cyclops
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I want to keep the specifics confidential
Oooooooo secret program.
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I want to keep the specifics confidential
Would that be oral? I feel a lot more effects from oral estroban but other steroids are better topically I think.
I did a progesterone challenge test with 600 mg.
What other tests would be helpful in your opinion?
Sprint's are the best workout for DHT.@DHT
In my experience squat, bench, deadlift didn't do much for my DHT over the years. Just recently I noticed increased DHT when training much more intense, and it doesnt even have to be heavy weight.
Guess it could be a combination between cold showers, intense training, creatine and caffeine.
I meant, have you tested your progesterone levels on a few blood tests?
Well, not sure people have tried progesterone + androsterone alone, or progesterone + DHEA, or progesterone + DHEA + androsterone. Also, I wanted to show that progesterone is an anti-catabolic steroid which even on its own should have a lot of benefit. And for the people that can stack it with a potent androgen like DHT it can be a very potent option. I guess the main message is that opposition to cortisol is one of the most protective things a person can do, especially when not in good health. Not sure if you remember the recent discussions with tyw and older ones where there was so much opposition to trying to block cortisol.
Over the past 3.5 years my weight has gone from 177 to 227. Many people on here know my history of excessive urination and stopping exercise. I've increased muscle mass by 30lbs +. I've done high doses of androsterone for sleep consistently, low dose Pansterone couple days a week, and I use progesterone 1x a week for recovery purposes. I've never noticed any high estrogen effects from any of these and I continue to gain mass; however many people think I only look 190-200lbs. There very well could be mass and done density gains as I've grown 1/2 inch in height as well. In my experience, the substances that destroy my metabolism is processed food, high starch, and the wrong physical activity. This combination has worked well for me. The fear of high estrogen I think can be overblown in my opinion, therefore, I like your research on progesterone to be a powerful and support substance...especially for a male.
Not having to get up to pee through the night anymore is priceless. When ever I miss the days of being rail thin/ripped, I remind myself of the awful things that come with that alt state.Over the past 3.5 years my weight has gone from 177 to 227. Many people on here know my history of excessive urination and stopping exercise. I've increased muscle mass by 30lbs +. I've done high doses of androsterone for sleep consistently, low dose Pansterone couple days a week, and I use progesterone 1x a week for recovery purposes. I've never noticed any high estrogen effects from any of these and I continue to gain mass; however many people think I only look 190-200lbs. There very well could be mass and done density gains as I've grown 1/2 inch in height as well. In my experience, the substances that destroy my metabolism is processed food, high starch, and the wrong physical activity. This combination has worked well for me. The fear of high estrogen I think can be overblown in my opinion, therefore, I like your research on progesterone to be a powerful and support substance...especially for a male.
So you’ve gained 30 lbs without working out? What would you say was the most important thing to gain healthy weight?
This would be hard to believe except I’ve had a similar experience. Over the course of a few months on androsterone I’ve gained several pounds while losing significant fat, so a gain of 5 pounds or more of lean tissue. (I’m now 173 at 69 inches.) My pecs, lats, traps, and neck all look more like they did back in my weightlifting days, and with no exercise. Never expected it and didn’t believe my own eyes until it became indisputable. I wondered if it would just continue over time but judging from your experience of 10 or 12 times the duration, yeah it will. (I wrote up my experience a couple weeks ago in the androsterone thread here: https://raypeatforum.com/community/posts/272453/)Over the past 3.5 years my weight has gone from 177 to 227. Many people on here know my history of excessive urination and stopping exercise. I've increased muscle mass by 30lbs +. I've done high doses of androsterone for sleep consistently, low dose Pansterone couple days a week, and I use progesterone 1x a week for recovery purposes. I've never noticed any high estrogen effects from any of these and I continue to gain mass; however many people think I only look 190-200lbs. There very well could be mass and done density gains as I've grown 1/2 inch in height as well. In my experience, the substances that destroy my metabolism is processed food, high starch, and the wrong physical activity. This combination has worked well for me. The fear of high estrogen I think can be overblown in my opinion, therefore, I like your research on progesterone to be a powerful and support substance...especially for a male.
Can you please give some details about how you dose your androsterone and progesterone and what effects you notice from said dosage? What is a high dose of androsterone for you? Have you tried 11-keto-dht?Be as accurate as you can the metabolic support you find in Peats wisdom. I could write a book on everything that I do; if you want to go gain muscle without working out, create an anabolic environment as much as possible
Carlson Vitamin D is the best available. Only added ingredient is MCT.Re an above post about oral vs topical vitamin D:
Vitamin D orally comes with a load of excipient. Microcrystalline cellulose and related fillers. They are very bad, and I think responsible for a lot of digestive reactions.
It's difficult to get "pure" D3 for topical use. But I know nothing better than vitamin D3 and calcium for fixing a lot of problems. I seem to feel a lot better with some D3 and eggshell calcium.
This post will be a bit long, but I hope it is worth it. I think @Jsaute21 and @dand will find it highly interesting but the information here applies just as much to females wishing to preserve lean tissue and prevent the catabolism that often occurs with aging.
Here we go. Lately, I have been researching the effects of various steroids on the glucocorticoid, androgenic and estrogenic receptors. There has been a great deal of interest in identifying steroids with anabolic effects but despite the decades of research on many synthetic ones the exact mechanism through which steroids like T or AAS stimulate protein synthesis is not really known.
My own personal experimentation with glucocorticoid antagonists like pregnenolone-16a-carbonitrile, RU486, progesterone, pregnenolone and DHEA led me to the theory that there is no such as anabolic hormones, only anticatabolic ones, and the "anabolic" effects from T and AAS are actually the result of their antagonism to cortisol (and potentially estrogen). An old study I found makes the same claim, and highlights the well-known fact that muscle contains almost exclusively glucocorticoid receptors (GR), while androgen receptors (AR) are mostly expressed in tissues like prostate, gonads, brain and skin. Thus, if a steroid if a steroid is found to have an "anabolic" effect in muscle that is due almost exclusively to antagonism of GR. Steroids with strong androgenic effects would also have anabolic effects but those would be secondary to GR antagonism and reserved mostly for tissues with high expression of AR - i.e. prostate, gonads, sex organs, brian, etc. This matches quite well the common knowledge that strong androgens are weakly anabolic for muscle but are highly anabolic for those tissues that express the AR. The studies I posted on androsterone's anabolism in kidney, heart, spleen, and thymus corroborate this theory further.
Binding of glucocorticoid antagonists to androgen and glucocorticoid hormone receptors in rat skeletal muscle. - PubMed - NCBI
"...Although the anabolic activity of androgenic steroids has been recognized for a long time, the way in which these steroids act in muscle is ill-understood. It is also known that glucocorticoids exert a catabolic and anti-anabolic effect on protein metabolism in skeletal muscle [l-3]. Androgen and glucocorticoid receptors have been demonstrated in this tissue [4-6]. Since several steroids, including androgens, behave as glucocorticoid antagonists when binding to the glucocorticoid receptor in other tissues [7,8] such steroids could antagonise the catabolic action of endogenous glucocorticoids by preventing binding of the latter to their cytosolic receptors in muscle [9, lo]. Thus, muscle anabolism could result either from agonist steroid binding to the androgen receptor, or from antagonist binding to the glucocorticoid receptor, or both."
"...Table 1 shows that rat skeletal muscle contains about 40 times less androgen receptors than glucocorticoid receptors. Thus, one might speculate that differentiated muscle cells contain only the glucocorticoid receptor, while the androgen receptors are restricted to the satellite cells since the latter contribute about 2-5% of nuclei in muscle [15, 161. Moreover, treatment with thyroxine, which has anabolic activity at physiological doses, results in elevated incidence of satellite cells per muscle fiber and in percentage of all muscle nuclei [27].
"...As to the glucocorticoid receptor, it bound four steroids with an affinity higher than the androgen receptor, namely RU486, 2001, 415 and DXB. The data for R 1881, testosterone, and nortestosterone are consistent with earlier work [5,26]. Interestingly, the potent anabolic steroid trenbolone [36,37] bound to the glucocorticoid receptor with an affinity almost as high as that of corticosterone, the endogenous glucocorticoid in the rat [12]. With the only exception of AY 13615, it is remarkable that all the steroids tested bound to the glucocorticoid receptor with an affinity that ranked in the same order as their antiglucocorticoid activity in the HTC system (compare Tables 2 and 3). The three weakest antiglucocorticoids, namely the androgens methyltestosterone, nortestosterone, and testosterone were also the steroids that bound the muscle glucocorticoid receptor with the lowest affinity."
"...These restrictions notwithstanding, these indices (Table 3) show how the high concentration of glucocorticoid receptor sites compensates for their relatively lower affinity towards some of the steroids tested, as compared to the androgen receptor. For instance, providing RU486 and R1881 both are anabolic agents, RU486 is expected, despite its 50-fold lower affinity for the androgen receptor, to be much more potent than R1881 if anabolism can result from antiglucocorticoid activity as well as from androgenic action proper. The latter possibility is supported by the observation that the anabolic action of androgens results from inhibition of protein catabolism rather than from stimulation of anabolism [37,39]. Indeed, antiglucocorticoid activity is expected to counteract protein catabolism, while androgenic activity would stimulate anabolism."
Thus, if one would like to combine the best of both worlds, one would need a steroid which is a strong antagonist at GR and a strong agonist at AR. This present a possible issue as the binding requirements for both receptors differ. Strong GR antagonists are usually pregnane derivatives, which also have at least one unsaturated (double) bond in the A-ring of the steroid core. Such steroids do not have great affinity for the AR.
On the other hand, strong AR agonists are usually fully saturated androstane steroids like DHT, and androsterone as well as synthetic derivatives like mesterolone and oxandrolone (among many others). However, fully reduced androstane steroids do not bind well to the GR even though they are antagonist to it. Thus, DHT is expected to be a relatively weak anabolic steroid in muscle and highly anabolic in AR-rich tissues, which has been confirmed in practice countless times.
In support of these assertions please see the attached study listing GR antagonism requirements and 50 steroids with various agonist or antagonist effects on GR. As can be immediately seen, progesterone is one of the most potent antagonists of GR as it satisfies all the requirements. Known "anabolic" steroids like testosterone and other AAS are also GR antagonists, but as the study above noted, relatively weak ones. In fact, as per the study, the only steroid stronger than progesterone is 1-dehydro-progesterone (delta-1-progesterone) - i.e another progestogen - but the differences are minuscule.
Btw, the study above lists RU486 as one steroid that satisfies the strong anticatabolism requirement but, as the study says, it is an AR antagonist. So while it may be anticatabolic a still better alternative is possible - i.e. combining a strong glucocorticoid antagonist with a strong androgen agonist. Be that as it may, given its opposition to cortisol and estrogen, RU486 has highly trophic effects on the brain which may explain some of its positive effects on the brain and in people with PFS. Its partial antagonism/agonism to progesterone likely has very little to do with its beneficial effects, and we can do better than that. But how?
Some people may have noticed that testosterone (T) is both an antagonist at GR and an agonist at AR. Unfortunately, as the study above shows, T is weak GR antagonist. Well, another thing we can try is a steroid stack. Progesterone would be my choice for a GR antagonist as per the attached study on structure/activity relationship and the other thread I posted on its antagonism to GR (The Anti-cortisol Mechanism Of Progesterone). In addition, as I posted in another thread, progesterone has proven anabolic effects at least in animal studies (The Anabolic Effects Of Progesterone). Needless to say, Peat has also written a ton on progesterone, of its opposition to cortisol and estrogen, and its role in protecting from tissue destruction.
As an androgen agonist I would of course pick DHT, especially given its own antagonism to GR and estrogen. However, given that is it not available OTC it is probably not an option for most people. That leaves androsterone and DHEA as legal substitutes, and in fact a combination of both may be even more powerful than either one alone, as shown by another study I posted in the past (Remarkable Synergistic Anabolic / Androgenic Effect Of Androsterone With DHEA). The doses for each steroid are based largely on Peat's recommendations and studies I have seen. We know that DHEA should not be used in daily doses over 15mg if we want estrogen to stay as is. Androsterone is likely optimal in a ratio 1:1 up to 1:4 in combination with DHEA. So, that means 5mg - 15mg androsterone. How about progesterone? Well, Peat mentioned it a few times in emails to people who asked him about melanoma treatment. He said progesterone in a ratio of least 2:1 to DHEA would be best. He gave an example of using 40mg progesterone and 25mg DHEA. So, that comes down to a stack where a single dose would have 5mg DHEA, 1mg-5mg androsterone and 10mg+ progesterone.
Btw, in confirmation of everything written above, this very recent human study found that progesterone was just as anabolic as testosterone in postmenopausal women, while estrogen had no effect! So, at least half of the theory seems confirmed by evidence in humans.
Progesterone Is As Anabolic For Muscle As Testosterone (in Women)
Thought, comments? Has anybody else experimented with something similar?
Sprint's are the best workout for DHT.
Really intelligent theory that would align with my own observations regarding "GR's" quite well. For me personally, i believe improving my AR is much more of a need than antagonizing GR. I have high Testosterone and low cortisol. When i take andro, KDHT, K2, excess caffeine, etc my libido, mood, etc generally do not improve. My face becomes more chiseled and muscles harden additionally (already hard and big.) I have found that when i take some of these supplements, i become less sensitive and patient. I become very self absorbed and obsessed with very specific things. I am not doubting their GR lowering properties what so ever, as i feel as if they pose great benefit to many folks, i am just highlighting how individual all of this experimentation is.
I am waiting on a life extension cortsiol measurement test so i can accurately assess intelligent supplementation to correlate with my own benefit. For the time being, i have limited supplementation to energin, tyromax and pregenolone. This stack makes me feel pretty damn good when i take it.
@haidut it seems as if you typically recommend administering these supplements before a meal for optimal effects? Tyromax and energin are oral while pregnenolone is topical.
Yes, I would try shortly before a meal as they can raise metabolism and if there is not enough glycogen the blood sugar can drop and cause a stress reaction. How much topical pregnenolone are you using?
I posted exactly the same for a steroid cycle in PFS thread a week ago. I said that if anyone would take steroids, they should take testosterone with progesterone. Since taking testosterone alone will tank 3 beta hsd. taking androsterone inhibits 5 alpha reductase that is why it works for PFS. I am anti Peat , I dont take any ideas from Peat
I block cortisol( or increase the need for it) to increase it sensitivity . Peat says cortisol is evil. and to lower it.I want cortisol to be more sensitive. DHEA does not block cortisol. It lowers pregnenolone conversions. Thus tanks the whole glucocorticoid branch. Thus many people crash on it and get hypokalemia.
Progesterone binds to cortisol receptors and activates glutamine synthase only at 21% of cortisol but agonizes cortisol receptors. That is why in cortisol deficiency , you get anxiety. this is understandable, since exogenous progesterone or progestins lower 3 beta hsd and zinc, and zinc is needed for glutamine synthase as active b6 depends on it.
Many women use progesterone to lose their muscular hands, progesterone will tank testosterone = NO MUSCLES
There is no anabolic supplement. Some people need more catabolism and some people need more anabolism. Read Revici work, some cancers are in anabolism and some in catabolism.
All you guys do here is opposite of what Peat says. You block cortisol, you make it more sensitive( I SAY THAT). It is not like you constantly block it to zero. Just block it to zero and live with it. YOU will die. Block serotonin to zero and live with it. You will die from it.
You are doing completely opposite of what you are saying. Your are blocking cortisol for a week. This makes it super sensitive. Then you get off and dont take the supplement. This is what fasting does.
You block serotonin receptor , then you get off the supplement. Serotonin becomes MORE not less.
And now you claim the opposite. LOL NO it is not me stealing the ideas, it is you will be stealing mine soon and spinning Peat into my understanding.
I dont rec any steroids. since if you take testosterone with progesterone, this will make your zinc biounvailable and many other vitamins and minerals biounvailable/
Your PH regulation will be screwed up. since zinc is used in many enzymes.
All these steroid cycles are nonsense and will ruin your health. Even taking pregnenolone will cause problems,since when you take pregnenolone. You make iron biounavailable since you tank 450scc
When you tank your biounavailable iron, you tank your progesterone to cortisol conversion, since you need iron in 11 beta. You also tank your 5 alpha . since DHT requires iron.
So pregnenolone will cause estrogen to go up, to oppose progesterone rise from pregnenolone intake. since conversion of progesterone to cortisol goes down. If iron was there, then metabolism could have gone up. since cortisol conversion depends on IRON.
This is why no one can tolerate thyroid with low iron level. WHY? since iron is needed to convert progesterone to cortisol, and without cortisol, you will have thyroid resistance.
Zinc will increase progesterone levels, THIS INCREASES CORTISOL IN SLOW OXIDIZERS and LOWERS IT IN FAST OXIDIZERS .
Progesterone and progestins also will always act differently on the receptor depending on the cell potassium level.
That guy always leaves when it gets interestingGbolduev,
I have never seen anything that would suggest that taking supplemental pregnenolone would "tank" P450scc, or in other words would lower the body's own production of pregnenolone. But what I would like to know is: How would the inhibition of 450scc make iron biounavailable as you say? Thanks.
I think he got banned.That guy always leaves when it gets interesting