Pointless

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I don't have any data on such conditions yes, but it seemed to make a psoriatic lesion disappear when a female friend of mine rubbed it on the lesion for 3 days. Psoriasis is another condition where excess estrogen is at play and currently there is a push to unite all "autoimmune" conditions under the same "spectrum" so they can be treated with the same drugs like Humira. People with psoriasis often have IBD or IBS as well.

We will see. I have bpc-157 on backup if it doesn't work.
 

vulture

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It seems really interesting to try.
I'm gonna be the cinical guy here: If it is so good at inhibiting catabolism without noticeable side effects, why did not get much more attention as AAS did?

In the other hand: it's great that idealabs has some kind of two sides, the commercial high quality supplement side, and the lab-research side. I think our experiments could help a lot of more people than ourselves...maybe in a few years great things could emerge from people here escaping the mainstream medical treatments.
 
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haidut

haidut

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why did not get much more attention as AAS did?

It is getting attention. The bodybuilders are all over it. It is sold commonly as "6-keto MASS", "6-keto progesterone" or just "6-keto". Jyst Google for any of these keywords, and maybe add "bodybuilding" if the results do not show up on the first page. It's just that the bodybuilders do not know its mechanism of action and are scratching their heads how/why it works. Maybe somebody can show them that thread on the structural requirements of optimal anticatabolic substance I linked in the beginning of the post.
 

Tarmander

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I think a lot of the hypertrophy seen in competitive bodybuilders is due to estrogenic AAS, and thus water retention. In fact, AFAIK estrogen is considered integral in bodybuilding circles for muscle growth and is only inhibited in the lean/cutting cycle. The fact that anti-estrogenic / anti-cortisol chemicals without any other known effects like RU486 are just as anabolic as the AAS (ab)used by the bodybuilders was conveniently ignored for decades. However, more recent studies showing heart and liver issues in AAS users showing up decades after ending use of these chemicals is making people reconsider what they (ab)use. Now everybody is jumping on "atypical" chemicals like RU486, and some of gbol's posts mentioned that.
Anyways, the main point is that inhibiting cortisol and estrogen is probably the main route to both quality muscle growth and maintaining overall systemic health, including immune system. AAS suppress the immune system almost as well as cortisol, and the most estrogenic AAS are the worst in this respect. Inhibiting estrogen is also immunity-boosting, just like inhibiting cortisol is.
https://raypeatforum.com/community/...-regenerates-thymus-destroyed-by-aging.22354/

Btw, I would not say Arnold did well. Two open heart surgeries so far, who knows how many bypass procedures, as well as a few "flu" episodes that almost killed him. Have not checked into how Zane is doing, but I doubt it is any better.

Yeah they are not doing well absolutely, but relatively I think they are doing well.

I think gbold once said that for bodybuilding, estrogen was an integral part, and that what you really need to worry about controlling is prolactin. I am not into body building but kind of interesting I guess
 
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haidut

haidut

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Yeah they are not doing well absolutely, but relatively I think they are doing well.

I think gbold once said that for bodybuilding, estrogen was an integral part, and that what you really need to worry about controlling is prolactin. I am not into body building but kind of interesting I guess

Estrogen and prolactin are two sides of the same coin. I don't think it is possible to have low prolactin and high estrogen. If you are controlling prolactin with drugs like bromocriptine and cabergoline then estrogen goes down too. Anti-prolactin drugs are known to lower estrogen.
https://raypeatforum.com/community/...etric-for-serotonin-and-estrogen-levels.3594/

I don't agree with estrogen necessity for muscle growth, since as I mentioned purely anti-cortisol chemicals like RU486 are also anabolic, and are actually anti-estrogenic to a degree.
 
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haidut

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"no progestin action"

isn't that a bad thing ?

Not really, if all you want is anti-catabolic effects. Progestin action would mean gonadal suppression in higher doses. I mention that in the original post. Progestin actin has its roles, but it would be nice to have the option to avoid it when desired.
 

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With an actual eat it would be quiet easy to assess anabolic potential of this chemical. Maybe even less than 1 mg would be a high dose in a rat and results shall be seen in just weeks. Think about it...
 
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haidut

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With an actual eat it would be quiet easy to assess anabolic potential of this chemical. Maybe even less than 1 mg would be a high dose in a rat and results shall be seen in just weeks. Think about it...

If it does block cortisol as shown for most progesterone isomers, then even low doses should have noticeable effect. I did notice that 1mg-5mg makes me sleepy at night.
 

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So basically this can increase muscle hypertrophy and cause no surpression? Is that wt this is besides the anti estrogen and anti cortisol effects
 

vulture

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If it does block cortisol as shown for most progesterone isomers, then even low doses should have noticeable effect. I did notice that 1mg-5mg makes me sleepy at night.
Sorry I meant with an actual Rat...I mean, 1 mg in a rat could be a high dose and changes shall be seen faster than in humans. Sadly edit buttom seems to be disabled after a few hours.
 
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haidut

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So basically this can increase muscle hypertrophy and cause no surpression? Is that wt this is besides the anti estrogen and anti cortisol effects

The muscle hypertrophy is due to its primarily to the anti-cortisol effects, as explained in the original thread and the links I posted there. In addition to muscles, it should help any tissue that expresses high levels of the glucocorticoid receptor (GR) and as such is vulnerable to high cortisol - brain, skin, gonads, liver, spleen, thymus, etc. The inhibition of estrogen synthesis would also be very nice, especially for thymus and gonadal health. Lowering estrogen should also increase DHEA synthesis in the adrenals. I don't think it opposes estrogen at the "receptor" level since the study did not find it affected the sexual cycle of female rats.
https://raypeatforum.com/community/...strogen-strongly-decreases-dhea-levels.20047/
 
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haidut

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Sorry I meant with an actual Rat...I mean, 1 mg in a rat could be a high dose and changes shall be seen faster than in humans. Sadly edit buttom seems to be disabled after a few hours.

Yes, the dose used in the study was 1/6 mg (0. 16mg) per rat, so even less than 1mg.
 

mogwog

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@haidut did you find any noticeable difference between oral and topical administration? I'm asking because of the options in solvent offered (tocopherol/MCT vs SFA esters/ethanol). Additionally, how long until you noticed a change?
 
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@haidut did you find any noticeable difference between oral and topical administration? I'm asking because of the options in solvent offered (tocopherol/MCT vs SFA esters/ethanol). Additionally, how long until you noticed a change?

For me, the change was visible almost immediately. When a person is under stress they tend to retain water (due to the cortisol). The 6-keto shrinks/dries me out within an hour or so of taking.
We offer the two options because some people prefer the tocopherol/MCT version as per Peat's advice. I can't officially advocate oral use, only topical. But when I tried oral, it worked just as well but he effect were more short lived.
 

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He repeatedly said tocopherol + oil is a great solvent for steroids, especially progesterone. He even explained why - the emulsifation of tocopherol/fats and conversion into chilomicrons helps steroid absorption as well as avoiding the liver to a large degree. His Progest-E uses vitamin E and "vegetable triglycerides" as solvent. Recently, he recommended using vitamin E + coconut oil (MCT) as a solvent for testosterone, and even said the vitamin E should protect to a degree the conversion of T into estrogen.
And as @Wagner83 mentioned - I meant it as a solvent, even though he actually does recommend vitamin E as a supplement, and has repeatedly said that diluting vitamin E with some oil reduces the risk of gut irritation. I have asked him this question directly, as have many others.
Which common available Testosterone products are possible to easily dissolve in E+coconut oil? What would be the process? Any study or info on absorption vs intramuscular and how long it last? (I'm trying to know how frequent shall be the supplementation to keep levels kinda stable)

Thanks again
 
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Which common available Testosterone products are possible to easily dissolve in E+coconut oil? What would be the process? Any study or info on absorption vs intramuscular and how long it last? (I'm trying to know how frequent shall be the supplementation to keep levels kinda stable)

Thanks again

I think raw T or the fatty esters like haptanoate would dissolve rather well in vitamin E + oil. I would prefer the raw T to make a solution. When this solvent is used the absorption is probably close to 100% and not much different from IM. But I don't know if there is a difference in metabolism AFTER the absorption in terms of oral/topical in tocopherol + oil vs. IM injection of one of the esters. I would still probably go for the oral/topical vitamin E+oil formulation over an IM injection of an ester. I don't think they do IM injections with raw T.
 

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I think raw T or the fatty esters like haptanoate would dissolve rather well in vitamin E + oil. I would prefer the raw T to make a solution. When this solvent is used the absorption is probably close to 100% and not much different from IM. But I don't know if there is a difference in metabolism AFTER the absorption in terms of oral/topical in tocopherol + oil vs. IM injection of one of the esters. I would still probably go for the oral/topical vitamin E+oil formulation over an IM injection of an ester. I don't think they do IM injections with raw T.
For the record I think schulz had posted a study on scrotal application of t raising dht a lot. This was attribute to high 5-ar in the skin, but the scrotum appeared to absorb more : https://raypeatforum.com/community/...pplements-on-scrotum.14887/page-2#post-234250

PS:

"The clinical significance of such increased DHT/T ratio, common to all non-parenteral routes of testosterone administration, is doubtful as studies
maintained circulating DHT levels of 10 times the physiological concentrations for up to 2 years without increasing prostate size or growth or any adverse sequelae (Idan et al., 2010) nor do exogenous androgens increase intraprostatic DHT (Marks et al., 2006; Page et al., 2011; Mostaghel et al., 2012; Thirumalai
et al., 2016)."
 
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haidut

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For the record I think giraffe had posted a study on scrotal application of t raising dht a lot. It was in one of the idealabs on scrotum thread.

Thanks. Btw, there are studies showing applying anywhere on the raises DHT a lot more than any other method. The skin has a lot of 5-AR, but so does liver so oral T in vitamin E+oil will probably also raise DHT. The question is if this DHT will be released in the bloodstream or will stay in the liver. With scrotal application most of it will end up in the blood so it is probably a better method for people who want to raise serum DHT.
 

Wagner83

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Thanks. Btw, there are studies showing applying anywhere on the raises DHT a lot more than any other method. The skin has a lot of 5-AR, but so does liver so oral T in vitamin E+oil will probably also raise DHT. The question is if this DHT will be released in the bloodstream or will stay in the liver. With scrotal application most of it will end up in the blood so it is probably a better method for people who want to raise serum DHT.
I have just finished editing my post lol.
 
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