When it comes to hair loss, no one-size-fits-all solution exists and that is because there are plenty of reasons why your hair could be falling out. The first step in choosing the most adequate treatment is realizing which factors contribute to hair loss in your case.

Firstly, knowing hair growth dynamics is essential for understanding why hair loss occurs. Hair growth is a recurring process. Each cycle consists of three major stages that hair follicles individually go through, unsynchronized from one another:

1. Growth (anagen). Scalp hair has an anagen phase of 2 to 10 The hair only grows in length during this stage.
2. Regression (catagen). A brief step which usually lasts 1 to 2 weeks.
3. Rest (telogen). The hair follicle stays dormant for 2 to 4 months prior to hair being shed.[1]
4. Some consider the shedding of hair a distinct 4th phase (exogen).[2] In a healthy subject, the scalp contains more than 80% anagen hair and less than 20% telogen hair, with approximately 1-2% of hair follicles being in the catagen state. [2,3]

Different types of hair can be distinguished, such as the long, thick and pigmented terminal hair (I.e. scalp hair), or the fine, short and very lightly pigmented vellus hair, which covers most of the body surface.[3]

There are different ways in which the hair’s biological activity can be disturbed, usually leading to a shorter life span and, therefore, perceived hair loss.

The term effluvium describes a transitory increase in hair shedding, while alopecia is the visible result of hair loss. However, both terms are nonspecific, as they do not offer information about the underlying cause.[2]

Different distributions of thinning can be encountered:

1. Specific patterns of hair loss, for example androgenetic alopecia;
2. A rather diffuse reduction in hair density, such as telogen or anagen effluvium;
3. One or more focal patches of missing hair, like alopecia areata. [2,4]

The disorders leading to alopecia can be scarring, consequently destroying permanently the hair follicles, or non-scarring, allowing for periods of regrowth after the shedding episodes.[2] A daily shedding of up to 100 hairs is considered normal.[2]

Also known as male or female pattern baldness, it is the most frequent cause of hair loss, affecting up to 50% of men by the age of 50 and 20-30% of women after menopause. [2,3]

In men, the classical M pattern is developed in time, with different grades of severity, starting with bitemporal recession and then extending to the vertex and frontal regions.[2,4] The pattern differs in female cases, where a diffuse loss starting at the central parting and respecting the frontal line is the most typical finding.[3] It is not uncommon for men to show female hair loss patterns and vice versa.[2,3] In severely affected individuals, some changes can already be noticeable around puberty.[3]

Both genetic predisposition and the individual’s hormonal profile play a role in the development of this condition. Susceptible cutaneous territories and age of disease onset is determined genetically.[2] The risk of androgenetic alopecia increases with a positive family history. Dihydrotestosterone (DHT), a more potent androgen derived from testosterone, suppresses hair growth in these receptive conditions.

Regional resistance to androgen action explains why the occipital area remains unaffected, thus creating the condition’s specific pattern of hair loss. Through fine molecular mechanisms, DHT modifies the hair cycle rhythm, leading to a progressively decreased anagen and increased telogen phase duration, therefore resulting gradually shorter hair. Moreover, it determines miniaturization of the hair follicle, which is the process of terminal hair being replaced by finer and smaller vellus hair.[5]

The second most frequent cause of hair loss is telogen effluvium, mostly affecting women.

It is characterized by a sudden, massive, non-patterned, diffuse hair shedding. In most cases, it is caused by a premature transition of hairs from the anagen into the catagen and telogen phase, which occurs because of a specific stimulus. The provoking agents can act for less than 6 months or a longer time, leading to acute, respectively chronic telogen effluvium.

Between the action of the agent and the hair shedding episode there is a 2 to 4 months latency, which is equal to the duration of the telogen phase. The hair loss is reversible, but regrown hair can be different in texture, color, curliness or even length.

Causes of telogen effluvium are:

• Discontinuing or changing oral contraceptive medication;
• Drugs: anticoagulants such as heparin; cimetidine; enalapril and captopril; imiquimod; metoprolol and propranolol; lithium; l-dopa; trimethadione; bromocriptine; etretinate and isotretinoin; cholesterol-lowering drugs; colchicin;
• Contamination with selenium, arsenic, thallium, mercury, lead;
• Rapid weight loss;
• Caloric, protein or essential fatty acids chronic deprivation;
• Chronic iron deficiency; possibly zinc and biotin deficiency;
• Surgical procedures, major trauma, hemorrhage;
• Acute or chronic psychological stress;
• Febrile illness;
• Renal dialysis;[2,6]
• Hypo- and hyperthyroidism, autoimmune diseases, psoriasis and seborrheic dermatitis
• Childbirth, miscarriage, abortion. In these cases, the biological mechanisms slightly differ. In pregnancy, there is a delay in anagen release due to the generally growth-promoting environment. Once the pregnancy is ended, multiple delayed hairs continue their cycle, finally entering the catagen and telogen phases. The sudden hair loss is caused by the simultaneous shedding of a larger number of terminal hairs.[3]

After radiation therapy or chemotherapy with vincristine, vinblastine, methotrexate, doxorubicin, fluorouracil or other drugs, the anagen phase is interrupted and the hair easily falls out in 7–14 days, after gentle pulling, without entering the catagen or telogen phase. The hair regrows after 4 months.[2]

This condition is the most common type of alopecia in children, although it can occur at any age.[4]

It typically manifests as sudden non-scarring hair falling, leaving one or multiple oval, well-circumscribed, usually asymptomatic bald patches with a smooth surface. The loss of the entire scalp hair is called alopecia totalis, and of the total body hair, alopecia universalis. [2,4]

This condition falls into the autoimmune category, as the hair follicle is being targeted by one’s own immune cells. However, the follicle is not destroyed, and regrowth is possible.

The evolution is chronic, with spontaneous remissions and repeated relapses. Major emotional stress is often a trigger. Other diseases, especially autoimmune ones, can be associated.[2,3,4]

Prolonged traction or pressure applied to the scalp can lead to hair loss, usually in the frontotemporal area. Women who wear tied back hairstyles, tight braids or wigs are at risk. Eliminating the source of traction allows for regrowth if subsequent scarring has not occurred.[3,4]

If hair is compulsively and repeatedly being plucked, alopecia can result.[4]

Inflammatory diseases and infections can sometimes cause focal alopecia. In most cases hair regrowth is still possible. Some examples are psoriasis, seborrheic and atopic dermatitis, bacterial and fungal infections (i.e. tinea capitis).[3]

Inflammatory or autoimmune diseases can cause permanent hair loss through destruction of the hair follicles. Examples include discoid lupus erythematosus and rather rare conditions such as lichen planopilaris, frontal fibrosing alopecia, or central centrifugal scarring alopecia. [3,4]

• Park, AM, Khan S, Rawnsley Hair Biology: Growth and Pigmentation. Facial Plastic Surgery Clinics of North America. 2018; 26(4): 415-424
• Wolff K, Goldsmith L, Katz S, Gilchrest B, Paller AS, Leffell Fitzpatrick'sDermatology in General Medicine. 8th Edition. New York: McGraw-Hill; 2011
• Wolff Diseases of Hair. Braun Falco´s Dermatology. Springer Berlin Heidelberg. 2020: 1–33
• Mounsey A, Reed SW. Diagnosing and treating hair loss. American Family Physician.2009;80(4):356-62
• Lolli F et al. Androgenetic alopecia: a review. Endocrine. 2017; 57:9–17
• Asghar F, Shamim N, Farooque U, Sheikh H, Aqeel Telogen Effluvium: A Review of the Literature. Cureus. 2020; 12(5)