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Strong Androgens (DHT) As Treatment For CVD, Obesity And Metabolic Syndrome

haidut

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The study used DHT as the active drug but since the positive effects were due to androgen receptor agonism, any other strong androgen agonist should do. I think the lack of estrogenicity also contributed to the benefits of DHT observed in this study, so this would explain the mixed results with T replacement therapy and positive results with human DHT studies on similar biomarkers. The most striking effects (at least in my opinion) were the 44% reduction in subcutaneous fat, 12% - 15% increase in lean muscle mass, and 41% reductions of established atherosclerotic lesions.
The HED was 0.1mg/kg for 8 weeks, so this means a daily dose of 7mg - 9mg for most humans should be able to replicate the findings/design of this study. Another interesting fact of note was that the study specifically used female animals to demonstrate that androgen deficiency is pathogenic for female organisms. So, DHT is not just the male hormone. I think the study really shows the detrimental effects of unopposed estrogen on CVD, body weight and lipid balance. Thus, the effects of DHT are likely to be mimicked by progesterone as well even though I don't know what dose would be needed to achieve the same effects.

The androgen receptor confers protection against diet-induced atherosclerosis, obesity, and dyslipidemia in female mice. - PubMed - NCBI

"...This is the first study to investigate atherogenesis in an animal model of female AR deficiency. Earlier studies to elucidate the effect of exogenous androgens on atherosclerosis in females report conflicting results (2328). An often-cited study reported that testosterone treatment of ovarian-intact female monkeys caused increased atherosclerosis (25); however, the treatment completely suppressed ovarian cyclicity, suggesting that a disturbed estrogen production may contribute to these results. By contrast, a number of studies in ovariectomized female mice showed atheroprotection by testosterone (27, 28), and similar to our findings, 1 study showed that the nonaromatizable AR agonist DHT protected against atherosclerosis in female apoE-deficient mice (26), supporting the importance of the AR. However, in all these earlier studies, pharmacologic doses of androgens were administered exogenously, and thus these studies do not provide information on the physiologic effects of endogenous androgens."

"...After 8 weeks on a high-fat diet, but not on a normal chow diet, atherosclerosis in aorta was increased in ARKO females (+59% vs. control apoE-deficient mice with intact AR gene). They also displayed increased body weight (+18%), body fat percentage (+62%), and hepatic triglyceride levels, reduced insulin sensitivity, and a marked atherogenic dyslipidemia (serum cholesterol, +52%). Differences in atherosclerosis, body weight, and lipid levels between ARKO and control mice were abolished in mice that were ovariectomized before puberty, consistent with a protective action of ovarian androgens mediated via the AR. Furthermore, the AR agonist dihydrotestosterone reduced atherosclerosis (−41%; thoracic aorta), subcutaneous fat mass (−44%), and cholesterol levels (−35%) in ovariectomized mice, reduced hepatocyte lipid accumulation in hepatoma cells in vitro, and regulated mRNA expression of hepatic genes pivotal for lipid homeostasis. In conclusion, we demonstrate that the AR protects against diet-induced atherosclerosis in female mice and propose that this is mediated by modulation of body composition and lipid metabolism."
 
B

Braveheart

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The study used DHT as the active drug but since the positive effects were due to androgen receptor agonism, any other strong androgen agonist should do. I think the lack of estrogenicity also contributed to the benefits of DHT observed in this study, so this would explain the mixed results with T replacement therapy and positive results with human DHT studies on similar biomarkers. The most striking effects (at least in my opinion) were the 44% reduction in subcutaneous fat, 12% - 15% increase in lean muscle mass, and 41% reductions of established atherosclerotic lesions.
The HED was 0.1mg/kg for 8 weeks, so this means a daily dose of 7mg - 9mg for most humans should be able to replicate the findings/design of this study. Another interesting fact of note was that the study specifically used female animals to demonstrate that androgen deficiency is pathogenic for female organisms. So, DHT is not just the male hormone. I think the study really shows the detrimental effects of unopposed estrogen on CVD, body weight and lipid balance. Thus, the effects of DHT are likely to be mimicked by progesterone as well even though I don't know what dose would be needed to achieve the same effects.

The androgen receptor confers protection against diet-induced atherosclerosis, obesity, and dyslipidemia in female mice. - PubMed - NCBI

"...This is the first study to investigate atherogenesis in an animal model of female AR deficiency. Earlier studies to elucidate the effect of exogenous androgens on atherosclerosis in females report conflicting results (2328). An often-cited study reported that testosterone treatment of ovarian-intact female monkeys caused increased atherosclerosis (25); however, the treatment completely suppressed ovarian cyclicity, suggesting that a disturbed estrogen production may contribute to these results. By contrast, a number of studies in ovariectomized female mice showed atheroprotection by testosterone (27, 28), and similar to our findings, 1 study showed that the nonaromatizable AR agonist DHT protected against atherosclerosis in female apoE-deficient mice (26), supporting the importance of the AR. However, in all these earlier studies, pharmacologic doses of androgens were administered exogenously, and thus these studies do not provide information on the physiologic effects of endogenous androgens."

"...After 8 weeks on a high-fat diet, but not on a normal chow diet, atherosclerosis in aorta was increased in ARKO females (+59% vs. control apoE-deficient mice with intact AR gene). They also displayed increased body weight (+18%), body fat percentage (+62%), and hepatic triglyceride levels, reduced insulin sensitivity, and a marked atherogenic dyslipidemia (serum cholesterol, +52%). Differences in atherosclerosis, body weight, and lipid levels between ARKO and control mice were abolished in mice that were ovariectomized before puberty, consistent with a protective action of ovarian androgens mediated via the AR. Furthermore, the AR agonist dihydrotestosterone reduced atherosclerosis (−41%; thoracic aorta), subcutaneous fat mass (−44%), and cholesterol levels (−35%) in ovariectomized mice, reduced hepatocyte lipid accumulation in hepatoma cells in vitro, and regulated mRNA expression of hepatic genes pivotal for lipid homeostasis. In conclusion, we demonstrate that the AR protects against diet-induced atherosclerosis in female mice and propose that this is mediated by modulation of body composition and lipid metabolism."

Thus, the effects of DHT are likely to be mimicked by progesterone as well even though I don't know what dose would be needed to achieve the same effects.
Would really like to learn/understand about this some more...seems very pertinent
 

Broken man

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When I have 11 Keto Dht, how much I need to replicate this study? Thank you.
 

haidut

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When I have 11 Keto Dht, how much I need to replicate this study? Thank you.

It should be same dose as both steroids have basically the same affinity for the androgen receptor.
 

Broken man

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It should be same dose as both steroids have basically the same affinity for the androgen receptor.
Thank you, is magnesium important for steroid production? I did some experiments with Keto dht and its very good for me but I have some cracking in my joints. I cant say that it hurts me but I can hear it when I am walking so I am just curious. I am taking b vits, eating 100+ g of protein, 2500+ calories, pregnenolone, kuinone. I am just thinking what I can do with this and I know that magnesium helps me with joint little bit. Thank you. I am very happy that you are back.
 

haidut

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Thank you, is magnesium important for steroid production? I did some experiments with Keto dht and its very good for me but I have some cracking in my joints. I cant say that it hurts me but I can hear it when I am walking so I am just curious. I am taking b vits, eating 100+ g of protein, 2500+ calories, pregnenolone, kuinone. I am just thinking what I can do with this and I know that magnesium helps me with joint little bit. Thank you. I am very happy that you are back.

Of course, it is a cofactor for most enzymes in the body. No magnesium = no ATP and without ATP no cholesterol can be converted into downstream steroids.
 

Broken man

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Of course, it is a cofactor for most enzymes in the body. No magnesium = no ATP and without ATP no cholesterol can be converted into downstream steroids.
I know that you was using magnesium carbonate but isnt transdermal using beter for absorption? I think dissolved magnesium chloride in vodka. Thank you.
 

Broken man

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I would like to ask, I have Keto-dht which I am using on my rat, why cant I use it more than few days until I develop knee pain and my head start itching? My rat is also using inosine for ATP and magnesium. The reason for this product is that my rat has spider veins around eyes and probably starting cvd which is okay when I am using keto dht.
 

dand

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Jul 3, 2014
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Georgi, going to try HED of 7-10 mg of 11 keto-dht. In the past, I think magnesium was a missing co factor for me when I tried to increase dose of androgens too much. Sound rational? Since I have add magnoil with this I don’t perceive any downsides. 11Keto would be about as good a surrogate I could get for dht it seems.
 

Cameron

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Is 11 keto dht better than dht? Are dht and T just pro hormones for the 11 keto versions? Maybe they’ll keto are the true goal end points steroids?
 

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