Just to let you know, I've started my first estrogen (estradiol) intake today.

I rubbed oestrogel all over my scalp and took a pill. I'll be doing this once per week, for a whole month, then skip for an entire month. I might post a new topic on the HRT forum to keep everyone updated.

I wonder if stopping and resuming hormones at an intermittent pace wouldn't be determential to your body.... I would think it would werak havoc on your body and make it continually confused, overworking it....

Quote from: MsDazzler on December 24, 2011, 11:53:58 AM
I wonder if stopping and resuming hormones at an intermittent pace wouldn't be determential to your body.... I would think it would werak havoc on your body and make it continually confused, overworking it....

Most HRT are titriated regimes (start at low doses, monitor liver enzymes for toxicity, increase or decrease or terrminate dosage.

Hormone effects are cummulative so if you start and stop you will reduce their effectiveness, and piss off your provider, that is all.

Jen61

In my case it's difficult to tell as I'd imagine it would be in any MTF case as we tend to start both hormone blockers and Estrogen. In my case I can't rightly tell you what effects were caused by the T-blockers and whitch was caused by the estrogen.

Overall tho friends have remarked about changes to the texture of my hair it's thicker fluffier much drier and less greasy than before and while I didn't think I had male pattern baldness I still got some hairs sprouting out of my hairline whitch I must have lost some time before. however I still have a male hairline.

While your post is intresting and well thought out. I don't think it's as simple as you make out because indivduals who've been castrated express similar effects on hair accociated with a loss of T rather than the introduction of Estrogen.

The exact mechanisms of MPB are complex and while shortening telomeres are a factor there are many young pepole who go bald dispite having normal length telomeres thus aging merely increases propensity towards the phenominon happening but not the trigger itself.
http://www.sciencedaily.com/releases/2010/04/100414134547.htm

My understanding of the process through what I've read is that WNT a cellular growth factor cascade is normally active in hair folicle cells encouraging them to divide. what I understand happens is that testosersone is converted to DHT through Alpha-5-reductase inside the cell this probably triggers an intercellular message (Mechanism unknown) whitch down regulates WNT and thus supresses the growth cycle of the hair, making it thinner and thinner until it's too small to reach through the skin.

However I've also seen some evidence that it's linked partly to a chronic inflammation reaction I suspect if this threoy is true then telomeres might be involved in it as misfolded protiens often occur in cells with shortened telomeres.

Both estrogen and testosterone act directly  or indirectly by regulating gene expression. Estrogen has been shown to be important for the up regulation of the telomerase gene.

Jen61

Carcinogenesis. 2011 Sep;32(9):1315-23. Epub 2011 Jun 21.

Indole-3-carbinol downregulation of telomerase gene expression requires the inhibition of estrogen receptor-alpha and Sp1 transcription factor interactions within the hTERT promoter and mediates the G1 cell cycle arrest of human breast cancer cells.

Marconett CN, Sundar SN, Tseng M, Tin AS, Tran KQ, Mahuron KM, Bjeldanes LF, Firestone GL.
Department of Molecular and Cell Biology and The Cancer Research Laboratory, University of California, Berkeley, CA 94720-3200, USA.

Abstract

Indole-3-carbinol (I3C), a naturally occurring hydrolysis product of glucobrassicin from cruciferous vegetables such as broccoli, cabbage and Brussels sprouts, is an anticancer phytochemical that triggers complementary sets of antiproliferative pathways to induce a cell cycle arrest of estrogen-responsive MCF7 breast cancer cells. I3C strongly downregulated transcript expression of the catalytic subunit of the human telomerase (hTERT) gene, which correlated with the dose-dependent indole-mediated G(1) cell cycle arrest without altering the transcript levels of the RNA template (hTR) for telomerase elongation. Exogenous expression of hTERT driven by a constitutive promoter prevented the I3C-induced cell cycle arrest and rescued the I3C inhibition of telomerase enzymatic activity and activation of cellular senescence. Time course studies showed that I3C downregulated expression of estrogen receptor-alpha (ERα) and cyclin-dependent kinase-6 transcripts levels (which is regulated through the Sp1 transcription factor) prior to the downregulation of hTERT suggesting a mechanistic link. Chromatin immunoprecipitation assays demonstrated that I3C disrupted endogenous interactions of both ERα and Sp1 with an estrogen response element-Sp1 composite element within the hTERT promoter. I3C inhibited 17β-estradiol stimulated hTERT expression and stimulated the production of threonine-phosphorylated Sp1, which inhibits Sp1-DNA interactions. Exogenous expression of both ERα and Sp1, but not either alone, in MCF7 cells blocked the I3C-mediated downregulation of hTERT expression. These results demonstrate that I3C disrupts the combined ERα- and Sp1-driven transcription of hTERT gene expression, which plays a significant role in the I3C-induced cell cycle arrest of human breast cancer cells.