Excessive Hair Shedding? Learn The Signs of Androgenetic Alopecia

Androgenetic Alopecia (also called androgenic alopecia) affects both men and women and is often referred to as male pattern baldness or female pattern baldness. It is a non-reversible form of genetically determined hair loss characterized by a marked decrease in terminal hair density as well as in hair shaft diameter. Although the pattern of hair loss appears differently in men and women, the underlying cause is the same: genetic disposition combined with the sex hormones called androgens. Androgens stimulate development of the male sex organs and also regulate hair growth and sex drive in both genders. learn how to make your healthy with natural ways without any harsh chemical. 

Specifically, the androgen testosterone converts into DHT (dyhydrotestosterone) with the help of 5 alpha reductase, an enzyme involved in steroid metabolism. A combination of DHT and genetic disposition facilitates a reduction in anagen (growth phase) as well as follicles that appear to shrink in diameter over time. According to Lacharriere et.al., "diversity in hair diameter is the main and most accurate clinical parameter linked to follicle miniaturization."1

Eventually, thick terminal hairs are replaced by fine vellus hairs (less than .03 mm in width). In some people, remaining terminal hairs may become shorter and coarser, resembling public hair. Of all ethnic groups, Caucasoids have been shown to suffer more from AGA than Afroids or Mongoloids.

Genetic research suggests that AGA is linked to genes on an X chromosome.2

In a major 2007 study, German researchers found that a specific variant of the androgen receptor gene, which is recessive, is needed to trigger AGA. Thus, a woman would need two X chromosomes with the defect to develop AGA.

In addition to genetics and androgens, women tend to have additional hormonal imbalances or conditions that may also play a role in the onset of AGA and its treatment.

Male Pattern Baldness

Men with AGA typically have higher levels of 5 alpha reductase, lower levels of total testosterone, higher levels of unbound/free testosterone, and higher levels of total free androgens including DHT.3 Age may also play a part in triggering the genetic onset of male AGA.

In the classic form of male pattern balding, hair is lost in a well-defined pattern beginning above both temples and at the crown of the head. As hair loss progresses, a rim of hair may be left from ear to ear in a pattern called "Hippocratic balding."4

A reliable scale to determine the progression of male pattern baldness was developed in the 1950s by Dr. James Hamilton and expanded in the 1970s by Dr. O'Tar Norwood. Actual progression varies from patient to patient and may not automatically lead to further balding.

In addition to consulting the Norwood-Hamilton Scale, trichoscopy can be helpful in diagnosing male AGA. Current trichoscopy magnifications range from 10-fold to 70-fold. Trichologists should look for the following criteria:

increased percentage of thin hairs

decreased average hair diameter

predominance of hair follicles with single hair shafts

presence of yellow dots

perifollicular hyperpigmentation

Female Pattern Baldness

In addition to genetic predisposition and the presence of androgens, other hormonal factors stemming from the endocrine system often play a part in cases of female AGA. Conditions to be aware of include:

Hypo- or hyperthyroidism

Insulin resistance

Metabolic syndrome

Polycystic Ovarian Syndrome

Peri-menopause and Menopause

Hysterectory

Ovarian Cancer

Anemia

Hormone-altering medications.

Female AGA is very different from men's in that it presents as diffuse thinning throughout the scalp. The Ludwig scale is the standard classification for female pattern baldness. However, in 1999, Olsen further categorized female AGA into 3 stages beginning with greater loss at the frontal region and tapering back toward less hair loss in the occiput.5

Stage 1: Mild to moderate frontal accentuation loss

Stage 2: More severe frontal accentuation mixed with diffuse hair loss

Stage 3: Continued diffuse thinning giving a more extreme appearance of hair loss.

According to Olsen, this "Christmas tree pattern" of hair loss accounts for 70% of female pattern loss.

Inga Zemite, MD, MTTS, offers an explanation for the unique pattern. She states that women with female pattern hair loss have higher levels of 5 alpha reductase and anagen receptors in frontal hair follicles, while having high levels of cytochrome p-450 aromatase in frontal and occipital follicles that saves some hairs from falling out.6

An abundance of estrogen may account for the somewhat slower progression of AGA in women than in men. Once menopause sets in, however, causing the permanent cessation of ovarian function including estrogen production, AGA may be triggered or sped up in women who are genetically predisposed.

Women exhibiting symptoms of AGA (thinning hair with decreased diameter of the hair shaft) can be further diagnosed using trichoscopy. According to Rakowska, et.al., major diagnostic criteria for female AGA using a trichoscope include:

increased number of yellow dots and thin hairs

decreased average hair thickness in frontal area.

Minor criteria include: increased frontal area to occiput ratio of single-hair units (>2:1) vellus hairs (>1.5:1) and follicles with perifollicular discoloration (>3:1) Fulfillment of 2 major criteria or 1 major and 2 minor is necessary for diagnosis.7

Treatments

Current effective treatments for AGA include:

Finasteride (Propecia, Proscar): An inhibitor of 5 alpha reductase, the enzyme that that converts testosterone to DHT. Approved only for use in men, as it can cause birth defects in women. Taken orally, the drug is shown to improve hair growth on the crown, with a recurrence of loss within 12 months when treatment is interrupted. Side effects include impotence and a possible increase in the risk of prostate cancer.

Minoxidil (Rogaine): A powerful vasodilator, Minoxidil is applied topically to prolong anagen in the vertex region of the scalp. It is approved for use in both men and women. It can take 6 to 12 months for hair to show an increase in number and diameter. Hair loss resumes if treatment is interrupted. Side effects include skin irritation.

Dutasteride (Avodart): Oral inhibitor of 5 alpha reductase not generally prescribed for female AGA. Side effects include impotence.

Spironolactone (Aldactone): Topical anti-androgen that inhibits DHT from attaching to receptor sites. Side effects include muscle weakness and drowsiness.

Hair Restoration Surgery: follicular grafting, scalp reduction, flap rotations. Side effects include scarring and infection.