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GAS6 protein

Has GAS6 been discussed here? I can’t find a thread here that discusses it. It was in the news here a few months ago. Is it anything to be excited about?

I hate to say it, but it sounds like they’re totally on the wrong track. Stress is NOT the primary cause of hair loss in males… It is androgenetic alopecia which is caused by dihydrotestosterone.


Stress is toxic and Testosterone activity is the rule and the healthy status-quo.

The receptors which are said receptors of T and make after their reception of T the DHT are there since 1st moments of creation, if you read texts of 2006 -if not prior to that-

Read in wikipedia

Distribution with age

5α-R1 is expressed in fetal scalp and nongenital skin of the back, anywhere from 5 to 50 times less than in the adult. 5α-R2 is expressed in fetal prostates similar to adults. 5α-R1 is expressed mainly in the epithelium and 5α-R2 the stroma of the fetal prostate. Scientists looked for 5α-R2 expression in fetal liver, adrenal, testis, ovary, brain, scalp, chest, and genital skin, using immunoblotting, and were only able to find it in genital skin.[8]

After birth, the 5α-R1 is expressed in more locations, including the liver, skin, scalp and prostate. 5α-R2 is expressed in prostate, seminal vesicles, epididymis, liver, and to a lesser extent the scalp and skin. Hepatic expression of both 5α-R1 and 2 is immediate, but disappears in the skin and scalp at month 18. Then, at puberty, only 5α-R1 is reexpressed in the skin and scalp.

5α-R1 and 5α-R2 appear to be expressed in the prostate in male fetuses and throughout postnatal life. In adulthood, 5α-R1-3[ clarification needed ] is ubiquitously expressed. 5α-R1 and 5α-R2 are also expressed, although to different degrees in liver, genital and nongenital skin, prostate, epididymis, seminal vesicle, testis, ovary, uterus, kidney, exocrine pancreas, and the brain.[3][8]

Stress causes a lot of toxic cascades and immune reactions

Women undergo a lot of stress, too, but rarely develop hair loss to the extrent seen in men.


Maryborough, in central Victoria has an approximate population of 8000 and census data is well matched for Australia overall. Australia has compulsory voting and registration on the electoral roll. To determine the age-related prevalence of balding among men and women in Maryborough we conducted a postal survey of 5000 men and women aged 20 or older, and 427 were invited to attend for examination. Additional data was collected on dandruff, presence of gray hair. Supplementary questionnaires were sent to 340 children aged 5-9, attending a coeducational primary school. 1456 adults (34.1%) responded to the questionnaire. 396 attended for examination. The prevalence of androgenetic alopecia (AGA) increased with advancing age. 98.6% of men had bitemporal recession and severity was significantly associated with vertex and mid-frontal hair loss (p <0.01) but not age (p = 0.06). In all, 64.4% of women had bitemporal hair loss, and similar to men there was a significant association with mid-frontal hair loss (p =0.042) but not age (p =0.467). One hundred and forty children with completed questionnaires were examined. All 72 females and 68 males were assessed as stage 1 on the mid-line part and with no bitemporal recession (frequency stage 1 = 100%, 95% CI (confidence interval) 97.4%-100%). A significant but weak positive association existed between presence of gray hair and history of dandruff (p<0.01). The prevalence of mid-frontal hair loss increases with age and affects 57% of women and 73.5% of men aged 80 and over.

Traditionally, more attention has been paid to male-pattern baldness; however, alopecia is common in females as well. More than 21 million females in the U.S. are affected by alopecia.

Androgenetic Alopecia: Also known as female-pattern or male-pattern hair loss, androgenetic alopecia is the most common type of alopecia. Caucasian females seem to have a higher prevalence, although precise numbers have not been determined.


Telogen Effluvium: During stressful times, the body may react by causing more hairs than normal to enter the resting phase. This is a form of alopecia called telogen effluvium . The body sheds a large amount of hair, which generally will regrow in 9 to 12 months without pharmacologic treatment. The hair loss occurring in telogen effluvium tends to be more rapid than in the case of androgenetic alopecia. The instigating factor or event typically occurs 2 to 4 months prior to noticeable hair loss, and the shedding lasts between 2 and 4 months.3 Stressful conditions that can cause telogen effluvium include pregnancy, thyroid disorders (hypothyroidism, hyperthyroidism), systemic lupus erythematosus, severe infections, major surgery, and deficiency disorders (protein, iron). Certain medications also can lead to telogen effluvium ( TABLE 1 ), but spontaneous regrowth usually occurs after the causative agent is discontinued.


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