Anti prolactin drug being developed for androgenic alopecia

[johnwester130]

View: https://www.reddit.com/r/tressless/comments/lx3yok/bayer_prolactin_receptor_antibody_for_male_and/



View: https://www.reddit.com/r/tressless/comments/qhik5r/this_might_actually_be_the_real_deal_i_dont_think/

 

[golder]

Was thinking of adding a small amount of a prolactin agonist to my topical hair spray recently. Never got around to it. I wonder what we could use before this promising compound becomes available.

 

[md_a]

Ray Peat: Both prolactin and TSH are increased by TRH, and I think both can contribute to hair loss.

Human Female Hair Follicles Are a Direct, Nonclassical Target for Thyroid-Stimulating Hormone​

Pituitary thyroid-stimulating hormone (TSH) regulates thyroid hormone synthesis via receptors (TSH-R) expressed on thyroid epithelial cells. As the hair follicle (HF) is uniquely hormone-sensitive and, hypothyroidism with its associated, increased TSH serum levels clinically can lead to hair loss, we asked whether human HFs are a direct target for TSH. Here, we report that normal human scalp skin and microdissected human HFs express TSH-R mRNA. TSH-R-like immunoreactivity is limited to the mesenchymal skin compartments in situ. TSH may alter HF mesenchymal functions, as it upregulates α-smooth muscle actin expression in HF fibroblasts. TSH-R stimulation by its natural ligand in organ culture changes the expression of several genes of human scalp HFs (for example keratin K5), upregulates the transcription of classical TSH target genes and enhances cAMP production. Although the functional role of TSH in human HF biology awaits further dissection, these findings document that intracutaneous TSH-Rs are fully functional in situ and that HFs of female individuals are direct targets for nonclassical, extrathyroidal TSH bioregulation. This suggests that organ-cultured scalp HFs provide an instructive and physiologically relevant human model for exploring nonclassical functions of TSH, in and beyond the skin.

Human Female Hair Follicles Are a Direct, Nonclassical Target for Thyroid-Stimulating Hormone

...........

Dr. Ray Peat: In hypothyroidism, thyrotropin-release hormone (TRH) is usually increased, increasing release of TSH. TRH itself can cause tachycardia, “palpitations,” high blood pressure, stasis of the intestine, increase of pressure in the eye, and hyperventilation with alkalosis. It can increase the release of norepinephrine, but in itself it acts very much like adrenalin. TRH stimulates prolactin release, and this can interfere with progesterone synthesis, which in itself affects heart function.

I consider even the lowest TSH within the “normal range” to be consistent with hypothyroidism; in good health, very little TSH is needed. When the thyroid function is low, the body often compensates by over-producing adrenalin. The daily production of adrenalin is sometimes 30 or 40 times higher than normal in hypothyroidism. The adrenalin tends to sustain blood sugar in spite of the metabolic inefficiency of hypothyroidism, and it can help to maintain core body temperature by causing vasoconstriction in the skin, but it also disturbs the sleep and accelerates the heart. During the night, cycles of rising adrenalin can cause nightmares, wakefulness, worry, and a pounding heart. Occasionally, a person who has chronically had a heart rate of 150 beats per minute or higher, will have a much lower heart rate after using a thyroid supplement for a few days. If your temperature or heart rate is lower after breakfast than before, it’s likely that they were raised as a result of the nocturnal increase of adrenalin and cortisol caused by hypothyroidism.

 

[LeeLemonoil]

Prolactin receptor antibody -

So, binding and then actually immune system destroying the receptors in situ?

 

[LeeLemonoil]

Prolactin receptor antibody -

So, binding and then actually immune system destroying the receptors in situ