Certain hair loss conditions are known as “effluviums,” a term denoting an outflow. Effluviums specifically impact various phases of the hair growth cycle. Hair follicles on the scalp don’t maintain a continuous production of hair. Instead, they cycle through a growth phase that can extend for two or more years, followed by a resting stage lasting up to two months before initiating the growth of a new hair fiber. At any given time on a healthy human scalp, approximately 80% to 90% of the hair follicles are actively growing hair. These active follicles are in what’s known as the anagen phase. This leaves around 10% to 20% of scalp hair follicles in a resting state called telogen, during which they don’t produce any hair fiber.

Telogen Effluvium

Telogen effluvium (TE) is likely the second most common type of hair loss encountered by dermatologists. It remains a vaguely defined condition, with minimal research conducted to fully understand TE. Essentially, TE occurs when there is a shift in the number of hair follicles that are actively growing hair. If the count of hair follicles producing hair significantly drops, particularly during the resting (telogen) phase, there’s a notable increase in dormant telogen-stage hair follicles. This results in shedding, or TE hair loss.

TE appears as a diffuse thinning of hair across the scalp, which may not be evenly distributed. It can be more pronounced in certain areas of the scalp. Typically, hair thinning is more evident on the top of the scalp compared to the sides and back. Hairline recession is generally absent, except in rare chronic cases.

The hairs shed in TE are typically telogen hairs, recognizable by a small bulb of keratin at the root end. Whether this keratinized mass is pigmented or not doesn’t affect the classification; these hair fibers remain typical telogen hairs.

Individuals with TE usually don’t experience complete scalp hair loss, but in severe cases, noticeable hair thinning can occur. While TE is typically localized to the scalp, more severe instances can affect other areas, such as the eyebrows or pubic region. Regardless of the form TE takes, it is completely reversible. The hair follicles aren’t permanently or irreversibly damaged; they simply enter a resting state in larger numbers than normal.

TE can develop in three primary ways:

  1. Environmental Shock: An abrupt environmental shock can trigger hair follicles to enter a resting state temporarily. This results in increased hair shedding and diffuse thinning of hair on the scalp. This form of TE can develop rapidly and might become noticeable one or two months after the triggering event. If the trigger is short-lived, the hair follicles will return to their growing state and start producing new hair fibers relatively quickly. This type of TE usually lasts less than six months, and affected individuals typically regain normal scalp hair density within a year.
  2. Gradual Accumulation: Hair follicles might transition more slowly to a resting telogen state and remain there for an extended period, leading to a gradual accumulation of telogen-stage follicles and progressive thinning of scalp hair. There might not be substantial hair shedding, but gradual thinning occurs. This form of TE is more likely in response to a persistent trigger.
  3. Truncated Growth Cycles: In this type of TE, hair follicles don’t stay in a resting state but rather cycle through shortened growth stages. This results in thin scalp hair and persistent shedding of short, thin hair fibers.

Causes of Telogen Effluvium: Stress and Diet

Numerous factors can trigger TE. Short-term TE often occurs in women shortly after childbirth, referred to as postpartum alopecia. The sudden hormonal change during childbirth can shock hair follicles into a temporary resting state, causing significant hair shedding. However, most women quickly regrow their hair after this phase.

Similarly, vaccinations, crash diets, physical trauma (such as a car crash), and surgeries can temporarily send a proportion of scalp hair follicles into hibernation. As the body recovers from these shocks, TE subsides, and new hair growth resumes.

Certain drugs, especially antidepressants, can also induce TE. Switching to a different medication might resolve this issue.

More persistent insults can lead to prolonged TE. For example, chronic illnesses can result in TE. Chronic stress and dietary deficiency are arguably the two most common triggers. Many dermatologists believe chronic stress gradually exerts a negative impact on hair growth, leading to persistent TE. Research with animal models supports this claim, indicating a connection between stress, changes in hair follicle biochemistry, and an increased number of hair follicles entering the telogen resting state.

Debates among dermatologists surround the role of dietary problems in causing TE in North America. While dietary deficiencies can certainly cause TE, particularly in third-world countries where diets may lack essential nutrients, it’s a contentious topic in developed nations. In first-world countries, the average diet is rarely entirely deficient in a particular vitamin or mineral. However, some dermatologists argue that reduced red meat consumption and a preference for vegetarian diets might result in imbalanced nutrient intake, particularly regarding iron deficiency in women due to regular iron loss during menstruation.

Other potential deficiencies in the modern North American diet, such as insufficient zinc, amino acid L-lysine, or vitamins B6 and B12, have also been proposed as contributors to TE.

When dietary deficiencies are suspected, supplements might be recommended. However, supplements can pose issues. Our bodies can only process a limited amount of iron each day, and high doses of iron can be toxic and lead to hair loss. Excessive vitamin A from supplements can also trigger TE reactions in some individuals, as excessive vitamin A can be toxic.

TE can occur independently or alongside other diseases. The early stages of androgenetic alopecia (male or female pattern baldness, AGA for short) are effectively TE. Early AGA is marked by an increase in resting telogen hair follicles, with up to 40% of scalp hair follicles in telogen phase.

TE can also manifest as a symptom of other conditions, such as inflammatory conditions like alopecia areata. Hair follicles are sensitive to thyroid hormones, and about one-third of individuals with thyroid disorders experience TE. Exposure to toxins can also cause TE as part of a broader set of symptoms.

Treatments for Telogen Effluvium

Treating TE depends on identifying the underlying trigger. For short-term TE linked to specific triggers like surgery, it’s advisable to wait for the follicles to recover naturally.

Persistent TE can be addressed by eliminating the causal factor if identified. Stress reduction helps for stress-related TE, and supplements can address identified deficiencies based on blood tests. Hormone supplements can be used for addressing thyroid hormone deficiencies.

However, when the cause remains unidentified, treatment options are limited. Dermatologists often prescribe minoxidil, a direct hair growth stimulator. While minoxidil can be effective for some individuals with TE, its use must continue if the underlying cause persists. With removal of the trigger, minoxidil use can be discontinued.

Before concluding the discussion on TE, it’s important to note that natural hair shedding is a normal process. Seasonal variations in hair shedding have been observed, with more hair loss occurring in the fall and to a lesser extent in the spring. This temporary increase in telogen hair follicles and shedding might be attributed to hormonal fluctuations in response to changes in daylight exposure.

Anagen Effluvium

Anagen effluvium mirrors telogen effluvium’s diffuse hair loss but develops much more rapidly and can lead to complete hair loss. This condition often arises in people taking cytostatic drugs for cancer treatment or those exposed to toxic substances like rat poison.

These substances inhibit rapid cell proliferation, a desirable effect for halting cancer cell growth. However, hair follicle cells are among the body’s fastest-growing noncancerous cells. Hair fibers from scalp hair follicles can grow at a rate of up to 0.4mm per day, requiring substantial cell proliferation. Cytostatic cancer drugs and toxins inhibit rapid cell growth, including hair follicle cell proliferation. This sudden inhibition halts hair fiber production.

The onset of anagen effluvium is swift. Individuals taking anticancer drugs may experience clumps of hair falling out within the first two weeks. Unlike telogen effluvium, the follicles don’t enter a telogen resting state but essentially freeze in time. Hair fibers shed quickly, often appearing as dystrophic anagen hairs with a tapered or feathered root end.

The extent of hair loss due to cytostatic drugs varies. Some individuals might experience a combination of anagen effluvium and telogen effluvium, resulting in limited hair loss.

Cold therapy, involving the use of ice packs or a specialized hood filled with cold water during anticancer drug administration, is employed by some cancer treatment centers to mitigate hair loss. Cold therapy induces a suspended animation in hair follicles before contact with the drug, preventing follicle cell uptake and damage. However, concerns exist that this approach might also shield cancer cells in the skin from the drug.

Experimental drugs to prevent drug-induced hair loss are being explored, but the same concern applies – these treatments could potentially safeguard cancer cells in the skin.

While anagen effluvium develops rapidly, recovery is equally swift. The follicles remain intact and poised for growth once the triggering factor is removed. After completing anticancer drug treatment, new hair growth may become visible within a month. Since the follicles are unharmed, normal hair density is restored. However, changes in hair fiber characteristics might occur, such as transitioning from straight to curly or experiencing altered hair color. These changes can be permanent.