, therefore, patients are advised to stop taking biotin supplements and food containing biotin a week before testing hormone levels.
  • Hair supplements and food containing high iodine content should also be avoided as they may interfere with the activity of thyroid medications.
  • Caffeine and alcohol intake is also known to exacerbate thyroid disease.


Thyroid-related hair loss tends to improve as soon as the underlying hypo or hyperthyroid conditions are corrected. According to experts, a visible decrease in hair fall is observed within a period of six to eight months.




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Vincent M, Yogiraj K. A descriptive study of alopecia patterns and their relation to thyroid dysfunction. International journal of trichology. 2013 Jan;5(1):57.

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Redondo P, Guzmán M, Marquina M, Pretel M, Aguado L, Lloret P, Gorrochategui A. Repigmentation of gray hair after thyroid hormone treatment. Actas Dermo-Sifiliográficas (English Edition). 2007 Jan 1;98(9):603-10.