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What causes AAS water retention?

FranJ

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Hi guys,

I was wondering if anyone knows the mechanism that make us to retain water while on AAS... We know estrogen interacts with aldosterone and renin-angiotensin system... but what about testosterone itself, and the less androgenic AAS (such as anavar, win, etc) ?

I have experienced that if I'm using aas, even non aromatizing AAS, I do retain loads of water if diet isn't in check. I guess all AAS make you hold subq water to some degree, I wonder how... if it's aldosterone, ADH...
 
Last edited:
Good topic. I retain water on just about anything -- even tren. What's worse is that I have real hard time telling the difference between water retention and body fat. This is not a big deal at the beginning of cut, but can cause serious miscalculations on diet and cardio toward the end.
 
This is quoted from patrick arnold blog:

People familiar with the use of anabolic steroids know that water retention and hypertension (high blood pressure) are potential side effects. This is due to the fact that all androgenic hormones have the capacity to cause some sodium retention (and hence water retention) through direct action via androgen receptors in the kidneys.

Furthermore, anabolic steroids that are estrogenic or can convert to estrogens can cause even more sodium retention via additional interaction with renal (kidney) estrogen receptors. So it’s often thought that an anabolic steroids propensity for water retention is related to its potency both as an androgen and as an estrogen (manifested via aromatization to estrogenic metabolites).

Confusion has often arisen however when people have noticed that some steroids – which traditional thinking tells us should not result in extraordinary water retention – end up doing just that. steroids that should not aromatize to estrogens such as oxymetholone (anadrol) and methyl-1-testosterone are known to result in extreme water retention in some individuals. A recent paper* suggests a heretofore unmentioned explanation for this.

There is an enzyme that is localized primarily in the kidneys whose function is to protect the kidneys from circulating cortisol. The kidneys have receptors called mineralcorticoid receptors (MR’s) which are meant to bind to specific adrenal hormones (called mineralcorticoids) in the body such as aldosterone. The result of this binding is a signal to increase sodium and water retention in the body, while stimulating the excretion of potassium. This is an important mechanism to maintain fluid and electrolyte balance in the body.

A problem exists though in that cortisol can also bind activate these receptors. Cortisol is a widely circulating hormone and serves a multitude of functions throughout the body. However its intended biological functions do not include mineralcorticoid action in the kidneys, so to prevent this from happening the kidneys are rich in the enzyme 11b-hydroxysteroid dehydrogenase 2 (11b-HSD2). This enzyme deactivates cortisol by converting it into cortisone before it can bind to the renal MRs.

Certain substances can block 11b-HSD2, and that can lead to problems. One example is a constituent of black licorice known as glycyrrhetinic acid. This enzyme inhibition potential is precisely why people that consume a lot of black licorice are known to retain water and experience high blood pressure and electrolyte disturbances. Interestingly, legend has it that Genghis Khan had his armies ingest licorice while on the march to prevent thirst and dehydration. Of course Genghis Khan had no idea that 11b-HSD2 inhibition was responsible for these effects, and today many have been similarly unaware that this property might be responsible for some of the salt/water effects of anabolic steroids.
 
This is quoted from patrick arnold blog:

People familiar with the use of anabolic steroids know that water retention and hypertension (high blood pressure) are potential side effects. This is due to the fact that all androgenic hormones have the capacity to cause some sodium retention (and hence water retention) through direct action via androgen receptors in the kidneys.

Furthermore, anabolic steroids that are estrogenic or can convert to estrogens can cause even more sodium retention via additional interaction with renal (kidney) estrogen receptors. So it’s often thought that an anabolic steroids propensity for water retention is related to its potency both as an androgen and as an estrogen (manifested via aromatization to estrogenic metabolites).

Confusion has often arisen however when people have noticed that some steroids – which traditional thinking tells us should not result in extraordinary water retention – end up doing just that. steroids that should not aromatize to estrogens such as oxymetholone (anadrol) and methyl-1-testosterone are known to result in extreme water retention in some individuals. A recent paper* suggests a heretofore unmentioned explanation for this.

There is an enzyme that is localized primarily in the kidneys whose function is to protect the kidneys from circulating cortisol. The kidneys have receptors called mineralcorticoid receptors (MR’s) which are meant to bind to specific adrenal hormones (called mineralcorticoids) in the body such as aldosterone. The result of this binding is a signal to increase sodium and water retention in the body, while stimulating the excretion of potassium. This is an important mechanism to maintain fluid and electrolyte balance in the body.

A problem exists though in that cortisol can also bind activate these receptors. Cortisol is a widely circulating hormone and serves a multitude of functions throughout the body. However its intended biological functions do not include mineralcorticoid action in the kidneys, so to prevent this from happening the kidneys are rich in the enzyme 11b-hydroxysteroid dehydrogenase 2 (11b-HSD2). This enzyme deactivates cortisol by converting it into cortisone before it can bind to the renal MRs.

Certain substances can block 11b-HSD2, and that can lead to problems. One example is a constituent of black licorice known as glycyrrhetinic acid. This enzyme inhibition potential is precisely why people that consume a lot of black licorice are known to retain water and experience high blood pressure and electrolyte disturbances. Interestingly, legend has it that Genghis Khan had his armies ingest licorice while on the march to prevent thirst and dehydration. Of course Genghis Khan had no idea that 11b-HSD2 inhibition was responsible for these effects, and today many have been similarly unaware that this property might be responsible for some of the salt/water effects of anabolic steroids.

Very interesting, so some aas can block 11b-HSD2 causing fluid retention...
 
I use all sciroxx products. Best domestic us source I've tried yet and best delivery and communication. I always run proviron during my aas cycles but am now using aromasin. Seems to be the best choice to keep you dry. My only question is do I continue running aromasin through my pct or do I stop after my cycle, run my pct than run aromasin after my pct for two weeks to avoid any estrogen rebound? Any takers
 
I hold a little water on everything. The worst high doses of testosterone, anadrol, dianabol. Puff city.
 
....



I have experienced that if I'm using aas, even non aromatizing AAS, I do retain loads of water if diet isn't in check. I guess all AAS make you hold subq water to some degree, I wonder how... if it's aldosterone, ADH...


....... Just how far removed from "isn't in check" are we talking?


Sent from my iPhone using Tapatalk
 
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...Once you start drinking more water, your body recognizes that it is getting a steady external supply, and it starts letting go of the water weight it’s been holding.

That water retention in your waist, face, and ankles is released because there is no longer a reason for your body to store it. I know this is true because I googled that sentence and it came up with a million hits of the very same sentence.

Just look at the fun you can have with water...
 

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