[Lotus]

Lotus thank you so much for chiming in, you explain things in a way my pea size brain can understand! haha!

 I've been digging through all of your threads trying to gather all the information I can. I'm super motivated to try to figure out a refined cycling plan for women so I hoping this thread continues!! I'd love to see that chart as well

Awesome,....though you might be cussing at me shortly for the complexity of things to come....lol (evil laugh) kidding. 

Updated 

I'll bet most can remember the " Flux Capacitor " from the movie " Back to the Future " right?. (Youngin's, go find it on YouTube.)

Anyways, the hypothalamus is similar to the Flux Capacitor in the way it can put the Gonads back in time...........aka- puberty.  Only, flash forward to 2015 in the movie and the 1.21 jigowatts needed to generate time travel in 1985 is replaced by Mr. Fusion in 2015, (powered by garbage..what a kicker lol).  

So our fuel (or should we say " Ms. Fusion ") needed to generate the gonads back to puberty will stem from the hypothalamus, albiet negative feedback loops via LH & FSH (lutenizing hormone & follicle stimulating hormone).....simple right?. It will make sense later. 

Here's the FSH relationship to aromatase: 

Binding distribution of principle endogenous steroid hormones in normal women during the menstrual cycle. ______________________________________________________
Of clinical importance is free testosterone, which is often elevated in hyperandrogenic women with clinical manifestations of hirsutism. The free testosterone is regulated by the concentration of SHBG in blood. The higher the SHBG level, the lower the free testosterone level, and vice versa. A number of factors can affect SHBG concentrations in blood. They include obesity, menopause, insulin, and androgens, each of which decreases SHBG levels. In contrast, SHBG levels are increased by estrogens, thyroid hormone, liver cirrhosis, and prolonged stress.

After menopause aromatase in adipose becomes the chief producer of estrogen, E1 estrone to be exact. But, as we know in adipose tissue estrone is weak, and it's produced from androstenedione of adrenal origin in relatively large quantities. 

Although aromatase level per adipose tissue fibroblast may be small, the sum of estrogen arising from billions of adipose tissue fibroblasts in the entire body makes a physiologic impact. The principal product of the ovary is the potent estrogen estradiol. In adipose tissue, estrogenically weak estrone is produced from androstenedione of adrenal origin in relatively large quantities. However, at least half of this peripherally produced estrone is eventually converted to estradiol in extraovarian tissues.

Molecular Bases and Phenotypic Determinants of Aromatase
http://downloads.hindawi.com/journals/ije/2012/584807.pdf


Physiological regulation of aromatase expression. FSH induces aromatase expression via a cAMP-dependent pathway in ovarian granulosa cells via promoter II. SF-1 mediates this action of FSH. On the other hand, a combination of a glucocorticoid and a member of the class I cytokine family induces aromatase expression in skin and adipose tissue fibroblasts via promoter I.4 located 73 kb upstream of the coding region. Binding of STAT-3 and glucocorticoid receptor (GR) upstream of promoter I.4 mediates regulation of aromatase expression in these fibroblasts.

Regulation of Aromatase Expression in Estrogen-Responsive Breast and Uterine Disease: From Bench to Treatment
http://pharmrev.aspetjournals.org/content/57/3/359.full.pdf

from the study above, promoter I.4 (skin and adipose) is the one we should focus on, (skin fibroblasts) to promote aromatase.