RP Email Advice Comment: Androsterone-Associated Joint Pain

[Daniel11]

Thanks GAF. You know, many moons ago I would take cordyceps (just because I was hippy-ish/counter culture and not because of any insight), and I did believe they gave me energy. Now, in light of Peat, I wonder if mushroom supps are prepared so that the toxins are processed/cooked away.....

I talked with a medicinal mushroom company today, they said all their products even if it says freeze dried always has to first go through a process of heat extraction to make digestible and potent.

 

[Regina]

I talked with a medicinal mushroom company today, they said all their products even if it says freeze dried always has to first go through a process of heat extraction to make digestible and potent.

I think we learned that freeze-dried retained the hydrazine.
Mushrooms, Preparation And "inflammation"

 

[Daniel11]

I think we learned that freeze-dried retained the hydrazine.
Mushrooms, Preparation And "inflammation"

Im not sure, maybe they heat enough there is no problem, also the company i buy from uses the mycelium not the fruiting body.
I have been taking for quite a while and feel very good.

 

[lollipop]

Im not sure, maybe they heat enough there is no problem, also the company i buy from uses the mycelium not the fruiting body.
I have been taking for quite a while and feel very good.

Interesting @Daniel11. Thank you for your efforts. If you are using Paul Stamets version you are probably fine. One of the most knowledgeable on planet about mushrooms. He would have certainly addressed this problem. He started the company you linked to for a recommendation of a good product.

 

[schultz]

Haidut is not the only one saying low estrogen causes joint pain and problems. Such joint issues are the number-1 report from people using an AI (aromatase inhibitor) to lower estrogen. There are literally tens of thousands of people who have posted such reports of EXACTLY this sort of "all over" joint pain on dozens of forums.

Further, lowering estrogen past a certain point is also well known to destroy male sexuality...no libido...no nocturnal erections...no morning wood. This is the second most commonly reported issue from users of AI's.

Again, these reports number in the >tens of thousands<, on dozens of forums. Many of these people spent serious coin to do repetitive bloodwork during their protocol, from which they were able to determine a specific >range< of E2-in-serum that maintained their sexuality.

Which brings to mind a 2nd point...

Ray is human too. He can be mistaken just like anyone else. :)

My take... Although significantly lowering estrogen has helped me (and many other 50+ men), there is >overwhelming< evidence that estrogen can indeed be made 'too low' for proper bodily function.

I disagree with this. For one thing, just because a pharmaceutical aromatase inhibitor is meant to be a drug strictly for the task of lowering estrogen does not mean that it doesn't do other things in the body that they have not discovered yet. Maybe the AI's can cause lipid peroxidation, or maybe they lower progesterone or maybe they lower blood estradiol levels but not tissue estrogen. The body is complex. I sincerely doubt that AI's just do the one thing that they were made for. So it's not really proof that low blood estradiol is bad when you take an AI to lower it and get negative symptoms.

Male sexual function can be maintained without aromatization: randomized placebo-controlled trial of dihydrotestosterone (DHT) in healthy, older me... - PubMed - NCBI
There is a study I posted a few months back where they give guys 70mg of DHT for 2 years. Serum estradiol went as low as 1.4 pg/mL, which is comparable to an aromatase inhibitor. Estradiol averaged 1.7 pg/mL in all men over the course of the entire study. They also had complete suppression of Testosterone. The study conclusion is

"We conclude that aromatization plays only a minimal role in maintenance of sexual function in healthy eugonadal middle-aged or older men"

and they use the word minimal. One thing that should be pointed out is that the men in the study didn't notice this minimal drop in libido.

"The effect on sexual desire is small in magnitude, being only detectable using a powerful study design, but was not sufficient for participants, unpaid volunteers, to notice or complain of."

This is actually amazing considering they had incredibly low estrogen and a complete suppression of testosterone as well, but still maintained normal sexual function!! Without testosterone!

Here is a very interesting paragraph from the study:

"An important issue for studies of the impact of selective estrogen deficiency is the degree of estrogen deficiency. The efficacy of aromatase inhibitors in men is questionable in that among 17 studies over a range of doses (modal dose 1 mg daily, range 0.5 mg daily to 80 mg over 5 days) and duration of treatment (5 days to 12 months), the magnitude of lowering in serum E2 was <50% (Supporting Information Table S1) raising the possibility that pharmacological inhibition of estrogen synthesis may be suboptimal. However, most studies (n = 9) used invalid direct (unextracted) E2 immunoassays [19], although other studies used more reliable indirect (using extraction and chromatography) immunoassays (n = 6, five from a single center) as well as mass spectrometry (n = 1) and in vitro bioassay (n = 1). Although reported serum E2 concentrations measured by mass spectrometry (MS) appeared to be comparable between studies, both had a high proportion of samples with undetectable serum E2 concentrations assigned an arbitrary low concentrations (as indicated by mean serum E2 concentrations below limits of quantitation) so that more sensitive analysis of left censored data would be required to verify whether the degree of suppression was comparable [20]. Furthermore, based on the affinity of estrogen receptors for estradiol, it is likely that serum E2 levels <1 pg mL may be biologically effective [21], consistent with evidence that, in subprimates, circulating serum E2 levels are undetectable under most physiological conditions by even the most sensitive MS-based methods [22]."

"Furthermore, the aromatization hypothesis that male sexual function is estrogen dependent predicts that estrogen receptor blockade may be detrimental to male sexual function. However, estrogen receptor blockers such as clomiphene, tamoxifen, raloxifene, or other mixed estrogen receptor agonist/antagonists have long been used off-label to treat men complaining of andropause, gynecomastia, infertility, and androgen abuseinduced hypogonadism. Although there are no specific studies of male sexual function, the best available evidence suggests that antiestrogen treatment does not impair male sexual function [47–53]."


I seriously doubt that the amount of Androsterone people are taking on this forum is lowering estrogen more than 70mg of DHT per day would.

 

[Broken man]

I disagree with this. For one thing, just because a pharmaceutical aromatase inhibitor is meant to be a drug strictly for the task of lowering estrogen does not mean that it doesn't do other things in the body that they have not discovered yet. Maybe the AI's can cause lipid peroxidation, or maybe they lower progesterone or maybe they lower blood estradiol levels but not tissue estrogen. The body is complex. I sincerely doubt that AI's just do the one thing that they were made for. So it's not really proof that low blood estradiol is bad when you take an AI to lower it and get negative symptoms.

Male sexual function can be maintained without aromatization: randomized placebo-controlled trial of dihydrotestosterone (DHT) in healthy, older me... - PubMed - NCBI
There is a study I posted a few months back where they give guys 70mg of DHT for 2 years. Serum estradiol went as low as 1.4 pg/mL, which is comparable to an aromatase inhibitor. Estradiol averaged 1.7 pg/mL in all men over the course of the entire study. They also had complete suppression of Testosterone. The study conclusion is

"We conclude that aromatization plays only a minimal role in maintenance of sexual function in healthy eugonadal middle-aged or older men"

and they use the word minimal. One thing that should be pointed out is that the men in the study didn't notice this minimal drop in libido.

"The effect on sexual desire is small in magnitude, being only detectable using a powerful study design, but was not sufficient for participants, unpaid volunteers, to notice or complain of."

This is actually amazing considering they had incredibly low estrogen and a complete suppression of testosterone as well, but still maintained normal sexual function!! Without testosterone!

Here is a very interesting paragraph from the study:

"An important issue for studies of the impact of selective estrogen deficiency is the degree of estrogen deficiency. The efficacy of aromatase inhibitors in men is questionable in that among 17 studies over a range of doses (modal dose 1 mg daily, range 0.5 mg daily to 80 mg over 5 days) and duration of treatment (5 days to 12 months), the magnitude of lowering in serum E2 was <50% (Supporting Information Table S1) raising the possibility that pharmacological inhibition of estrogen synthesis may be suboptimal. However, most studies (n = 9) used invalid direct (unextracted) E2 immunoassays [19], although other studies used more reliable indirect (using extraction and chromatography) immunoassays (n = 6, five from a single center) as well as mass spectrometry (n = 1) and in vitro bioassay (n = 1). Although reported serum E2 concentrations measured by mass spectrometry (MS) appeared to be comparable between studies, both had a high proportion of samples with undetectable serum E2 concentrations assigned an arbitrary low concentrations (as indicated by mean serum E2 concentrations below limits of quantitation) so that more sensitive analysis of left censored data would be required to verify whether the degree of suppression was comparable [20]. Furthermore, based on the affinity of estrogen receptors for estradiol, it is likely that serum E2 levels <1 pg mL may be biologically effective [21], consistent with evidence that, in subprimates, circulating serum E2 levels are undetectable under most physiological conditions by even the most sensitive MS-based methods [22]."

"Furthermore, the aromatization hypothesis that male sexual function is estrogen dependent predicts that estrogen receptor blockade may be detrimental to male sexual function. However, estrogen receptor blockers such as clomiphene, tamoxifen, raloxifene, or other mixed estrogen receptor agonist/antagonists have long been used off-label to treat men complaining of andropause, gynecomastia, infertility, and androgen abuseinduced hypogonadism. Although there are no specific studies of male sexual function, the best available evidence suggests that antiestrogen treatment does not impair male sexual function [47–53]."


I seriously doubt that the amount of Androsterone people are taking on this forum is lowering estrogen more than 70mg of DHT per day would.

Thank you for this study, do you think that NAD is crucial factor for this? I am fighting with arthritis few months now and I have it even I am not taking Androsterone.

 

[pone]

Not getting around to the post at the moment, but in order to avoid leaving you guys hanging...

Mark Donahue has put together a really interesting series of reports on Multiple Chemical Sensitivity, but with information that I found useful/interesting for a number of things.

Report #11 "Sulfoxidation and Sulfation" is the one that primarily deals with what we're discussing here

Mark J Donohue - Toxipedia

Does anyone know where we can find Mark Donohue (note different spelling from above passage)? He used to maintain a page on Toxipedia. The entire website is now on hold. Does he have a blog or participate in any online forums? Does he have a Facebook profile?

 

[Mauritio]

A compound called laxogenin seems to be an antagonist of 7-keto-DHEA, and has a supposed anabolic effect while preventing lactate from rising. Supposedly, Russians have been aware of it for some time. I see it's available in Australia, which makes me assume it's probably ineffective.

Here's the link: Laxogenin and 5-hydroxy-laxogenin: natural anabolics that can enhance real anabolic steroids

Has anybody tried this ??