Androsterone - Liquid Androsterone For Lab/R&D

[cyclops]

So, on monday, I did 2 drops androsterone and 2 drops lisuride before I left for aikido class. I walked into the dojo and immediately spoke to the teacher-- who was arriving at the same time -- about something that was bothering me. This is very unusual for me. (usually I am a shy stammering worm). For sure, he was taken aback to see me have anything like off-mat assertiveness. Like 'wow, she means business.'
This afternoon, I did 2 drops androsterone and then about an hour later, 2 drops lisuride and left for class. (There is an hour between leaving my house and warming up and class starting). 2nd to enter the mat was a senior black belt. He said, "Wow, someone's in a good mood." Just by looking at me.

Regina, you seem to do ok with taking some supplements I would only normally figure males to use. Are these safe for women too?

 

[Regina]

Regina, you seem to do ok with taking some supplements I would only normally figure males to use. Are these safe for women too?

I have no idea. Just thought I'd give it a try and in tiny doses, I like the effect.

 

[Andman]

are you using topically or orally?

sorry for late reply, always topically so far

 

[Wagner83]

I experienced with this product on my rat again a few times. In tocopherols/mct 10 mg can be used topically without noticing much at all besides some pheromone-like effects. With the new solvent there is relaxation of muscles at night and pheromone-like effects with 1-2mg. Combined with pansterone there may be light effects on strength however it still seems to be a lot less powerful than when I last used it (long while ago, dmso), I'm not sure why, there used to be intense effects on the brain, mood, voice even orientation of sexual fantasies.

I have no idea. Just thought I'd give it a try and in tiny doses, I like the effect.

From what I saw it has been studied in men less than in women.

 

[Steene]

I have no idea. Just thought I'd give it a try and in tiny doses, I like the effect.

I wouldn't take it as a woman. Nobody knows its long term effects on women.

 

[milk_lover]

@Wagner83 any studies connecting Andro/pheromones to the pituitary gland?

 

[Wagner83]

I wouldn't take it as a woman. Nobody knows its long term effects on women.

Not that I disagree but the only "long term" (1year) study I've seen was on women , it used massive doses and there were apparently no issues, not even side effects reported from the participants.

 

[Wagner83]

@Wagner83 any studies connecting Andro/pheromones to the pituitary gland?

There are some on rats that haidut sent me, some are in the references spoilers of the mail exchange with Ray.
SAGE Journals: Your gateway to world-class journal research

Abstract
Conclusions

The daily administration of 200 γ of androsterone for 15 days into sexually mature spayed rats caused no significant change either in pituitary weight or pituitary lactogen content and produced no detectable growth of the mammary glands.

You may need to scroll down for androsterone: Vitamins and Hormones

From haidut:

Finally, this study shows that androsterone suppressed pituitary directly. More notably, while steroids like DHEA has estrogenic effects androsterone did not.
The effect of high doses of androgenic substances on the weights of the testes' accessory reproductive organs and endocrine glands of young male guinea-pigs - Bottomley - 1938 - The Journal of Physiology - Wiley Online Library
"...As far as it is possible from our results to draw conclusions as to the relative pituitary suppression potencies of any of the substances used by us, it may be said that the power of causing pituitary suppression appears to be correlated with androgenic potency rather than with gynaecogenic properties. Thus in these experiments, administration both of A5-tr-androstendiol and of cis-androsterone caused pituitary suppression as evidenced by testicular atrophy, while A6-tr-dehydroandrosterone had no effect. With regard to gynaecogenic properties on the other hand, cis-androsterone has little or no activity [Warren, 1935; Deanesly & Parkes, 1936], while A5-tr-androstendiol and A5-tr-dehydroandrosterone are active [D e a ne s ly & Parkes, 1936; see also Koch, 1937]."

"...On the other hand, it is noteworthy that with respect to the power of producing pituitary suppression, the two male hormones found in male urine fall into the order of potency, cis-androsterone > A5-tr-dehydroandrosterone which is the same as their relative order of potency on the basis of the capon comb test [see Koch, 1937]."

So, basically matches with that has been known about androsterone for quite some time - i.e. no estrogenic effects, in physiological doses probably a good precursor to DHT, in higher doses becomes suppressive of pituitary like other androgens including dihydrotestosterone, 17-methyltestosterone, and testosterone (what the study tested).

----------------------------------------------------------------------

This may be interesting for those who are supplementing hormones in "physiological doses":

Even Minor Stress Substantially Decreases DHEA-S Levels

Why DHEA Must Be Taken In Small Doses Only

 

[haidut]

I have no idea. Just thought I'd give it a try and in tiny doses, I like the effect.

Didn't you say another girl started hitting on you when you used androsterone? Also, didn't the hairy Bulgarian gorilla also seem more interested in wrestling you than usual?
Maybe I am just misremembering, but I thought you said something along those lines...

 

[Regina]

Didn't you say another girl started hitting on you when you used androsterone? Also, didn't the hairy Bulgarian gorilla also seem more interested in wrestling you than usual?
Maybe I am just misremembering, but I thought you said something along those lines...

Haha. That was at the old dojo. Yeah, it was a 15 yr old super strong Serbian girl.
I don't know what to say about the hairy Bulgarian. He's just a lousy aikidoist.
Since then, I've had a huge amount of changes--besides a completely different training environment, many more egos to face--and mostly had to re-wire myself.
But I do get to train with my favorite Bulgarian female, who is tremendously talented and altogether class act.

For now 2 drops androsterone in the afternoon before training seems like a hit.

As long as I am mindful about eating enough, it is working out. (Sugar, B's, protein, mins)
I just bought a product called SaltStick caps buffered electrolyte salts and will pop one before class.

 

[cyclops]

You really seem to love aikido; I'm interested, what's the best part about it?

 

[Regina]

You really seem to love aikido; I'm interested, what's the best part about it?

It hits so many notes. The principles that get embodied through direct physical training make normal life easier to navigate. The atmosphere is highly formal and therefore allows for very sophisticated partner interaction in a martial setting.
Great aikido happens when there is "ukemi both sides." Ukemi is how to receive or "catch" a technique. When one gets good at it, (staying supple and relaxed, but whole body coherence) it feels awesome. As practitioners mature in their training outlook, the two sides press into each other in a highly dynamic way. You train with everybody in the room and one's ego is dissolved. It's a way to develop your Self, your shadow side, by interacting with so many different bodies and egos. It's amazing how you learn to be present in the moment. You see how you fail every time you bring judgment to every unfolding second.

 

[johnsmith]

I just took my first drop of Androsterone in a month or so, this is the first time I haven't been depressed in a couple days. Interesting.

 

[Wagner83]

This is a very nice link if you are looking for a page packed with information on a compound, just replace "androsterone" in the search bar with an other term:
Androsterone - an overview | ScienceDirect Topics

This is a funny study , not sure what to make of it, perhaps the metabolites are the reason for the issues, or androsterone is not as strong a pheromone as androstenone or androstenol:

Current Issues in the Study of Androstenes in Human Chemosignaling - ScienceDirect (Jan Havlicek⁎, ... S. Craig Roberts†, in Vitamins & Hormones, 2010)

Spoiler: quote

Behavioral effects
Evidence about context-dependent effects of androstenes on mood change and perception is certainly important, but leaves open the question of whether these effects translate into behavioral changes. To answer this, we should examine evidence on behavioral effects, and in particular those investigated in naturalistic settings. In the first study of this kind, researchers impregnated seats in a dentist's waiting room with androstenone (Kirk-Smith and Booth, 1980). Female patients approached the treated seats, while male patients avoided them. In a second elegant study, researchers impregnated doors of student restroom stalls with ethanol, androstenol, or androsterone (a compound that smells similar to androstenol, but is not a constituent of human body odor), and monitored men's and women's usage (Gustavson et al., 1987). Men but not women avoided cubicles impregnated with androstenol, but not the two controls.

A third group of researchers used a “necklace technique” to test the effect of androstenol and copulines in natural settings (Cowley and Brooksbank, 1991). Participants wore a plastic tube with open ends that had been impregnated with the target substance (0.25 ml chloroform with 1 mg/ml androstenol) as a necklace from the afternoon until the next morning, when they were asked to record details of all their morning social interactions, including sex of their interlocutor, length and depth of the conversation, and details of who initiated the interaction. Women who wore androstenol reported more interactions with men but not with other women, and longer and deeper conversations.

A paper on clofibrate/atromid:

Spoiler: paper

The Search for Cholesterol-lowering Drugs (Daniel Steinberg M.D., Ph.D., in The Cholesterol Wars, 2007)

CLOFIBRATE
The discovery of clofibrate is a curious example of serendipity in science. In the early 1960s, J.M. Thorp and colleagues, working at Imperial Chemical Industries Limited in England, were experimenting with the effects of steroid hormones on metabolism. It had been shown by Hellman et al. that the adrenal steroid androsterone could lower blood cholesterol levels when given intramuscularly but was without effect when given orally (36). Androsterone itself is not well absorbed from the intestine so Thorp and colleagues were hoping to find some way to increase its absorption. They found that clofibrate (α-p-chlorophenoxyisobutyrate), when administered orally along with androsterone, yielded a consistent fall in blood cholesterol levels (37;38). They inferred, logically enough, that the clofibrate was enhancing the absorption of androsterone, the presumed active component. Michael E Oliver, at the University of Edinburgh, demonstrated the effectiveness of this combination in humans. He also reported that there was no response to the clofibrate when given alone at the same dosage. (It should be noted that Oliver only studied six patients at the time.) He, like Thorp, concluded that the effectiveness of the combination was attributable to the androsterone. In any case, after some small-scale safety studies, the combination of androsterone and clofibrate was put on the market under the trade name Atromid (each capsule containing 5.5 mg androsterone “dissolved in” 245 mg clofibrate). It was recommended “for the control of blood abnormalities in coronary heart disease.” Concurrently the drug company started a large, multicenter trial to further evaluate safety and efficacy. In fact, plans were already afoot for a full-scale clinical trial of Atromid to see if lowering blood cholesterol would reduce risk of coronary events. Then something most unexpected happened. In 1963, a group of investigators at the Sloan-Kettering Institute in New York led by Dr. Leon Hellman reported that in their hands the clofibrate contained in Atromid, without the androsterone, was fully as effective as the combination (39;40). Subsequent studies by Oliver (41) and by other investigators quickly confirmed that the androsterone in the preparation could indeed be totally omitted with no change in efficacy, i.e. clofibrate alone was just as effective as the combination. The drug company did not lose a beat. They simply rechristened it “Atromid-S” instead of “Atromid” the “S” presumably denoting the Latin “sine” – without. Without androsterone, that is.

So, the theory – that clofibrate enhanced the oral availability of steroid hormones – was wrong, but clofibrate, by itself, was actually quite effective. It reduced blood cholesterol levels by about 15 percent and it did not appear to have any serious side effects. Two groups in the United Kingdom, one in Scotland under the leadership of Michael F. Oliver and one in England under the leadership of H.A. Dewar, went to work on designing randomized, placebo-controlled, double-blind studies of the effectiveness of clofibrate in preventing progression of coronary heart disease in high-risk individuals, men and women, who already had clinically evident heart disease (42;43). At about the same time, the World Health Organization sponsored an even larger cooperative primary prevention study, involving Edinburgh, Prague, and Budapest, to determine whether clofibrate treatment of men at high risk because of hypercholesterolemia but without clinically evident heart disease would reduce risk.

CLOFIBRATE REDUCES RISK OF INFARCTION
The results in the two UK studies (in patients who had had their first infarct or who had angina) were not entirely concordant but they did agree in general (44). Both showed that in patients who were having angina at the beginning of the study there was a significant reduction in mortality, especially in sudden deaths, and a significant reduction in events. In both trials there was also a reduction in the incidence of nonfatal infarcts, and again this was more marked in patients with angina. However, the degree of protection did not parallel the plasma lipid responses, and the authors speculated that clofibrate might have additional modes of action. The bottom line was that there was a trend toward protection against a second cardiac event. The next question was whether starting treatment earlier – patients who had not yet developed symptomatic disease – would be effective. That was the question addressed by a large-scale WHO-sponsored study.

The WHO study was started in 1965 and included over 15,000 healthy men, aged 30–59 (3). About 10,000 of these were men with high blood cholesterol levels, levels found in the upper third of the population. Half of these (5,000) were assigned to the placebo group and half to the clofibrate group. (A second, untreated control group was made up of men having blood cholesterol levels in the lower third of the population to allow comparison of their prognosis with that of the men treated with clofibrate.) Clofibrate, instead of giving the predicted 15 percent drop in blood cholesterol, only decreased it by an average of 9 percent. Despite that, over the approximately 5 years of the study, clofibrate reduced the overall incidence of nonfatal heart attacks by 20 percent, and this result was statistically significant at the canonical p < 0.05 level. Moreover, the degree of protection was greatest in the men with the highest initial levels of plasma cholesterol and in the men showing the greatest drop in cholesterol level in response to clofibrate. In other words, the data suggested that the preventive effect was directly ascribable to the cholesterol-lowering effect of the drug. (Interestingly these data conform nicely to the generalization reached many years later that whatever the nature of the cholesterol-lowering intervention – diet or drugs – a 1 percent drop in cholesterol level causes an approximate 2 percent reduction in cardiac risk.) If there were no catch, these findings lent strong support to the lipid hypothesis. But there was a catch.

CLOFIBRATE IS TOXIC
The catch was that total mortality, i.e. all deaths irrespective of cause, was actually greater in the clofibrate-treated group. The overall death rate was 20 percent higher and this difference was statistically significant (p < 0.05). So, even though clofibrate had reduced the number of nonfatal heart attacks significantly, overall it had apparently done more harm than good. To paraphrase an old aphorism: “The experiment was a success but the patient died.”

The investigators looked carefully at the causes of death by category. There were no differences in the number of deaths from other vascular diseases nor from accidents or violence. The total number of cancers in the clofibrate group was slightly higher, irrespective of the site of the cancer, but that difference was not statistically significant. The excess deaths were predominantly associated with diseases of the liver, gall bladder, and intestine, including cancers in these locations. The authors hypothesized that clofibrate might be responsible by increasing cholesterol mobilization and excretion into the bile, but there was no direct evidence for that.

The key question was whether the increase in non-CHD deaths was due, directly or indirectly, to the lowering of serum cholesterol brought about by the drug or rather to some other pharmacologic effect of clofibrate not necessarily related to its cholesterol-lowering effect. If the former, then any other cholesterol-lowering regimen would be similarly toxic and research in the field might as well come to a complete halt. If the latter were true, then other pharmacologic or dietary approaches might very well reduce serum cholesterol and risk of heart attack without increasing deaths from other diseases. At the time no one could answer the question unambiguously and therefore an understandable conservatism held sway for some time regarding treatment of hypercholesterolemia.

Michael E Oliver, who was a prime mover in the design and execution of these trials, and the many clinician-scientists who participated must have been bitterly disappointed in the outcome. Dr. Oliver, his close collaborator George S. Boyd, and their colleagues in Edinburgh had for many years done pioneering work on lipoproteins and atherosclerosis, especially on the role of hormones in the process (45;46). They must have felt reasonably sure there was a causal relationship between blood cholesterol and atherosclerosis or else they would not have invested so much time and energy in the design and execution of these clinical trials. It would be readily understandable that Oliver and the others involved would henceforth take a skeptical if not frankly negativistic view of any proposals to treat hypercholesterolemia. Oliver spoke out passionately against such recommendations for years, even after the 1984 Consensus Conference at which the National Heart, Lung and Blood Institute endorsed a national program for lowering blood cholesterol to prevent heart disease (47). He was indeed “The Cholesterol Pessimist” – possibly because the clofibrate trials had left scars.

Later studies, using more effective drugs for lowering cholesterol levels and involving many thousands of subjects, would clearly show that lowering cholesterol levels does not per se increase deaths from any other causes, including cancers, violence or accidents, or diseases of the gastrointestinal tract. The unfortunate side effects in the WHO study must have been due to some other effect of the clofibrate molecule or due to chance alone. Ironically, the fact that clofibrate treatment had in fact reduced the incidence of nonfatal myocardial infarctions by 20 percent seemed to be lost sight of. Later studies using the statins would show that not only coronary heart disease mortality but also total mortality is decreased when serum cholesterol is lowered, even when it is lowered by more than 40 percent. At the time, however, none of this was known, and the concerns about safety dampened efforts to make lowering cholesterol a high-priority public health goal.

It should be noted that an analogue of clofibrate, gemfibrozil, was introduced in the mid-1970s and shown to have comparable effects on serum lipid levels but without the side effects encountered in the clofibrate trials. Moreover, the Helsinki Heart Study, an intervention study in over 4,000 men at high risk because of dyslipidemia showed that gemfibrozil reduced incidence of coronary events by 34 percent without affecting overall mortality (48;49). Follow-up at 18 years showed a 32 percent lower relative risk in the original gemfibrozil-treated group and no difference in all-cause or cancer mortality (50).

Maybe this will interest @haidut :
Cell Biology of Leydig Cells in the Testis (Syed G. Haider, in International Review of Cytology, 2004)

Adult Leydig Cells
Hardy et al. (1989) subdivided the postnatal differentiation of rat Leydig cells into three stages: (1) progenitor stage: Leydig cells originate from mesenchyme-like fibroblasts (pnd 14–28) and produce androsterone as the predominant androgen end product; (2) immature stage: Leydig cells produce small amounts of testosterone on about pnd 35 and metabolize most of this testosterone, the predominant androgen end product being 5α-androstane-3α, 17β-diol; and (3) mature stage: Leydig cells actively produce testosterone as androgen end product and are fully functional in the sexually mature animal, by pnd 90 (Hardy et al., 1990; Shan and Hardy, 1992; Shan et al., 1995, 1997). Figure 7 schematically represents the main steps in the differentiation of ALCs in rat.

 

[Jsaute21]

EDIT: Since I keep getting questions about androsterone, here is Ray's response when asked about it:
Ray Peat Email Advice Depository Discussion/Comment Thread
"...I think it would be safe enough to try in treating cancer or brain degenerative diseases."

Here is one reference that gives backing to his statement above:
Antitumor Steroids - ScienceDirect
"...Androsterone (11) effected a 63% inhbition of bronchiogenic carcinoma A-42, 42% inhibition of epidermoid carcinoma HEp3, 81% inhibition of sarcoma HS1, and 35% inhbition of intestinal adenocarcinoma HAd1, all tested in egg [9]."

Unlike other products that we have released over the years, this one is almost completely unknown outside bodybuilding circles. Even among die-hard bodybuilders it is exclusively known as its ability to function as pro-hormone for more potent androgens like DHT and 5-androstanedione. See attached images for tha pathways of androsterone conversion back into potent androgens like DHT.

The backdoor pathway to dihydrotestosterone. - PubMed - NCBI
"...Because androsterone is an efficient precursor of DHT, a moderate production rate might produce a considerable physiological effect, even if androsterone is not the most abundant 19-carbon steroid produced in 21OHD."

Androsterone - Wikipedia, the free encyclopedia
"...Androsterone, or 3α-hydroxy-5α-androstan-17-one, is an endogenous steroid hormone, neurosteroid, and putative pheromone.[1] It is a weak androgen with a potency that is approximately 1/7th that of testosterone.[2]In addition, it can be converted to dihydrotestosterone (DHT) from 3α-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase, bypassing conventional intermediates such as androstenedione and testosterone, and as such, can be considered to be a metabolic intermediate in its own right.[3][4] Androsterone is also known to be an inhibitory androstane neurosteroid,[5][6] acting as a positive allosteric modulator of theGABAA receptor,[7] and possesses anticonvulsant effects.[8] The unnatural enantiomer of androsterone is more potent as a positive allosteric modulator of GABAA receptors and as an anticonvulsant than the natural form.[9] Androsterone's 3β-isomer is epiandrosterone, and its 5β-epimer is etiocholanolone."

Dihydrotestosterone synthesis pathways from inactive androgen 5α-androstane-3β,17β-diol in prostate cancer cells: Inhibition of intratumoural 3β-hydroxysteroid dehydrogenase activities by abiraterone : Scientific Reports
Androgen deprivation promotes intratumoral synthesis of dihydrotestosterone from androgen metabolites in prostate cancer
Dihydrotestosterone synthesis bypasses testosterone to drive castration-resistant prostate cancer
"...The four 5α-reduced 19-carbon steroids [5α-dione, DHT, androsterone, and Adiol] are interconvertible through reversible reactions (Fig. 1). Comparison of the accumulation of total 5α-reduced steroids with [3H]-AD and [3H]-T treatments further shows that AD→5α-dione is the dominant entryway to 5α-reduced steroids (Fig. 2E)."

However, androsterone is a very interesting steroid in its own right and for a lack of a better analogy I would call it the "mirror image of DHT" due to identical structure but with reversed functional groups. It also seems to share quite a few of progesterone's effects - i.e. anti-estrogenic, sedative, anti-convulsant, pro-thyroid, pro-metabolic, brain protective, promoting insulin sensitivity, anti-adrenaline, anti-cortisol, anti-cancer, anti-depressant, etc. Some studies have gone as far as to suggest that it is androsterone that is the actual steroid with real metabolic activity while all other steroids before it in the pathways (including T and DHT) are the actual pro-hormones.

Studies with Androsterone-3-3H,4-14C | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic
"...These two studies demonstrate the surprising extent to which an important, biologically active, hormone metabolite is further utilized in vivo in man. They raise many further problems. Perhaps the most important of these is the fate of the large portion that was not detected in urine or feces. From the extent of the oxidation of the C-3 hydroxyl group, it might be concluded that a part of the androsterone could serve an important function in man as the coenzyme in a transhydrogenase system, as has indeed been demonstrated with bacterial (15) and rat liver (16) preparations."
"...In view of its biological activity and its participation in oxidation-reduction systems, it seems clear that androsterone may have metabolic functions equal to those of the hormones which generate it. Since, with the exception of testosterone, the physiological role of the other androgens is unclear, it is perhaps not too speculative to suggest that one function of these hormones may be the production of this important "metabolite."

Unlike progesterone androsterone does not have the potential for anti-androgenic effects of high doses progesterone in males. It is truly a pity that this amazing chemical saw so much research in the middle of the 20th century and even wild commercial success as the drug Atromid, only to be forgotten and replaced by much more toxic alternatives.

The units listed on the label are just for measurement purposes. They do not indicate or suggest optimal dose. Please note that similar to the products sold by companies like BlueSky, this product if for lab/research use only. The product can be ordered from the link below:
http://www.idealabsdc.com/lab

*******************************************************************************
Androsterone is an androgenic steroid derived via the activity of the enzyme 5-AR and is a donwstream metabolite of the more potent androgen DHT. Like all 5-AR derived androgens, androsterone displays anti-estrogenic and anti-glucocorticoid activity and in addition serves as a pro-hormone for DHT and other potent androgens. In addition, androsterone is a neurosteroid with potent GABA agonist activity, and is known to function as a pheromone in many animal species including humans. It has been shown to possess anti-depressant and anti-proliferative effects. Perhaps most importantly, it has been found to act like as a potent thyroid mimetic / surrogate and as such to increase basal temperature, oxygen consumption and lower lipid levels in humans.

Drops per container: about 240
Each drop contains the following ingredients:

Androsterone: 1 mg

Other ingredients: (1) DMSO, ethanol; or (2) tocopherols, MCT
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References:

1. Androgenic / pro-sexual
Remarkable Synergistic Anabolic /androgenic Effect Of Androsterone And DHEA Combination
Androsterone - Androgenic Neurosteroid Required For Male Sexual Behavior
Androsterone - The Legal Pro-hormone For Potent 5-AR Derived Androgens

2. Anti-estrogenic
Androsterone - A Potent Steroidal Aromatase Inhibitor

3. Thyroid mimetic / surrogate
Androsterone - The Forgotten But Potent Thyroid Mimetic
Androsterone Is A Potent Agonist / Activator Of The Farnesoid X Receptor (FXR)

4. Anti-adrenaline
Androsterone Inhibits Catecholamine Release

5. Anti-cancer
Androsterone - A Neurosteroid With Anti-cancer Activity

6. Insulin resistance / sensitivity, diabetes
Androsterone - A Potential Treatment For Insulin Resistance And Diabetes

7. Neurosteroid / anti-sepressant
Androsterone - An Andidepressant Neurosteroid
The Antidepressant Mechanism Of Androsterone
Androsterone - A Potent Anxiolytic, Sedative, And Anti-convulsant Neurosteroid

May seem silly but would there be any difference between administering

EDIT: Since I keep getting questions about androsterone, here is Ray's response when asked about it:
Ray Peat Email Advice Depository Discussion/Comment Thread
"...I think it would be safe enough to try in treating cancer or brain degenerative diseases."

Here is one reference that gives backing to his statement above:
Antitumor Steroids - ScienceDirect
"...Androsterone (11) effected a 63% inhbition of bronchiogenic carcinoma A-42, 42% inhibition of epidermoid carcinoma HEp3, 81% inhibition of sarcoma HS1, and 35% inhbition of intestinal adenocarcinoma HAd1, all tested in egg [9]."

Unlike other products that we have released over the years, this one is almost completely unknown outside bodybuilding circles. Even among die-hard bodybuilders it is exclusively known as its ability to function as pro-hormone for more potent androgens like DHT and 5-androstanedione. See attached images for tha pathways of androsterone conversion back into potent androgens like DHT.

The backdoor pathway to dihydrotestosterone. - PubMed - NCBI
"...Because androsterone is an efficient precursor of DHT, a moderate production rate might produce a considerable physiological effect, even if androsterone is not the most abundant 19-carbon steroid produced in 21OHD."

Androsterone - Wikipedia, the free encyclopedia
"...Androsterone, or 3α-hydroxy-5α-androstan-17-one, is an endogenous steroid hormone, neurosteroid, and putative pheromone.[1] It is a weak androgen with a potency that is approximately 1/7th that of testosterone.[2]In addition, it can be converted to dihydrotestosterone (DHT) from 3α-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase, bypassing conventional intermediates such as androstenedione and testosterone, and as such, can be considered to be a metabolic intermediate in its own right.[3][4] Androsterone is also known to be an inhibitory androstane neurosteroid,[5][6] acting as a positive allosteric modulator of theGABAA receptor,[7] and possesses anticonvulsant effects.[8] The unnatural enantiomer of androsterone is more potent as a positive allosteric modulator of GABAA receptors and as an anticonvulsant than the natural form.[9] Androsterone's 3β-isomer is epiandrosterone, and its 5β-epimer is etiocholanolone."

Dihydrotestosterone synthesis pathways from inactive androgen 5α-androstane-3β,17β-diol in prostate cancer cells: Inhibition of intratumoural 3β-hydroxysteroid dehydrogenase activities by abiraterone : Scientific Reports
Androgen deprivation promotes intratumoral synthesis of dihydrotestosterone from androgen metabolites in prostate cancer
Dihydrotestosterone synthesis bypasses testosterone to drive castration-resistant prostate cancer
"...The four 5α-reduced 19-carbon steroids [5α-dione, DHT, androsterone, and Adiol] are interconvertible through reversible reactions (Fig. 1). Comparison of the accumulation of total 5α-reduced steroids with [3H]-AD and [3H]-T treatments further shows that AD→5α-dione is the dominant entryway to 5α-reduced steroids (Fig. 2E)."

However, androsterone is a very interesting steroid in its own right and for a lack of a better analogy I would call it the "mirror image of DHT" due to identical structure but with reversed functional groups. It also seems to share quite a few of progesterone's effects - i.e. anti-estrogenic, sedative, anti-convulsant, pro-thyroid, pro-metabolic, brain protective, promoting insulin sensitivity, anti-adrenaline, anti-cortisol, anti-cancer, anti-depressant, etc. Some studies have gone as far as to suggest that it is androsterone that is the actual steroid with real metabolic activity while all other steroids before it in the pathways (including T and DHT) are the actual pro-hormones.

Studies with Androsterone-3-3H,4-14C | The Journal of Clinical Endocrinology & Metabolism | Oxford Academic
"...These two studies demonstrate the surprising extent to which an important, biologically active, hormone metabolite is further utilized in vivo in man. They raise many further problems. Perhaps the most important of these is the fate of the large portion that was not detected in urine or feces. From the extent of the oxidation of the C-3 hydroxyl group, it might be concluded that a part of the androsterone could serve an important function in man as the coenzyme in a transhydrogenase system, as has indeed been demonstrated with bacterial (15) and rat liver (16) preparations."
"...In view of its biological activity and its participation in oxidation-reduction systems, it seems clear that androsterone may have metabolic functions equal to those of the hormones which generate it. Since, with the exception of testosterone, the physiological role of the other androgens is unclear, it is perhaps not too speculative to suggest that one function of these hormones may be the production of this important "metabolite."

Unlike progesterone androsterone does not have the potential for anti-androgenic effects of high doses progesterone in males. It is truly a pity that this amazing chemical saw so much research in the middle of the 20th century and even wild commercial success as the drug Atromid, only to be forgotten and replaced by much more toxic alternatives.

The units listed on the label are just for measurement purposes. They do not indicate or suggest optimal dose. Please note that similar to the products sold by companies like BlueSky, this product if for lab/research use only. The product can be ordered from the link below:
http://www.idealabsdc.com/lab

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Androsterone is an androgenic steroid derived via the activity of the enzyme 5-AR and is a donwstream metabolite of the more potent androgen DHT. Like all 5-AR derived androgens, androsterone displays anti-estrogenic and anti-glucocorticoid activity and in addition serves as a pro-hormone for DHT and other potent androgens. In addition, androsterone is a neurosteroid with potent GABA agonist activity, and is known to function as a pheromone in many animal species including humans. It has been shown to possess anti-depressant and anti-proliferative effects. Perhaps most importantly, it has been found to act like as a potent thyroid mimetic / surrogate and as such to increase basal temperature, oxygen consumption and lower lipid levels in humans.

Drops per container: about 240
Each drop contains the following ingredients:

Androsterone: 1 mg

Other ingredients: (1) DMSO, ethanol; or (2) tocopherols, MCT
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References:

1. Androgenic / pro-sexual
Remarkable Synergistic Anabolic /androgenic Effect Of Androsterone And DHEA Combination
Androsterone - Androgenic Neurosteroid Required For Male Sexual Behavior
Androsterone - The Legal Pro-hormone For Potent 5-AR Derived Androgens

2. Anti-estrogenic
Androsterone - A Potent Steroidal Aromatase Inhibitor

3. Thyroid mimetic / surrogate
Androsterone - The Forgotten But Potent Thyroid Mimetic
Androsterone Is A Potent Agonist / Activator Of The Farnesoid X Receptor (FXR)

4. Anti-adrenaline
Androsterone Inhibits Catecholamine Release

5. Anti-cancer
Androsterone - A Neurosteroid With Anti-cancer Activity

6. Insulin resistance / sensitivity, diabetes
Androsterone - A Potential Treatment For Insulin Resistance And Diabetes

7. Neurosteroid / anti-sepressant
Androsterone - An Andidepressant Neurosteroid
The Antidepressant Mechanism Of Androsterone
Androsterone - A Potent Anxiolytic, Sedative, And Anti-convulsant Neurosteroid

What do we estimate the difference being of taking a downstream hormone like androsterone opposed to a product like pine pollen? I know PP contains andro but for some reason i view it as being potentially less confusing to our HPTA?

 

[cyclops]

It hits so many notes. The principles that get embodied through direct physical training make normal life easier to navigate. The atmosphere is highly formal and therefore allows for very sophisticated partner interaction in a martial setting.
Great aikido happens when there is "ukemi both sides." Ukemi is how to receive or "catch" a technique. When one gets good at it, (staying supple and relaxed, but whole body coherence) it feels awesome. As practitioners mature in their training outlook, the two sides press into each other in a highly dynamic way. You train with everybody in the room and one's ego is dissolved. It's a way to develop your Self, your shadow side, by interacting with so many different bodies and egos. It's amazing how you learn to be present in the moment. You see how you fail every time you bring judgment to every unfolding second.

beautiful description!...thanks for sharing!

 

[Wagner83]

May seem silly but would there be any difference between administering


What do we estimate the difference being of taking a downstream hormone like androsterone opposed to a product like pine pollen? I know PP contains andro but for some reason i view it as being potentially less confusing to our HPTA?

That's an argument that doesn't make sense to me yet, the battle of "natural" supplements (vitamins, minerals, herbs) vs unnatural (dhea, preg etc..).

 

[Wagner83]

After more days the review is still the same as the one in post 964, this is not androgenic to the brain for some reason. I wonder if dmso affects compounds uptake in the cell (as if the body had no choice but to use the compound) and through the blood brain barrier, I also wonder if reducing estrogens levels too much without enough dht can have negative effects given the studies which showed supplementing dht and tanked estrogens did not have bad effects . Estroban for a few days is a lot more powerful for me but after a week/10 days the benefits come to a brutal halt. Btw I've tried to replicate the effects of estroban with vitamins A, K2, E and it did not produce the same effects at all.

 

[Black Ops]

Is their a possibility of adrenaline rebound upon discontinuation of androsterone?

 

[cyclops]

Btw I've tried to replicate the effects of estroban with vitamins A, K2, E and it did not produce the same effects at all.

You forgot the D.