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• General Questions About Hair Loss

THE HAIR LOSS DIRECTORY

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A: "The adult human body averages five million hairs, of which 100,000 to 150,000 are on the scalp. Hair is composed of keratin, the same protein that makes up nails and the outer layer of our skin. The part seen rising out of the skin is called hair shaft or strand. Each strand consists of three layers. The outermost protective layer (cuticle) is thin and colorless. The middle layer, or cortex , is the thickest. It provides strength, determines your hair color and texture.

Hair color is determined by melanin from your pigment cells. The more pigment granules there are, and the more tightly packed, the darker the hair. Two kinds of melanin contribute to hair color. Eumelanin colors hair brown to black, and an iron-rich pigment, pheomelanin colors it yellow-blonde to red. Whether hair is mousy, brown, brunette or black depends on the type and amount of melanin and how densely it's distributed within the hair. For example, deep-black African hair contains closely packed melanin in the cortex, a few in the cuticle. Very dark European hair, quite apart from having more melanin granules than lighter or blonde hair, has more melanin per granule. When pigment-producing cells cease to function, the result is the uncolored white or gray hair.

In Caucasians, true blonds typically have more hair (about 140,000 hair) than brunettes (about 105,000) or redheads (about 90,000).

Below your skin is the hair root which is enclosed by a sack-like structure called the hair follicle. Tiny blood vessels at the base of the follicle provide nourishment. A nearby gland secretes a mixture of fats (called sebum) which keep the hair shiny and waterproof to some extent. At the base of the follicle is the papilla, which is the "hair manufacturing plant." The papilla is fed by the blood-stream which carries nourishment to produce new hair. Male hormones or androgens regulate hair growth. Pubic and axillary (armpit) hair are particularly androgen-sensitive and grow at lower androgen levels than hair on the chest or legs. In boys, most pubic hair is grown by age 15, followed by the development of armpit hair two to three years later. In girls, too, an increase in androgens at puberty triggers growth of pubic and armpit hair. Scalp hair, not directly androgen-responsive, is influenced by local amounts of a testosterone derivative called dihydrotestosterone.

Hair follicles initially form in utero. No new follicles are created after birth, and none are lost in adult life. The first hair to be produced by the fetal hair follicles is Lanugo hair, which is fine, soft, and unpigmented. This is usually shed in about the eighth month of gestation. The first postnatal hair is vellus hair, which is fine, soft, usually unpigmented, and seldom more than 2 cm long. Vellus hair remains on the so-called hairless regions of the body, such as the forehead and balding scalp. At puberty, the vellus hair in some areas is replaced by terminal hair, which is longer, coarser, and pigmented. Growth starts in the pubic region; then the eyelashes and eyebrows become thicker. Axillary hair and male facial hair appear about two years after growth of pubic hair begins. Body hair continues to develop long after puberty, stimulated by male hormones that paradoxically, also cause terminal hair to be replaced by vellus hair when balding begins.

Scalp hair fibers grow from 100,000 to 350,000 follicles which are reported to occupy the human scalp; however, not all the follicles are productive. In each producing follicle, the duration of the hair's life cycle is influenced by age, pathology and a wide variety of physiological factors. The life cycle is divided into the anagen (active), catagen (transitional) and telogen (resting) phases.

The anagen phase is the period of active hair growth where protein synthesis and keratinization are continuously occurring. In normal subjects, this phase lasts for up to five years, although longer durations have been documented. The cessation of the anagen phase is characterized by a transitory phase known as catagen. This phase lasts for two to three weeks. Following the catagen phase, the hair enters the telogen or "resting" phase. In normal subjects, telogen hair is retained within the scalp for up to 12 weeks before the emerging new hair dislodges it from its follicle.

During the anagen phase, protein synthesis is the main distinction of the hair bulb. In the telogen phase, the dermal papilla undergoes renewal. It is at this time that structural characteristics can be modified. The new hair should be identical to its predecessor, but with advancing age, and in some pathological states, a strict copy is not maintained. In these circumstances, the hair may become finer and shorter, modifying the esthetic profile. Since these effects occur over several hair cycles, years may elapse before the affected individual recognizes the difference.

Like skin cells, hair grows and is shed regularly. Shedding anywhere from 50 to 100 hairs per day is considered normal. The average rate of growth is about 1/2 inch a month. It is now known that hair grows fastest in the summer, slowest in the winter, speeds up under heat and friction, but slows down when exposed to cold. Hair grows the best between the ages of 15 to 30. But, hair growth begins to wind down sometime between the ages of 40 and 50. Progressive hair loss begins naturally in both sexes about age 50, accelerating in the 70s. About 40 percent of Caucasian men lose hair to some extent by age 35."*

*Source: Health Review Magazine, January 1996. All rights reserved.
**Source: Hair Loss FAQ, Peter H. Proctor, PhD, MD.

A: There is much debate on this topic. While the link between certain forms of hair loss and the immune system is well-accepted, there is also evidence of a connection between the immune system and pattern loss (androgenic or androgenetic Alopecia). In line with this, it appears that male hormones--especially DHT--trigger an autoimmune response in pattern loss, initiating an attack on the hair follicle that can be observed microscopically. This results in destructive inflammation that gradually destroys the follicle's ability to produce terminal hair. The reason for this could be that androgens somehow alter the follicle, causing it to be labeled as a foreign body. A possibly related factor is that elevated androgens also trigger increased sebum (oil) production, which can favor an excessive microbial and parasitic population, also leading to inflammation. In any case, hair progressively miniaturizes under the withering autoimmune attack, so that with each successive growth cycle it gets shorter and thinner until it finally turns into tiny unpigmented vellus hair (peach fuzz).

In men, balding typically follows the classic horseshoe pattern known as male pattern baldness or MPB, though diffuse thinning can also occur. It has been noted that both the number of androgen receptors and the level of 5-alpha reductase, which converts testosterone to DHT, are higher in susceptible areas than in the rest of the scalp. Women's hair loss tends to be diffuse but is also primarily hormonally driven.

The story of balding is, however, not the story of androgens alone. Rather pattern loss appears to have multiple contributing factors once the process is underway. For instance, damage to blood vessel linings can inhibit a growth factor they ordinarily produce: endothelium-derived relaxing factor (EDRF) or nitric oxide (NO). Minoxidil probably works in part by mimicking this growth factor. Similarly it has been noted that severe baldness is strongly correlated with heart disease and even diabetes, so there appears to be some common etiology outside of the strictly androgen paradigm for pattern loss. There are likely other factors as well.