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What Is Hair, Really? By |
"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 consist of three layers. The
outermost protective layer (cuticle) is thin and colorless. The middle layer, or cortex ,
is the thicknest. It provides strength, determines your hair color and whether your hair
is straight or curly.
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 brunette
(about 105,000) or redhead (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,
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.[1,2] 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 hairloss begins naturally in both sex about age 50, accelerating in the
70s. About 40 percent of Caucasian men lose hair to some extent by age 35."*
Alopecia Universalis is when all or almost all hair on
the body is lost (hair on head, eyebrows, eylashes, etc.)
"By far the most common form of hairloss is determined by our genes and hormones:
Also known as androgen-dependent, androgenic, or genetic hairloss. It is the largest
single type of recognizable alopecia to affect both men and women. It is estimated that
around 30% of Caucasian females are affected before menopause. Other commonly used names
for genetic hairloss include common baldness, diffuse hairloss, male or female pattern
baldness."*
"The rate of hair shedding in androgenic alopecia is
speeded up by three forces: advancing age, an inherited tendency to bald early, and an
over-abundance of the male hormone dihydrotestosterone (DHT) within the hair follicle. DHT
is a highly active form of testosterone, which influences many aspects of manly behavior,
from sex drive to aggression. The conversion from testosterone to DHT is driven by an
enzyme called 5-alpha reductase, which is produced in the prostate, various adrenal
glands, and the scalp. Over time, the action of DHT causes the hair follicle to degrade
and shortens the anagen phase. Though the follicle is technically still alive and
connected to a good blood supply--it can successfully nurture a transplanted follicle
which is immune to the effects of DHT--it will grow smaller and smaller. Some follicles
will gradually die, but most will simply shrink to the size they were when you were born
which produce weaker hairs. With a steadily shorter anagen growing cycle, more hairs are
shed, the hairs becoming thinner and thinner until they are too fine to survive daily wear
and tear. Balding hair gradually changes from long, thick, coarse, pigmented hair into
fine, unpigmented vellus sprouts."*
"Current research also indicates an immunological factor in balding. Basically, the
immune system begins to target the hair follicles in the hairloss area. The current
theory is that the rise in male hormones such as DHT during puberty INITIATES this
process. This is why many drugs which lower male hormone levels do not completely stop and
reverse the hairloss process. One other target of treatment is to manipulate the
messenger chemicals in the body that tell follicles to initiate anagen and telogen phases.
Super Oxide radical is believed to be one of the messenger substances causing hair to
enter telogen (resting phase), while nitric oxide is one of the messenger substances
causing hair to enter anagen (growth) phase. These treatments use topical treatments to
stimulate nitric oxide levels while decreasing Super Oxide Radical levels using Super
Oxide Dismutase (SODases). Many of the drugs currently being researched and studied by the
FDA are SODases."**
"However, the sebaceous gland attached to it remains the same size. As the hair
shafts become smaller, the gland continues to pump out about the same amount of oil. So as
your hair thins, you will notice that your hair becomes flatter and oilier.
Other physiological factors might cause hairloss. Recently, a group of Japanese
researcher reported a correlation between excessive sebum in the scalp and hairloss.
Excessive sebum often accompanying thinning hair is attributed to an enlargement of the
sebaceous gland. They believed excessive sebum causes an high level of 5-alpha reductase
and pore clogging, thus malnutrition of the hair root.
Although this condition could be hereditary, they believe diet is a more prominent cause.
The researchers note that Japanese hair was thick and healthy, with a small gland and
little scalp oil, until the occidental habit of consuming animal fat crept into their diet
after World War II. This change has led to a significant height increase in the Japanese
population, but it has also resulted in more Japanese men losing hair. To some extent,
their observation makes sense since problems with greasy hair have often been noted as
much as six months to a year prior to when thinning hair becomes noticeable, but this
might be just one of the symptons, not underlying cause, more research is needed. Most
doctors agree that if you have a oily scalp with thinning hair, frequent shampooing is
advised. Shampooing can reduce surface sebum, which contains high levels of testosterone
and DHT that may reenter the skin and affect the hair follicle."*
*Source: Health Review Magazine, January 1996.
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**Source: Hairloss FAQ, Peter H. Proctor, PhD, MD.

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