Real Way to Handle DHT, Estrogen, and SHBG

J987 wrote:So Im on board with

- Correcting all vitamin/mineral deficiencies ( especially iodine and vitamin D)
- Perfecting an anti inflammatory, nutritional diet ( minimize all inflammation in the body)
- IH top 6 type regimen maybe with some variation
- Healthy levels of exercise
- Increase SHBG and testosterone ( maintain youthful levels of test)
- Increase body/scalp circulation
- and for some people mildly decrease DHT through natural means.

The most ive seen on increasing SHBG is through green tea and iodine?
Does an increase in SHBG mean an increase in testosterone also generally!?

Im pretty sure my thinning was a product of bad scalp inflammation triggered by up-regulated hormonal excess in my scalp due to very low shbg, which expressed itself because I probably have a slightly less robust capillary network in the scalp
(which gets damaged by androgens?) to begin with...
I say that because I think most people who bald tend to naturally have higher hair lines and thinner hair than non balders are born with, or perhaps just larger upper head dimensions from my observation, so I can see how there'd be more susceptibility in androgenic damage or scalp tightening/stress and/or inflammation induced blood flow restriction ...

Not sure If I Agree with the part about people with higher hairlines tend to go bald more often. Black men have some of the lowest straightest hairlines and they go bald very often.

Estrogens, Breast Cancer, and Intestinal Flora

Sherwood L. Gorbach

+ Author Affiliations

Division of Infectious Diseases, Department of Medicine, Tufts-New England Medical Center and Tufts University School of Medicine, Boston, Massachusetts

Please address requests for reprints to Dr. Sherwood L. Gorbach, Tufts-New England Medical Center, 171 Harrison Avenue, Boston, Massachusetts 02111

Abstract

Epidemiologic evidence has linked diet to breast cancer, with the highest cancer rates observed in women who eat a high fat-low fiber diet. There is also substantial information, both clinical and experimental, that implicates estrogens in the etiology of breast cancer. A recent study from our laboratory has shown that diet influences levels of estrogens, and the main mechanism is metabolism of estrogens in the intestine. The intestinal microflora plays a key role in .the enterohepatic circulation of estrogens by deconjugating bound estrogens that appear in the bile, thereby permitting the free hormones to be reabsorbed. By suppressing the microflora with antibiotic therapy, fecal estrogens increase and urinary estrogens decrease, changes indicating diminished intestinal reabsorption. A low fat-high fiber diet is associated with similar findings — high fecal estrogens and low urinary estrogens. It appears that the microflora plays a key role in the metabolism of female sex hormones.

Studies on the role of intestinal bacteria in metabolism of synthetic and natural steroid hormones.
Adlercreutz H, Pulkkinen MO, Hämäläinen EK, Korpela JT.
Abstract

Administration of antimicrobial agents to subjects taking oral contraceptives has been reported to lead to contraceptive failure and subsequent pregnancy. In women taking oral contraceptives antimicrobial agents could have an effect on both endogenous hormone levels and on the metabolism of the exogenously administered steroids. To investigate these possibilities, antimicrobial agents were administered for short periods to normal women taking various steroid drugs: Megestrol acetate (MA), medroxyprogesterone acetate (MPA), norethisterone (NET), a combination of NET and ethinylestradiol (EE) or a combination of lynestrenol and EE. During ampicillin administration the 24-h morning plasma concentrations of MA, MPA and NET were increased compared to the control values. In the MA and MPA experiments the afternoon values were determined and also found to be increased. In the subjects taking oral contraceptives plasma EE concentration showed a tendency to decrease during ampicillin administration on the third, fourth or fifth morning of ampicillin administration, but was never lower than the pretreatment values. In other experiments plasma estrone (E1) and estradiol (E2), urinary total E1, E2 and estriol (E3) and fecal unconjugated and conjugated E1, E2 or E3 were determined by RIA before, during and after administration of oxytetracycline (2 X 500 mg/day for 5 days) to 5 young male subjects. Furthermore urinary and fecal estrogens were determined in 1 male subject after administration of erythromycin for 6 days and in 2 normally menstruating women after tetracycline and trimethoprim administration, respectively. During treatment with antimicrobial drugs an increase in the excretion of fecal conjugated and, with the exception of the oxytetracycline experiments, also of unconjugated estrogens paralleled a decrease in urinary estrogen excretion, especially for E2 and E3. In both urine and feces the E1/E2 and E1 + E2/E3 ratios increased due to diminished reductive metabolism of estrogens in the gut. No significant effects on plasma unconjugated estrogen concentrations were observed. The results suggest that the intestinal bacterial flora plays a significant role in estrogen metabolism. However, further studies are necessary, because our results do not explain why administration of antibiotics may cause contraceptive failure.