Anagen phase represents the part of the hair cycle when the hair enters a state of active growth and it lasts about three to five years. The cells in the root of the hair are dividing rapidly. A new hair is formed and pushes the club hair (a hair that has stopped growing or is no longer in the anagen phase) up the follicle and eventually out.
During this phase, the hair grows about 1 cm every 28 days. At that time, approximately 85 to 90% of scalp follicles are in the anagen phase of hair growth.
Body hair has the same mechanism of growth with the scalp hair. However, body hair remains in the active phase for a short period (about 30 to 45 days). This is why body hair grows remarkably shorter than scalp hair.
Genetics may influence the anagen phase. Some people have difficulty growing their hair beyond a certain length because they have a short active phase of growth. On the other hand, people with very long hair have a long active phase of growth.
The catagen phase represents the second part of a hair’s lifecycle and it is a transitional stage. This phase lasts for about two to three weeks. Growth stops, and the outer root sheath shrinks and attaches to the root of the hair. Once the hair bulb no longer has access to the blood supply, it begins to convert to keratin. During this keratinisation process, the hair bulb becomes shaped like a club.
Telogen phase is the third phase of the hair’s cycle, occurring after both the anagen phase and catagen phase. During this phase, the hair growth is ceased and the hair becomes fully keratinized. The dermal papilla enters a resting state and does not supply any nutrition to the hair, which is fully grown. Telogen is the resting phase and usually accounts for 6% to 8% of all hairs. This phase lasts for about 100 days for hairs on the scalp and longer for hairs on the eyebrow, eyelash, arm, and leg. During this phase, the hair follicle is completely at rest and the club hair is completely formed. Each day are shed about 25 to 100 telogen hairs. At the end of the telogen phase, the original hair falls out (exogenous phase) and is replaced by a new hair at the early growth stage.
What are the causes of hair loss?
Hair loss, also known as alopecia has a significant effect on the social and psychologic well-being of both men and women of all ages.
Etymologically, the word “alopecia” comes from the Greek ἀλώπηξ (alōpēx), which means “fox”. It is an allusion to the constant hair loss suffered by these animals during life.
One or more of the following factors may lead to the occurrence of hair loss:
Family history (heredity)
Hormones, such as abnormal levels of androgens;
Drugs, including chemotherapy drugs used in cancer treatment, blood thinners, beta-adrenergic blockers used to control blood pressure, and birth control pills;
Burns, injuries, and X-rays;
Cosmetic procedures, such as shampooing too often, perms, bleaching, dyeing hair, tight braiding, using rollers or hot curlers
Medical conditions like thyroid disease, lupus, diabetes, iron deficiency anaemia, eating disorders;
Low-protein diet or severely calorie-restricted diet.
Hair loss disorders
Male pattern hair loss
Male pattern hair loss, also known as androgenetic alopecia, represents the most common type of hair loss in men. This condition was described since antiquity when Hippocrates observed that eunuchs and men castrated before puberty did not develop baldness. Androgenetic alopecia usually has a specific pattern of temporal-frontal loss in men and central thinning in women.
The following changes can be observed in patients diagnosed with androgenetic alopecia:
A reduction in the percentage of hair follicles in the anagen growth phase;
Reduction in the length of hair grown;
An increase in the proportion of vellus hair followed by a reduction of hair density;
Men with androgenetic alopecia present an increased activity of 5 alpha-reductase, an enzyme which converts testosterone in its active metabolite dihydrotestosterone. The androgens determinate the shortening of the anagen phase starting at puberty. Therefore, they promote follicular miniaturization and lead to a vellus-like hair formation and gradual hair thinning.
The treatment options for androgenetic alopecia are based on decreasing the activity of androgens. The most used medicines for the treatment of androgenetic alopecia are minoxidil (Rogaine) available as a topical solution and Finasteride (Propecia) available as 1 mg film-coated tablets.
In 1970’s, Minoxidil was initially introduced as an antihypertensive agent. It was found to cause hypertrichosis, a rare condition that causes excessive hair growth anywhere on person’s body. The dermatologist decided to test topical formulation of minoxidil in order to avoid the side effect of oral minoxidil like weight gain and severe water retention. Clinical trials were performed with 1%, 2% and 5% topical formulation of minoxidil versus placebo to test the efficacy of this drug in the treatment of androgenetic alopecia. The studies have shown that for men 2% and 5% topical formulation is more effective than 1% and placebo, and for women 2% topical formulation is better than the placebo and safer to use than the 5% formulation.
The mechanism by which minoxidil promotes hair growth is still unknown. Present evidence suggests that minoxidil acts mainly on the hair cycle and it may also increase the hair diameter. Minoxidil was shown to increase the duration of anagen phase which explains its effect on hair growth.
Female pattern hair loss called also in the past female androgenetic alopecia represents the major cause of hair loss in adult women with a major impact on their quality of life. The follicular changes that lead to alopecia are similar between men and women, but clinical presentation and response to antiandrogen therapy are different. Furthermore, the participation of androgens in the development of female pattern hair loss has not been yet fully elucidated. For these reasons, the term female pattern hair loss has been preferred over female androgenic alopecia.
Female pattern hair loss is characterized by a progressive miniaturization of hair follicles and subsequent reduction of the number of hairs, especially in the central, frontal and parietal scalp regions.
The pathophysiology of female pattern hair loss is not fully understood. Genetic, hormonal and environmental factors could be involved. Women diagnosed with female pattern hair loss present a reduced anagen phase and a delay between the end of the telogen phase and the beginning of the new anagen phase. It could be observed a miniaturization of the dermal papilla, which size determinates the diameter of hair follicles. Therefore, hair follicles became thinner.
Alopecia areata is characterised by a localized area of complete hair loss. This may extend to the entire scalp (alopecia totalis) or the entire body (alopecia universalis).
Alopecia areata is caused by an abnormality in the immune system that damages the follicles. Hair follicles are attacked by the body’s own immune system and the normal hair formation is disrupted.
Alopecia areata is occasionally associated with other autoimmune conditions such as:
Spontaneous recovery of hair usually occurs within 6 to 12 months, with hair often being pigmented differently. However, the prognosis is not good if the condition persists for more than one year or occurs before puberty.
The treatments for alopecia areata include immunomodulating agents and biologic response modifiers (minoxidil).
Telogen effluvium is a condition that occurs when the normal balance of hairs in growth and rest phases is disrupted and the telogen phase predominates. About 30 to 50% of body hair can be lost in telogen effluvium. Normally, only 15% of hairs are in the telogen phase, while in case of telogen effluvium, up to 50% of hairs are in the telogen phase.
Telogen effluvium can be triggered by several different events, including:
Severe chronic illness;
An extreme change in diet;
Extreme weight loss
Severe psychological stress (life-threatening situations);
There is no specific treatment for telogen effluvium. Hair growth can occur after the resolution of the causes that lead to this condition.
Trichotillomania also called hair-pulling disorder is a psychiatric impulse control disorder that involves recurrent, irresistible urges to pull out hair from scalp, eyebrows or other areas of your body, despite trying to stop. It represents the most common cause of childhood alopecia, but it may persist into adulthood. The mean age of onset is 12 years in girls and 8 years in boys.
Because of its psychologic nature, the treatment for trichotillomania consists of counselling, behaviour modification techniques, and hypnosis.
Traction alopecia is a form of unintentional hair loss associated with specific social, cultural, and cosmetic practices. It also occurs commonly in female athletes who pull their hair tightly in ponytails.
The main risks include:
Using curling rollers;
The main affected area in the frontal-temporal area, although it can vary.
Eliminating the stressor or source of traction on the hair commonly cures the problem and returns hair growth to normal.
Tinea capitis is a fungal infection of the skin of the scalp, eyebrows and eyelashes caused by Microsporum or Trichophyton species of dermatophytes and usually occur in pre-pubertal patients.
Tinea capitis can result in widespread hair loss with increased fragility of the hairs and frequent breakage. In its most severe form, tinea capitis causes a boggy inflammatory mass called kerion, which may heal with scarring and subsequent localized alopecia.
Treatment for tinea capitis includes oral antifungal agents such as griseofulvin, itraconazole, terbinafine and fluconazole. For patients presenting kerion, oral steroids are necessary to decrease the inflammation.
Cicatricial alopecia or scarring alopecia causes permanent hair loss. The hair follicles are destroyed without re-growth by inflammatory or autoimmune diseases. The inflammatory process involves stem-cell failure at the base of the follicles, which inhibits follicular recovery from the telogen phase.
The most common disorders involved in the occurrence of cicatricial alopecia are:
Discoid lupus erythematosus;
Pseudopelade in whites;
Follicular degeneration syndrome in blacks;
The goals of treatments for cicatricial alopecia are to reduce inflammation, eliminate infection if present, reduce morbidity, and prevent complications.
The main classes of drugs used in the treatment of scarring alopecia are:
Corticosteroids (used for their anti-inflammatory properties);
Immunosuppressants (promote immune reactions resulting from diverse stimuli);
Diet and hair loss
The structure of hair and hair growth may be affected by a nutritional deficiency. Studies have shown that sudden weight loss or decreased protein intake leads to telogen effluvium, and niacin deficiency leads to diffuse alopecia. Androgenic alopecia, female pattern hair loss and alopecia areata are also associated with nutritional deficiency. If you want to diet effectively and safely, take a look here.
Iron deficiency is the world’s most common nutritional deficiency and is a well-known cause of hair loss. The mechanism by which iron impacts hair growth is unknown. Iron deficiency may contribute to hair loss via its role as a cofactor in the dividing process of hair follicle matrix cells.
The risk factors for iron deficiency include:
Gastrointestinal blood loss;
Vegan and vegetarian food.
Niacin deficiency leads to pellagra, a disease including photosensitive dermatitis, diarrhoea, dementia and alopecia. Pellagra became rare in many developed countries after niacin fortification of food was introduced.
The main causes of pellagra are:
Deficiency of the polyunsaturated essential fatty acids linoleic acid (an omega-6 fatty acid) and alpha-linolenic acid (an omega-3 fatty acid) may be determinate by malabsorption disorders such as cystic fibrosis. Hair changes include loss of scalp hair and eyebrows as well as lightening of hair.
Studies have shown that unsaturated fatty acids have the capacity to modulate androgen action by inhibition of 5-alpha reductase, like finasteride. Hair growth may also be promoted by arachidonic acid, am omega-6 fatty acid, by enhancing follicle proliferation.
Vitamin D plays an important role in hair follicle cycle. The main risk factors for vitamin D deficiency include:
Inadequate sun exposure;
One study of eight females with telogen effluvium or female pattern hair loss showed that serum vitamin D2 levels were significantly lower than in controls.
Vitamin A is a group of compounds including retinal, retinol, retinoic acid, and provitamin A. The role of dietary vitamin A in the optimal function of hair follicle was shown in murine studies.
In case of vitamin A, hair loss is not associated with its deficiency. In humans, hypervitaminosis A resulted from over supplementation, has a strong known link to hair loss with other effects such as skin, vision, and bone changes.
Biotin, or vitamin H, serves as a co-factor for carboxylation enzymes. Biotin deficiency is rare, as intestinal bacteria are typically able to produce adequate levels of biotin and it is associated with eczematous skin rash, alopecia, and conjunctivitis.
The efficacy in treating hair loss with biotin supplementation in the absence of deficiency was not shown in clinical trials.
Guo EL, Katta R. Diet and hair loss: effects of nutrient deficiency and supplement use. Dermatol Pract Concept. 2017 Jan 31;7(1):1-10.
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