Interesting Study On Why Not To Destroy Estrogen Balance

[EricMM]

Looks like here we see estradiol is an important factor in Serotonin uptake. Suppression of estradiol increased insulin resistance and obesity.

I think insulin resistance works in this way:

Muscle cells are the primary preferred clearing mechanism. Fat cells seem to be the last line of defense and the last to achieve insulin resistance. Thus it's important to take our insulin sensitizers with our meals! Also, supports the Team Juggernaut theory of carb backloading ONLY when you finish exercise. I know personally it works!

ALA
Bitter Melon
Cinnamon Extract
Chlorogenic Acid

Sci Rep. 2017 Apr 25;7(1):1137. doi: 10.1038/s41598-017-01291-5.
Serotonin transporter deficiency drives estrogen-dependent obesity and glucose intolerance.

Zha W1, Ho HTB1, Hu T1, Hebert MF2,3, Wang J4,5.
Author information
Abstract
Depression and use of antidepressant medications are both associated with increased risk of obesity, potentially attributed to a reduced serotonin transporter (SERT) function. However, how SERT deficiency promotes obesity is unknown. Here, we demonstrated that SERT -/- mice display abnormal fat accumulation in both white and brown adipose tissues, glucose intolerance and insulin resistance while exhibiting suppressed aromatase (Cyp19a1) expression and reduced circulating 17β-estradiol levels. 17β-estradiol replacement in SERT -/- mice reversed the obesity and glucose intolerance, supporting a role for estrogen in SERT deficiency-associated obesity and glucose intolerance. Treatment of wild type mice with paroxetine, a chemical inhibitor of SERT, also resulted in Cyp19a1 suppression, decreased circulating 17β-estradiol levels, abnormal fat accumulation, and glucose intolerance. Such effects were not observed in paroxetine-treated SERT -/- mice. Conversely, pregnant SERT -/- mice displayed normalized estrogen levels, markedly reduced fat accumulation, and improved glucose tolerance, which can be eliminated by an antagonist of estrogen receptor α (ERα). Together, these findings support that estrogen suppression is involved in SERT deficiency-induced obesity and glucose intolerance, and suggest approaches to restore 17β-estradiol levels as a novel treatment option for SERT deficiency associated obesity and metabolic abnormalities.

 

[MARK_]

Interesting to read

 

[cheftepesh1]

Found interestiing

 

[dvw]

I ran original novedex xt 10 years ago and I noticed rapid fat gain in hips lower pecs upon ceasing ATD at 75mgs. Crashing e2 definitely leads to fat gain in my opinion. I think indole 3 carbinol is perfect not to strong.

 

[chainsaw]

Bump for more of a discussion

 

[HIT4ME]

This is interesting. Testosterone increases 5-HT binding in the brain, so I guess it would make some sense that estrogen would sensitive the brain to serotonin. Kind of a good backup for a testosterone drop, which may ultimately still be the mechanism here - low testosterone and high aromitase would compound the issue, so some signaling is reducing aromitase and this estrogen. Supplying exogenous estrogen will allow for further aromitase suppression and this would provide a testosterone sparing effect maybe?