"In summary, the results of this study show that estrogen is
the dominant reproductive hormone that supports and sustains
an experimental vaginal C. albicans infection and reduces the
inhibitory activity of epithelial cells against Candida. Progesterone,
on the other hand, has no demonstrable effect on the
vaginal infection or on systemic and/or local immune responsiveness
associated with the infection. Taken together, these
results suggest that estrogen, but not progesterone, is important
in the reproductive-hormone-associated susceptibility to
vaginal C. albicans infection." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC97188/
"Yeast infections appear to occur more frequently in women with increased estrogen levels — for instance, in women who are pregnant, those taking high-dose estrogen birth control pills or those taking estrogen hormone therapy." http://www.mayoclinic.org/.../risk-factors/con-20035129
"In a normal menstrual cycle, estrogen deposits glycogen (a form of sugar) in the cells that are found in the lining of the vagina. The release of progesterone causes the cells to shed into the vagina, so the sugar becomes available for yeast to feed on, multiply and grow. Estrogen and sugar production peak at the midpoint between periods, and then progesterone begins to build and sugar is released. Yeast infection symptoms can follow the hormonal pattern of this cycle. Usually, the most severe symptoms occur before the onset of a woman's period when more sugar is available. During and after the flow, symptoms are likely to subside. Additionally, changes in the vaginal pH can disrupt the immune system or destroy the so-called friendly bacteria that populate the vaginal canal and keep the yeast fungus in check." http://health.howstuffworks.com/.../the-basics-of-yeast...
See here about estrogen and endometriosis: http://endocomprehensive.blogspot.com/2013/11/estrogen-receptors-importance-in.html
"Aberrant estrogen synthesis and metabolism have been suggested to increase local estradiol (E2) concentration in endometriosis and thus to promote the growth of the lesions. However, tissue estrogen concentrations within the endometrium and different types of endometriosis lesions have not been described....Endometrial or endometriotic intratissue E2 concentrations did not reflect the corresponding serum levels. In the proliferative phase, endometrial E2 concentration was five to eight times higher than in the serum, whereas in the secretory phase the E2 concentration was about half of that in the serum. Accordingly, a markedly higher E2/E1 ratio was observed in the endometrium at the proliferative phase compared with the secretory phase. In the endometriosis lesions, E2 levels were predominating over those of E1 throughout the menstrual cycle. Among the hydroxysteroid (17β) dehydrogenase (HSD17B) enzymes analyzed, HSD17B2 negatively correlated with the E2 concentration in the endometrium, and HSD17B6 was strongly expressed, especially in the deep lesions." http://www.ncbi.nlm.nih.gov/pubmed/22969138
