House Treatments For Hair Loss
I’d like to begin by saying how superb this webpage is and all of the great information that Ted and all the members provide. A little background; I started Acctuane July of 2010 and bought off it in December of 2011. I took wherever from 40-eighty mg a day. I saw a previous post on Acctuane and hair loss on this discussion board and I’ve been following it to a T for the final four months will little success. I’m 18 years old and had the thickest head of hair earlier than Accutane and that i don’t have any household historical past of baldness on either aspect of my household. I am 100% certain that I am losing hair as a result of Accutane. It is not in the MPB sample, it is usually diffusing all over. I have taken so many supplements in try and counteract my hair loss, here are some:
N-acetyl Cysteine (1500mg)
Riboflavin 5- Phosphate (36.5mg)
B Advanced (Activated/co-enzymated 3x daily)
Molybdenum Picolinate (1, 000mg)
Phytisone Adrenal Complex (3x day by day)
AC Grace Vitamin E (1200 IU)
Glutathione (2x each day)
Thorne Mediclear (2x daily)
Prescript Assist soil primarily based probiotic (2x daily)
Niacinamide (1, 000 mg)
Manganese Sulfate (400mg)
Fish oil (2x a day)
Vitamin C (5000mg)
Vitamin D (6000 IU)
As you can see, I have experimented with quite a bit of various supplements and it is quite overwhelming. The hair loss didn’t start until 2 months after my course was over. I feel like none of these are attending to the bulk human hair wholesale source of my drawback which I imagine to be cell divison. Accutane is a chemotherapy agent and acts by suppressing cell division and proliferation. I have executed copious amounts of analysis over the last eight months and really feel like I get so close to the reply.
“Retinoic acid (lively form of Accutane) induces differentiation and reduces proliferation of stem and progenitor cells. It works on acne by inducing comparable occasions in basal sebocytes. These similar actions additionally lead to 13-cis-retinoic’s (Accutane’s) side effects, and these are directed towards proliferating cells in the adult reminiscent of within the skin, intestine and bone. “
“A wide ranging effect of retinoic acid is to inhibit proliferation in dividing cells, and this accounts for its frequent consideration as an anti-cancer agent.”
“Deleting telomere elongation capability throughout the body would even be life-threatening, as a result of it will imply that our regular, proliferating cells (like these in the skin or the lining of the intestine) would all of the sudden have iron limits on their skill to reproduce themselves and thus replenish tissue. From the second that we denuded our cells of telomerase, a clock would be ticking. With each division the telomere would shorten by a notch from no matter it had been once we took telomerase out. We would be under the specter of a moderately horrible loss of life, as our stem cells went offline one after the other beneath replicative senescence with each failure of a stem cell liable for supplying key capabilities, the tissue would fail to be renewed and would slowly degenerate. “(De Gray, 297)
To sum all of this up, the proof we at present have is that long term therapy with ATRA (all-trans retinoic acid), which is almost chemically equivalent to Accutane, causes “telomere shortening, growth arrest, and cell death.”
Accutane induces cell apoptosis. It down-regulates the telomerase enzyme and shortens the telomere size so the cells cannot divide as a lot anymore.
Quite a few elements have an effect on the number and activity of androgen receptors in dermal papilla cells. Retinoic acid (vitamin A derivative), if used for a very long time, may scale back the variety of androgen receptors by 30 – 40 p.c.  Vitamin B6 reduces by 35-40% the extent of protein synthesis observed after androgen receptor activation.  A polypeptide with molecular weight of 60 kDa, analogous to an intracellular calcium-binding protein called calreticulin, prevents binding of the androgen-receptor complex to DNA and in addition results in the production of calreticulin.
Medicine producing hair loss:
Medicine may affect hair follicles in anagen in two methods: by stopping mitosis in matrix cells (anagen effluvium) or by inducing transition of hair follicles from anagen to premature telogen (telogen effluvium). Anagen effluvium ensues a couple of days or weeks after drug administration,  and telogen effluvium only after two to four months. In each instances hair loss is reversible. Anagen effluvium may be produced by cytotoxic medication (alkylating agents, alkaloids) and telogen by: heparin, vitamin A and its derivatives, interferons, angiotensin changing enzyme blockers, beta-blockers (propranolol, metoprolol), the antiepileptic trimethadione, levodopa, nicotinic acid, salts of gold, lithium, cimetidine, amphetamine, isoniazid and antiinflammatory medicine (ibuprofen, acetylsalicylic acid).
I really feel as if there was a means to extend cell division that the hair loss could possibly be reversed. It states in the last paragraph that “in each cases hair loss is reversible”. I hope that this is the case and that I simply have telegon effluvium and not permenant alopecia.
Without having a scientific background it is tough to connect the pieces and come up with an answer. Ted- if you possibly can decipher all of this and make some connection between it, it will imply the world to me and plenty of different Accutane sufferers.
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