This is likely one of the most unintelligent and ill informed, generalized statements I've ever heard.
Maybe you just aren't educated on the matter..but first.
1.) It's not that simple, and tongkat ali doesn't have much of an effect on estrogen and progesterone - which are opiate modulators.
2.) Net androgen activity and responsivity also correlates with genetics.
3.) Enlarged prostate is related to estrogen, several studies show that dihydrotestosterone treatments can reduce prostate enlargement.
Sorry to burst your bubble, but you are still consuming propaganda like maple syrup.
4.) MPB , though has some relevance to androgens..it has more to do with 5-alpha reductase localization and genetics.
5.)Testosterone and androgens do NOT just affect dopamine..in fact, androgens like DHT have little to no effect on dopamine...
DHT however may raise epinephrine and alter adrenaline receptor expression, and it may actually decrease dopamine turnover..but not directly alter the serum or whole level. Then again it may allow for more dopamine interactions by it's modulation of hippocampal plasticity and calcium nerve terminals....
6.)Free T that converts into estrogen, when in the proper ratio with androgens..upregulates multiple dopamine and serotonin subtypes, inhibits PDE AND MAO's..and affects many other pathways including nitric oxide, glutamate etc, histamine h1 mRNA..all that.
7.) DHT modulates opiate receptor bioavailability and may enhance the effects of naltrexone by re routing beta endorphin to more acceptable and less harmful receptors.
Do some reading, check out these articles..you'll learn a lot!
http://area1255.blog...how-of-dht.html
http://well.blogs.ny...-exercise/?_r=0
http://www.ncbi.nlm..../pubmed/4000546
Why are you so quick to call me unintelligent, just because I disagreed with you? You're not going to convince anyone of your views with that attitude.
Please provide a link to the studies that show that prostate enlargement is caused by estrogen. This is an extraordinary claim that completely contradicts standard medical practice. If this is true, how do you explain the studies which show that finasteride is effective in treating prostate enlargement and preventing prostate cancer? Wouldn't finasteride have the opposite effect?
You mention that male pattern baldness "has some relevance to androgens" but "it has more to do with 5-alpha reductase localization." 5-alpha reductase is involved in the metabolism of androgens and other steroids. Do you believe that DHT causes hair loss? What other genes could be responsible?
I have read your article, and you have obviously done a lot of research, but you're taking bits and pieces of unrelated and highly specialized studies and making unwieldy generalizations from them. It's tough to draw the kind of conclusions you're making without high-quality human studies. Most of these points are only theoretical, such as the relationship between DHT and naltrexone.
It's a paradox of sorts..yes DHT can** cause some enlargement, but only to a certain point itself, the reason behind this is solely between the interactions of DHT and SHBG. In other words, it's a coincidence that 5-ar inhibitors may help prostate enlargement..the reason is because SHBH controls the uptake of estrogen and androgens, and extreme alterations of this and other binding proteins that may occur naturally may result in abnormal variations of hormones concentrating and accumulating in the prostate. THERE is an inverse correlation between these these binding proteins and how androgen receptors are localized, what occurs here is that DHT inhibits SHBG - and in this case then more testosterone is "freed up" - leaving more possible estrogen floating around and in the prostate to where the uptake may be altered yet again.
Think about how hormones attach and de-attach, high levels of freely circulating test are a good thing IF the ratios are genetically sound, or otherwise in good shape. In other words, having high free T itself is not bad, but having high free T with a genetic disposition and more estrogen conversion sets one up for issues.
*study on aromatase inhibitors and prostate enlargement*
Now if androgens were the whole story, common sense would tell you that aromatase inhiibitors would cause or worsen prostate enlargement..because by inhibiting aromatase and estrogen..you would have nearly a 4 fold increase in both testosterone and DHT!!!
It's not always as clear cut as you might think....and it's not that I am saying this to disagree, I just hate to see people deceived by propaganda!
You have to read the fine print of the studies, and draw your own conclusions....
But here's an image for your head....estrogen and prolactin are basically growth hormones...wet hormones, or bloating hormones...it's a generalization a bit..but the point is that studies have shown that very little estrogen and / or prolactin leads to a very thin, or lean build....because of their interactions with insulin...now interestingly , insulin is also involved in altering SHBG and other sex hormone binding proteins..and yet is now being seen as playing a role in prostate issues.
Med Hypotheses. 2011 Apr;76(4):474-8. doi: 10.1016/j.mehy.2010.11.024. Epub 2010 Dec 14.
Role of insulin and testosterone in prostatic growth: who is doing what?
Abstract
Previous studies have demonstrated increased incidence of benign prostatic hyperplasia in insulin-resistant individuals. In addition to androgens, prostatic growth is sensitive to the peptide growth factors including insulin. Experimental studies employing intervention of selective β-cell toxin streptozotocin and castration suggest that depletion of either insulin or testosterone results in the severe prostatic atrophy (>80%). Exogenous testosterone and diet-induced experimental hyperinsulinemia induces prostatic enlargement in rats. Further, hyperinsulinemia sensitizes prostate towards the growth promoting effect of testosterone, and testosterone augments prostatic growth even in the hypoinsulinemic rats. However, in castrated rats diet-induced hyperinsulinemia fails to promote prostatic growth. Based on these evidences it is hypothesized that in the presence of testosterone insulin plays an important role in the prostatic growth. The epidemiological reports witnessing increased incidences of prostatic enlargement in men with metabolic syndrome, which are known to have increased level of insulin, provides a validating clue to the hypothesis. Further, the hypothesis suggests that targeting insulin signaling pathway could be a new objective for the treatment of prostatic enlargement.
