Androsterone - Liquid Androsterone For Lab/R&D

[haidut]

I found that girls have better orgasms when I am taking Androsterone. Just curious, where to apply androsterone for maximal pheromone effect? Neck? Thank you.

I think any area with large blood vessels near the surface would be good. Neck, shoulders, pelvic area, inside of elbows, etc.

 

[haidut]

Would this be good to stack with real DHT?

Probably not, as it is a precursor to DHT. Why would you want to stack it with DHT?

 

[cyclops]

Probably not, as it is a precursor to DHT. Why would you want to stack it with DHT?

Experimenting with some of the "Peat" hormones in an effort to be and feel my best. Not sure which ones are good to combine with others though, so I was asking.

 

[Wagner83]

I found that girls have better orgasms when I am taking Androsterone. Just curious, where to apply androsterone for maximal pheromone effect? Neck? Thank you.

The few times I used it (with pansterone) it looked like it could increase penis size some over time, by that I mean improving night woods, hardness and just maximizing our potential. Also since it is relaxing it makes sense that the pelvic floor muscles could be more relaxed and let the penis fill up more fully before erection.

 

[Lukas]

You could combine DHEA and/or Pregnenolone with either DHT or Androsterone. But I would test each hormone on its own before combining them and start with the lowest dose possible.

 

[Broken man]

The few times I used it (with pansterone) it looked like it could increase penis size some over time, by that I mean improving night woods, hardness and just maximizing our potential. Also since it is relaxing it makes sense that the pelvic floor muscles could be more relaxed and let the penis fill up more fully before erection.

Ye, I am doing some PE and I can say that Andro is important because you can almost see how he is growing .

 

[Wagner83]

Ye, I am doing some PE and I can say that Andro is important because you can almost see how he is growing .

Be prepared for pms lol. It would be interesting to see how you'd grow without PE, as I said it may very well be working on its own . I've been wondering what kind of blowjob one would get if androsterone is applied on glans...

 

[Broken man]

Be prepared for pms lol. It would be interesting to see how you'd grow without PE, as I said it may very well be working on its own . I've been wondering what kind of blowjob one would get if androsterone is applied on glans...

I think that doing PE increase genetic potetial cuz I have great recovery from andro, not so much from Keto DHT.

 

[Jsaute21]

Experimenting with some of the "Peat" hormones in an effort to be and feel my best. Not sure which ones are good to combine with others though, so I was asking.

There are a lot of posts on various synergies between hormones and different supplements. Below is a good place to start. Don't be afraid to use that search browser in the top right. It can be a real helpful SOB.

Remarkable Synergistic Anabolic / Androgenic Effect Of Androsterone With DHEA

 

[cyclops]

You could combine DHEA and/or Pregnenolone with either DHT or Androsterone. But I would test each hormone on its own before combining them and start with the lowest dose possible.

What do you think the difference would be in using Pregnenolone+Androsterone VS. Pregnenolone+DHT?

 

[haidut]

What do you think the difference would be in using Pregnenolone+Androsterone VS. Pregnenolone+DHT?

The latter would probably be stronger in terms of androgenic response but I have tried both and they are pretty close. Androsterone seems to have more pronounced mood lifting effects than DHT it does have at least one advantage. DHT seems to be stronger in terms of generating muscle response but even that can be matched by androsterone if it is taken in doses twice as high as DHT.

 

[Wagner83]

@haidut, several points worth looking into. Chapter Five - Steroid Metabolism and Excretion in Anorexia Nervosa - ScienceDirect

Anorexia
Wassif Samuel Wassif*1, Andrew Rashad Ross†, in Vitamins & Hormones, 2013

"
Steroid Excretion in AN
Capillary gas chromatography (GC) is the method of choice for obtaining detailed urinary steroid profile (Shackleton and Honour, 1976). Because of its high specificity and resolution, GC can clearly identify urinary cardinal steroid metabolites. However, a number of preparatory steps are required prior to GC analysis including extraction of conjugated steroids, hydrolysis of glucuronide/sulfate conjugates, and reextraction. Internal standards are then added, and a purification step is included to remove water-soluble material that may interfere with the derivatization process. Following derivatization, steroid identity is checked by gas chromatography–mass spectrometry. Metabolites are quantified by relating peak heights with those of the internal standards (Bevan et al., 1986). The concentration of steroid present in the original urine sample is calculated according to the following formula:

Unknownpeakheight×μgstandardinderivativeStandardpeakheight×fractionofextractusedforderivative×fractionof24-hurinevolumeanalyzed.
The principal urinary metabolites of cortisol measured by GC are shown in Fig. 5.2. Steroid metabolites are typically analyzed in 24 h collections of urine, and steroid profile is used to obtain direct assessments of daily production rates of androgen metabolites (AM, androsterone and etiocholanolone) and cortisol metabolites (CM, tetrahydrocortisone, 5α- and 5β-tetrahydrocortisol, 20α- and 20β-cortolone, and 20α- and 20β-cortol). Urine metabolites are sensitive indicators of suppression of adrenal steroidogenesis (Fink et al., 2002). Ratios of urine metabolites provide indices of activity of the major routes of peripheral phase 1 metabolism as follows: 5α- compared with 5β-reduction:androsterone (5α)/etiocholanolone (5β) and 5α-/5β-tetrahydrocortisol; 11-oxidoreduction compared with 11-dehydrogenation:tetrahydrocortisols (11-OH)/tetrahydrocortisone (11-oxo); 20-oxidoreduction compared with 20-dehydrogenation:cortols + cortolones (20-OH)/tetrahydrocortisone + tetrahydrocortisols (20-oxo); and 20α- compared with 20β-reduction:20α-cortolone + 20α-cortol/20β-cortolone + 20β-cortol. The biosynthesis and origin of urinary steroid metabolites are described in Fig. 5.3 and a typical chromatogram is shown in Fig. 5.4.

Underweight AN patients tend to have relatively lower concentrations of urinary excretion of total CM and total AM. In untreated patients, urinary androsterone, 5α-tetrahydrocortisol (5α-THF), α-cortolone, and α-cortol are low (Table 5.1). Before refeeding, anorexic patients have reduced 5α- and 5β-reductases activities: both of the androsterone/etiocholanolone (andro/etio) ratio as well the 5α-/5β-THF ratio are significantly low (Wassif et al., 2011). The andro/etio and 5α-/5β-THF ratios reflect relative activities of the same 5-reductase enzymes. Changes in these ratios are accounted for by the 5α-reduced component, since androsterone and 5α-THF are reduced, while the 5β-epimers are not different from normal. In contrast, the 5β-reduced components (etiocholanolone, 5β-THF) are comparable to normal weight subjects (Bradlow, Boyar, O'Connor, Zumoff, & Hellman, 1976; Wassif et al., 2011). Low ratios mimic findings in patients with 5α-reductase deficiency and during treatment with the 5α-reductase inhibitor finasteride. In 5α-reductase deficiency, the 5α-reductase II enzyme is deficient, and both ratios are very low. Steroid metabolic changes in AN are similar to those in hypothyroidism (Bradlow et al., 1976). The 5α-/5β-THF ratio and andro/etio ratio are significantly higher in hyperthyroid patients and significantly lower in hypothyroid patients compared to normal subjects (Hoshiro, Ohno, Masaki, Iwase, & Aoki, 2006). This may be explained by anorexics being essentially hypothyroid due to metabolic adaptation that lowers the resting energy expenditure during chronic starvation (Usdan, Khaodhiar, & Apovian, 2008).

Similarly, starving AN patients have abnormal 20α- and 20β-hydroxysteroid dehydrogenase (HSD) activities and the 20-OH/20-oxo [20-hydroxycorticosteroid (cortolone + cortol)/20-oxocorticosteroid (THE + THFs)] metabolite ratio is reduced before refeeding (Table 5.1). However, the 20α-cortol + α-cortolone/20β-cortol + β-cortolone ratio, which examines 20α- versus 20β-reduction, is not altered in AN patients. Anorexic patients also appear to have reduced 11β-HSD activity (reflected by higher ratio of tetrahydrocortisols/tetrahydrocortisone; THFs/THE). There are two main 11β-HSD enzymes: type-1 is predominant in the liver and acts as a reductase (converting cortisone to cortisol) while type-2 is predominantly renal and acts as a dehydrogenase (converting cortisol to cortisone) (Fig. 5.3). Cortisol metabolic clearance rate is greatly influenced by 11β-HSD activity. In most conditions in which the ratio of cortisol:cortisone metabolites changes (apart from specific enzyme deficiencies), such as differences of fat deposits and growth hormone status, it is the type-1 enzyme activity which is changed (Gelding et al., 1998). Increased activity results in a lower clearance rate, while decreased activity (or increased 11β-HSD 2 activity) results in a higher clearance rate (Boyar et al., 1977; Müssig et al., 2008). Studies of steroid excretion in AN have indicated reduced activity of the 11-oxidation component of 11β-HSD (Lawson & Klibanski, 2008; Wassif et al., 2011). This is supported by the finding of higher ratios of THFs/THE. As in the situation with 5α-reductase, changes in 11β-HSD activity are similar to those in hypothyroidism with a THFs/THE ratio that is lower in hyperthyroid patients and higher in hypothyroid patients compared to normal subjects (Hoshiro et al., 2006). In specific type-2 enzyme deficiency (apparent mineralocorticoid excess), the THFs/THE ratio is very high, but the 5α-reduced steroids are also relatively increased and this is evidently a secondary phenomenon. In AN, increase in the THFs/THE ratio is accompanied by decrease in 5α-reduction, so the latter clearly has another origin.

In contrast to AN patients, overweight individuals show enhanced androgen and cortisol metabolite excretion and increased net 5α-reductase and 11-oxidation activities (Boyar et al., 1977; Vassiliadi et al., 2009). Adipose tissue samples taken from obese subjects show increased expression of 11β-HSD1 (Rask et al., 2001) which would be expected to lead to a stimulated conversion of cortisone to cortisol and subsequently increased intracellular glucocorticoid reactivation and activity (Svendsen, Madsbad, Nilas, Paulsen, & Pedersen, 2009).

Weight-reducing diets for obese subjects are associated with an increased 11β-HSD1 and diminished 5-reductase activities (Svendsen et al., 2009). Wassif et al. (2011) have shown that a high-calorie diet in AN patients achieves the opposite changes, with decrease of THFs/THE. Previous studies have demonstrated that weight loss (Engeli et al., 2004) and a low-carbohydrate diet (Stimson et al., 2007) are not associated with changes in 5α-reductase and 11β-HSD1 activities in adipose tissue. Hence, these changes are likely to occur predominantly in the liver.

A novel finding in AN patients of reduced 20-OH/20-oxo ratio, indicating decreased 20-reduction over 20-dehydrogenation, has been recently reported (Wassif et al., 2011). This phenomenon is likely to be responsible for decreased cortisol metabolic clearance rate."

 

[haidut]

@haidut, several points worth looking into. Chapter Five - Steroid Metabolism and Excretion in Anorexia Nervosa - ScienceDirect

Anorexia
Wassif Samuel Wassif*1, Andrew Rashad Ross†, in Vitamins & Hormones, 2013

"
Steroid Excretion in AN
Capillary gas chromatography (GC) is the method of choice for obtaining detailed urinary steroid profile (Shackleton and Honour, 1976). Because of its high specificity and resolution, GC can clearly identify urinary cardinal steroid metabolites. However, a number of preparatory steps are required prior to GC analysis including extraction of conjugated steroids, hydrolysis of glucuronide/sulfate conjugates, and reextraction. Internal standards are then added, and a purification step is included to remove water-soluble material that may interfere with the derivatization process. Following derivatization, steroid identity is checked by gas chromatography–mass spectrometry. Metabolites are quantified by relating peak heights with those of the internal standards (Bevan et al., 1986). The concentration of steroid present in the original urine sample is calculated according to the following formula:

Unknownpeakheight×μgstandardinderivativeStandardpeakheight×fractionofextractusedforderivative×fractionof24-hurinevolumeanalyzed.
The principal urinary metabolites of cortisol measured by GC are shown in Fig. 5.2. Steroid metabolites are typically analyzed in 24 h collections of urine, and steroid profile is used to obtain direct assessments of daily production rates of androgen metabolites (AM, androsterone and etiocholanolone) and cortisol metabolites (CM, tetrahydrocortisone, 5α- and 5β-tetrahydrocortisol, 20α- and 20β-cortolone, and 20α- and 20β-cortol). Urine metabolites are sensitive indicators of suppression of adrenal steroidogenesis (Fink et al., 2002). Ratios of urine metabolites provide indices of activity of the major routes of peripheral phase 1 metabolism as follows: 5α- compared with 5β-reduction:androsterone (5α)/etiocholanolone (5β) and 5α-/5β-tetrahydrocortisol; 11-oxidoreduction compared with 11-dehydrogenation:tetrahydrocortisols (11-OH)/tetrahydrocortisone (11-oxo); 20-oxidoreduction compared with 20-dehydrogenation:cortols + cortolones (20-OH)/tetrahydrocortisone + tetrahydrocortisols (20-oxo); and 20α- compared with 20β-reduction:20α-cortolone + 20α-cortol/20β-cortolone + 20β-cortol. The biosynthesis and origin of urinary steroid metabolites are described in Fig. 5.3 and a typical chromatogram is shown in Fig. 5.4.

Underweight AN patients tend to have relatively lower concentrations of urinary excretion of total CM and total AM. In untreated patients, urinary androsterone, 5α-tetrahydrocortisol (5α-THF), α-cortolone, and α-cortol are low (Table 5.1). Before refeeding, anorexic patients have reduced 5α- and 5β-reductases activities: both of the androsterone/etiocholanolone (andro/etio) ratio as well the 5α-/5β-THF ratio are significantly low (Wassif et al., 2011). The andro/etio and 5α-/5β-THF ratios reflect relative activities of the same 5-reductase enzymes. Changes in these ratios are accounted for by the 5α-reduced component, since androsterone and 5α-THF are reduced, while the 5β-epimers are not different from normal. In contrast, the 5β-reduced components (etiocholanolone, 5β-THF) are comparable to normal weight subjects (Bradlow, Boyar, O'Connor, Zumoff, & Hellman, 1976; Wassif et al., 2011). Low ratios mimic findings in patients with 5α-reductase deficiency and during treatment with the 5α-reductase inhibitor finasteride. In 5α-reductase deficiency, the 5α-reductase II enzyme is deficient, and both ratios are very low. Steroid metabolic changes in AN are similar to those in hypothyroidism (Bradlow et al., 1976). The 5α-/5β-THF ratio and andro/etio ratio are significantly higher in hyperthyroid patients and significantly lower in hypothyroid patients compared to normal subjects (Hoshiro, Ohno, Masaki, Iwase, & Aoki, 2006). This may be explained by anorexics being essentially hypothyroid due to metabolic adaptation that lowers the resting energy expenditure during chronic starvation (Usdan, Khaodhiar, & Apovian, 2008).

Similarly, starving AN patients have abnormal 20α- and 20β-hydroxysteroid dehydrogenase (HSD) activities and the 20-OH/20-oxo [20-hydroxycorticosteroid (cortolone + cortol)/20-oxocorticosteroid (THE + THFs)] metabolite ratio is reduced before refeeding (Table 5.1). However, the 20α-cortol + α-cortolone/20β-cortol + β-cortolone ratio, which examines 20α- versus 20β-reduction, is not altered in AN patients. Anorexic patients also appear to have reduced 11β-HSD activity (reflected by higher ratio of tetrahydrocortisols/tetrahydrocortisone; THFs/THE). There are two main 11β-HSD enzymes: type-1 is predominant in the liver and acts as a reductase (converting cortisone to cortisol) while type-2 is predominantly renal and acts as a dehydrogenase (converting cortisol to cortisone) (Fig. 5.3). Cortisol metabolic clearance rate is greatly influenced by 11β-HSD activity. In most conditions in which the ratio of cortisol:cortisone metabolites changes (apart from specific enzyme deficiencies), such as differences of fat deposits and growth hormone status, it is the type-1 enzyme activity which is changed (Gelding et al., 1998). Increased activity results in a lower clearance rate, while decreased activity (or increased 11β-HSD 2 activity) results in a higher clearance rate (Boyar et al., 1977; Müssig et al., 2008). Studies of steroid excretion in AN have indicated reduced activity of the 11-oxidation component of 11β-HSD (Lawson & Klibanski, 2008; Wassif et al., 2011). This is supported by the finding of higher ratios of THFs/THE. As in the situation with 5α-reductase, changes in 11β-HSD activity are similar to those in hypothyroidism with a THFs/THE ratio that is lower in hyperthyroid patients and higher in hypothyroid patients compared to normal subjects (Hoshiro et al., 2006). In specific type-2 enzyme deficiency (apparent mineralocorticoid excess), the THFs/THE ratio is very high, but the 5α-reduced steroids are also relatively increased and this is evidently a secondary phenomenon. In AN, increase in the THFs/THE ratio is accompanied by decrease in 5α-reduction, so the latter clearly has another origin.

In contrast to AN patients, overweight individuals show enhanced androgen and cortisol metabolite excretion and increased net 5α-reductase and 11-oxidation activities (Boyar et al., 1977; Vassiliadi et al., 2009). Adipose tissue samples taken from obese subjects show increased expression of 11β-HSD1 (Rask et al., 2001) which would be expected to lead to a stimulated conversion of cortisone to cortisol and subsequently increased intracellular glucocorticoid reactivation and activity (Svendsen, Madsbad, Nilas, Paulsen, & Pedersen, 2009).

Weight-reducing diets for obese subjects are associated with an increased 11β-HSD1 and diminished 5-reductase activities (Svendsen et al., 2009). Wassif et al. (2011) have shown that a high-calorie diet in AN patients achieves the opposite changes, with decrease of THFs/THE. Previous studies have demonstrated that weight loss (Engeli et al., 2004) and a low-carbohydrate diet (Stimson et al., 2007) are not associated with changes in 5α-reductase and 11β-HSD1 activities in adipose tissue. Hence, these changes are likely to occur predominantly in the liver.

A novel finding in AN patients of reduced 20-OH/20-oxo ratio, indicating decreased 20-reduction over 20-dehydrogenation, has been recently reported (Wassif et al., 2011). This phenomenon is likely to be responsible for decreased cortisol metabolic clearance rate."

Interesting, thanks a lot. So, basically AN patients have lower 5-AR activity (thus lower DHT, androsterone and 5-AR metabolites of cortisol) and increased 11b-HSD1 (higher cortisol). I think serotonin is also involved. SSRI drugs are known as "anorectics" and are known to cause extreme weight loss. If this is common knowledge, I wonder why cyproheptadine is not used as main treatment for them...I mean, it seems rather obvious, especially given that cypro is known to cause weight gain.

 

[Wagner83]

Interesting, thanks a lot. So, basically AN patients have lower 5-AR activity (thus lower DHT, androsterone and 5-AR metabolites of cortisol) and increased 11b-HSD1 (higher cortisol). I think serotonin is also involved. SSRI drugs are known as "anorectics" and are known to cause extreme weight loss. If this is common knowledge, I wonder why cyproheptadine is not used as main treatment for them...I mean, it seems rather obvious, especially given that cypro is known to cause weight gain.

It seems to be quite a "Peaty" study, besides , not sure if you read the end which is not only focused on AN patients but also dieting etc.. It's also worth reading :

"[...]This may be explained by anorexics being essentially hypothyroid due to metabolic adaptation that lowers the resting energy expenditure during chronic starvation[...]

In contrast to AN patients, overweight individuals show enhanced androgen and cortisol metabolite excretion and increased net 5α-reductase and 11-oxidation activities (Boyar et al., 1977; Vassiliadi et al., 2009). Adipose tissue samples taken from obese subjects show increased expression of 11β-HSD1 (Rask et al., 2001) which would be expected to lead to a stimulated conversion of cortisone to cortisol and subsequently increased intracellular glucocorticoid reactivation and activity (Svendsen, Madsbad, Nilas, Paulsen, & Pedersen, 2009).

Weight-reducing diets for obese subjects are associated with an increased 11β-HSD1 and diminished 5-reductase activities (Svendsen et al., 2009). Wassif et al. (2011) have shown that a high-calorie diet in AN patients achieves the opposite changes, with decrease of THFs/THE. Previous studies have demonstrated that weight loss (Engeli et al., 2004) and a low-carbohydrate diet (Stimson et al., 2007) are not associated with changes in 5α-reductase and 11β-HSD1 activities in adipose tissue. Hence, these changes are likely to occur predominantly in the liver."

From what they say I wonder if just eating enough calories can reverse a lot of issues. Of course the main problem with aneroxia is in the head, I don't know how much they address it.

 

[Jsaute21]

The latter would probably be stronger in terms of androgenic response but I have tried both and they are pretty close. Androsterone seems to have more pronounced mood lifting effects than DHT it does have at least one advantage. DHT seems to be stronger in terms of generating muscle response but even that can be matched by androsterone if it is taken in doses twice as high as DHT.

Good post. When you say "DHT" are you talking about DHT such as Proviron or your own Keto DHT?

 

[haidut]

Weight-reducing diets for obese subjects are associated with an increased 11β-HSD1 and diminished 5-reductase activities (Svendsen et al., 2009)

Right, I saw that and the above part is troubling because weight loss diet was associated with even bigger increase in 11b-HSD1 and a decrease in 5-AR. At least when there was obesity the 5-AR was higher so some cortisol was getting diverted via the 5-AR pathway.

 

[haidut]

Good post. When you say "DHT" are you talking about DHT such as Proviron or your own Keto DHT?

I meant biodidentical DHT like Andractim. The methylated DHT derivatives are dangerous IMO, and I would not use them unless it is a dire situation.

 

[milk_lover]

@haidut do you thinking combining andro with pregnenolone topically near the pelvic area too much kill for the libido? I am talking about low doses like one drop of Andro and one drop of Stressnone..

 

[sladerunner69]

Has anyone noticed a fragrance with women made with some androsterone?
I have smelt it on two different women, it makes sense since a lot of them should enjoy it.

ehmmm.... nope?

 

[Andman]

Androsterone (in SFA) is probably my rats fav. idealabs substance. As with 5a-dhp and Pansterone the dosages are kept low, like 2-4 drops at most.
Great benefit on overall mood, and doesnt seem to lose effects if used too often like for example 5a-dhp which i need to take breaks from.