Jump to content

Supplemental estradiol/estrogen to increase longevity?


Recommended Posts

So, like, testosterone bad, estrogen good. Has anyone thought of bica/spiro + estradiol?

 

https://docs.google.com/document/d/1cdlrbsuCfwxR9pykGyMgezHZAAlsc7VJFdKw50_qRrE/edit 

Castration reduces DNA methylation age - https://www.biorxiv.org/content/10.1101/2020.11.16.385369v1?__cf_chl_jschl_tk__=a9f7af7214e36934ecad24ee42b813a5cf7cbb42-1605739115-0-AQtO5lHUsJJx27iHzXoRFSrHV2T79mQMKKj-snCHEsCZvqwOL2Bqe_6Wic9Mtu_DQ8xA1MfwsBR27EfGAeZqu7csupkiY0Skwqrlbrvns64mbXQ-BReg88_RXX8rrc-jozSGVj0p41vltobtze_W9n3jiMmKzxdgLbLXjHsp-lfhAkaDBcuuC8pI3HOUjx17oNMCwOu33onKjI-oOHGuVVp8yKn3cmXo38VQykSbR22oUfVAbTzN9450un4TG_kpMMnTPj6otv2-OcuCSL3IpnsVw1h2qMi15U_2G5gW9IqCevniQE4w-9gdhMtzSN_XcXTKX7x_fyHesY7hkE0-IRKfFBOpMWQyXCvl3f8rTxK4

17-alpha estradiol increases longevity in males and makes their longevity competitive with females. It's not easy to get. Estradiol is easy to get and is supposedly mixed isomers AND you can stop it when you get breast growth.

 

Edited by InquilineKea
Link to comment
Share on other sites

You'll probably experience some feminizing effects. Even if you say for example, used the estrogen at a low dose, if you're also suppressing Testosterone and DHT, you'll probably start noticing budding and experience skin changes within 2-4 weeks. It's not as simple to stop and start, but you could probably manage a really low dose and significantly prolong the time it takes for changes to happen.

Edited by Matt
typo
Link to comment
Share on other sites

  • 3 weeks later...

I try lots of ground flaxseeds for 3 months for my curiosity about the effects of phytoestrogens. (This is my experience not claim anything) It messed me up, I lose muscle, oiling in my chest, my skin becomes much softer, my eyelashes and hair grow faster. Even I'm doing an exercise I can't stop oiling in the body and I quit. I think Moroccan tea is a better option if you want to suppress testosterone levels.

Link to comment
Share on other sites

  • 3 weeks later...
Quote

 

14.4  Estrogen and Neuroprotection

Estrogen mediated neuroprotection has been described in several neuronal culture models of neuronal toxicity including that of the serum deprivation (Gollapudi and Oblinger 1999), β amyloid-induced toxicity (Behl et al. 1997; Gridley et al. 1997) and excitotoxicity systems (Weaver et al. 1997; Singer 1999). It has also been demonstrated in experimental models of oxidative stress (Moosmann and Behl 1999). Estrogen has a large number of cellular effects including the modulation of apoptotic factors, which has been shown to enhance neuronal survival (Green and Simpkins 2000). The Bcl-2 family of proteins are important modulators of neuronal apoptosis and include both inhibitors (Bcl-2 and Bcl-XL) as well as promoters (Bax and Bad). A marked increase in the Bcl-2 immunoreactivity has been observed in NT2 neuronal cell cultures (Singer et al. 1998) and in the neurons of the arcuate nucleus of rat following 17α estradiol administration (Gollapudi and Oblinger 1999). Similarly, 17β estradiol increased i) Bcl-XL mRNA levels in PC 12 cells transfected with ERα (Gollapudi and Oblinger 1999) and ii) Bcl-XL immunoreactivity in primary rat hippocampal neurons (Pike 1999). 17β estradiol exposure also caused a marked decrease in the levels of pro-apoptotic protein BAD in ERα transfected PC 12 cells (Gollapudi and Oblinger 1999). The expression of a member of Bcl-2 binding proteins family (BNIP) was significantly reduced by treatment with 17β estradiol in

 

Quote

n addition to regulation of gonadal functions, ERα and ERβ are also present in both female and male brains, specifically in brain areas involved in memory and cognition (McEwen 2001). Among the brain regions, major interest is focused on hippocampus and neocortex (Mehra et al. 2005). In rat and mouse, different regions and cell-populations in the brain, including hypothalamus, hippocampus, cerebellum and pituitary appear to express ERα and ERβ (Mitchner et al. 1998; Osterlund et al. 1998). While the protein sequences of ERα and ERβ are highly homologous, they represent two distinct gene products. In humans, the gene for ERα is located on chromosome 6 while that for ERβ is on chromosome 14 (Couse and Korach 1999).
Since estrogen is a potent neuroprotective hormone, to reveal its exact mo lecular and cellular mechanisms of action would offer putative drug target points. Gonadal steroids act on both genomic and nongenomic pathways related to nuclear as well as membrane and cytoplasmic receptors, respectively. Extensive research activity is going on worldwide, including our recent research work, to define both genomic and intracellular signaling pathways in order to determine the molecular actions of estrogens. For example: (1) Activation of Src/ERK/CREB/Bcl-2 signaling pathways by estrogen triggers neuroprotective mechanism (Sharma and Mehra 2008), (2) Estradiol (E2)-induced formation of dendritic spines in hippocampus acts via Akt (protein kinase B)-mediated signaling events (Zhou et al. 1996), and
(3) modulation of cyclic AMP response element binding protein (CREB) pathway (Szegõ et al. 2006; Wappler et al. 2009) provides an insight into the existence of the ‘nongenomic’ action of the ovarian hormone. According to Falkenstein et al. (2000), estrogen rapidly activates adenylate cyclase, ERK 1 and 2, and MAPK

 

Edited by InquilineKea
Link to comment
Share on other sites

Join the conversation

You can post now and register later. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
 Share

×
×
  • Create New...