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(Study) Boldenone-mediated hepatorenal impairment in Rats (2021)

As @MasteroniPepperoni says, UDCA is a drug. TUDCA is taurine-conjugated UDCA and is the primary UDCA metabolite. TUDCA is not quite as efficacious, but is comparable. Specifically, both are satisfactory in the dissolution of gallstones, improving GGT values (but UDCA > TUDCA), and tolerability (but UDCA >> TUDCA).
Unrelated, but do you have an opinion on DHEA?

Have been taking 200mg orally for about six weeks now for bumping up some hormonal pathways (test, e2,...), the DHEA acting as a test and estrogen base somewhat (am using it since test results came back low repeatedly since PCT for last AAS cycle didn't bring up test values back to baseline again).

am thinking of hopping on Test again, I simply wanted to do a "natty" SARM cycle between hopping off on TEST again (maybe permanently now, depending on next round of hormonal blood panels later this year),

had in mind DHEA was relatively safe, however coming across a few studies I've been wary of using it too high now, don't know how much relevant this really is (had instances of kidney issues in the paast, nwo resolved I think):

The effect of dehydroepiandrosterone (DHEA) on renal function and metabolism in diabetic rats
 
Unrelated, but do you have an opinion on DHEA?

Have been taking 200mg orally for about six weeks now for bumping up some hormonal pathways (test, e2,...), the DHEA acting as a test and estrogen base somewhat (am using it since test results came back low repeatedly since PCT for last AAS cycle didn't bring up test values back to baseline again).

am thinking of hopping on Test again, I simply wanted to do a "natty" SARM cycle between hopping off on TEST again (maybe permanently now, depending on next round of hormonal blood panels later this year),

had in mind DHEA was relatively safe, however coming across a few studies I've been wary of using it too high now, don't know how much relevant this really is (had instances of kidney issues in the paast, nwo resolved I think):

The effect of dehydroepiandrosterone (DHEA) on renal function and metabolism in diabetic rats
DHEA (as DHEAS, DHEA sulfate) is itself a potent estrogen (without any AR activity) & in men, essentially just dose-dependently increases E2 & E1 (estrone; via 3β-HSD). That is a high dose.

It's fine to use to replace serum DHEA levels to normal if low (i.e., to 16.33 nmol/L; 4.71 ng/mL). It's performance-enhancing in women only.
 
DHEA (as DHEAS, DHEA sulfate) is itself a potent estrogen (without any AR activity) & in men, essentially just dose-dependently increases E2 & E1 (estrone; via 3β-HSD). That is a high dose.

It's fine to use to replace serum DHEA levels to normal if low (i.e., to 16.33 nmol/L; 4.71 ng/mL). It's performance-enhancing in women only.
yes it'a high dose but from my understanding it's poorly bioavailable orally as well
 
That first study (the relevant one) shows that UDCA is efficacious for (chemotherapy-induced) cholestasis with (complete) biliary obstruction in man.

There is some hypothetical risk that hasn't been borne out that it may disrupt biliary integrity.

Again, in my view it's a potent drug usually unnecessary, but seems most appropriate with Superdrol & methyltrienolone use.
Do you know if tudca/udca can have impact the effect of oral drugs such a SD? If so should it be dosed as far away from oral drug dosing or what do you suggest?
 
From an aromatizing like look okay to use boldenone up untill competition a few days before competition, while using arimidex last week , does arimidex lower boldenone s unique estrogen , is arimidex enough to rid body of all estrogens?

Was going to switch to Masteron two weeks out but realized today this is my last bottle and it may have half a ml or less. Have some primo but the same batch stung like test prop and it very well may be test prop. but will try it. Can't hurt with arimidex. Have SD and that'll be run five to six days a week last two weeks, been running it ten mgs for a week. Other than that smaller dose of good ole test enth.
 
Regarding and degree of hepatoxicity, our body has the ability to heal, providing the right foundation.
Raw greens... a few times a year I do raw juice cleansing, focusing on the dark greens. Usually 3-5days does it. The juices are very alkalizing, and the dark green raws will cause gentle squeezing and contracting of the liver and kidneys even starting in the mouth, with vagus nerve contact.
The raw greens are very healing, and can help even with daily physical housekeeping.
 
Do you know if tudca/udca can have impact the effect of oral drugs such a SD? If so should it be dosed as far away from oral drug dosing or what do you suggest?
There are no timing issues that apply to TUDCA/UDCA in combination with SD and it does not impact on the latter's potency. If anything it can potentiate it by increasing skeletal muscle insulin sensitivity.
 
From an aromatizing like look okay to use boldenone up untill competition a few days before competition, while using arimidex last week , does arimidex lower boldenone s unique estrogen , is arimidex enough to rid body of all estrogens?

Was going to switch to Masteron two weeks out but realized today this is my last bottle and it may have half a ml or less. Have some primo but the same batch stung like test prop and it very well may be test prop. but will try it. Can't hurt with arimidex. Have SD and that'll be run five to six days a week last two weeks, been running it ten mgs for a week. Other than that smaller dose of good ole test enth.
You should probably find a coach brother.

EQ doesn't really fit into contest prep, it's an off-season drug. It doesn't yield a unique estrogen, but E2 and E1. Adex reduces aromatase activity, the enzyme responsible for androgens being converted to E2 (a potent estrogen), so essentially yes: Adex will substantially reduce estrogenic activity.

You may still have other issues relating to all the other compounds I've seen you mention, progestins like allopregnanolone/progesterone, effective estrogens like DHEA, and God knows what else - not to mind nutrition/diet, etc.

Sounds like you do basically cut out injectables during peak weak: that's good. SD wouldn't be something I'd use for peaking but it can rationally be used to keep you full (might make sense if you're very dry & grainy approaching flat - but I suspect you're not).
 
You should probably find a coach brother.

EQ doesn't really fit into contest prep, it's an off-season drug. It doesn't yield a unique estrogen, but E2 and E1. Adex reduces aromatase activity, the enzyme responsible for androgens being converted to E2 (a potent estrogen), so essentially yes: Adex will substantially reduce estrogenic activity.

You may still have other issues relating to all the other compounds I've seen you mention, progestins like allopregnanolone/progesterone, effective estrogens like DHEA, and God knows what else - not to mind nutrition/diet, etc.

Sounds like you do basically cut out injectables during peak weak: that's good. SD wouldn't be something I'd use for peaking but it can rationally be used to keep you full (might make sense if you're very dry & grainy approaching flat - but I suspect you're not).
Since when does Eq not fit into a contest prep? The endurance benefit alone is a tremendous reason to keep it in. Have you ever prepped for a show WITH Eq?
 
You should probably find a coach brother.

EQ doesn't really fit into contest prep, it's an off-season drug. It doesn't yield a unique estrogen, but E2 and E1. Adex reduces aromatase activity, the enzyme responsible for androgens being converted to E2 (a potent estrogen), so essentially yes: Adex will substantially reduce estrogenic activity.

You may still have other issues relating to all the other compounds I've seen you mention, progestins like allopregnanolone/progesterone, effective estrogens like DHEA, and God knows what else - not to mind nutrition/diet, etc.

Sounds like you do basically cut out injectables during peak weak: that's good. SD wouldn't be something I'd use for peaking but it can rationally be used to keep you full (might make sense if you're very dry & grainy approaching flat - but I suspect you're not).
Only EQ was used this prep very small amount test and Masteron, nothing else. SD toward end Thank you.
 
Since when does Eq not fit into a contest prep? The endurance benefit alone is a tremendous reason to keep it in. Have you ever prepped for a show WITH Eq?
Worry a little less about me and more about yourself bro.

Now if you had said that your rationale for maintaining a low dose of EQ through prep was to supplant Test's role (taking its place) in maintaining anti-catabolism, supporting a dry look and vascularity through prep (while reducing injection frequency), I'd say OK, great. Though I'd argue that it is a poor T replacement for sexual function and well-being.

But your rationale that EQ gives you an "endurance benefit" through prep is absurd. What are you, doing high frequency Zone 3 cardio/HIIT despite muscle and strength risks/loss? Besides, EQ doesn't in truth doesn't even support this particularly well (PROVE to me that it's a particularly potent hematinic agent).

So, was this basically a post intended to say that unless you've done it, despite its illogical ends, you can't fairly characterize it?
 
you understand endurance is a broad term and it is very useful in prep? Smart man, you understand muscular endurance right? What happens when you’re deep in prep (oh wait, that’s never happened I bet) and your energy falls off in the gym? Every aspect of prep or bodybuilding in general we supplement with tools that enhance the stage we’re in. Eq is one of those tools that can be utilized. Your broad term of Eq has no place is so far from the truth. You understand these drugs have been used for decades before your pubmed articles were able to be found on the internet right? Want to know why they were used? Because they work. Period.
 
Unrelated, but do you have an opinion on DHEA?

Have been taking 200mg orally for about six weeks now for bumping up some hormonal pathways (test, e2,...), the DHEA acting as a test and estrogen base somewhat (am using it since test results came back low repeatedly since PCT for last AAS cycle didn't bring up test values back to baseline again).

am thinking of hopping on Test again, I simply wanted to do a "natty" SARM cycle between hopping off on TEST again (maybe permanently now, depending on next round of hormonal blood panels later this year),

had in mind DHEA was relatively safe, however coming across a few studies I've been wary of using it too high now, don't know how much relevant this really is (had instances of kidney issues in the paast, nwo resolved I think):

The effect of dehydroepiandrosterone (DHEA) on renal function and metabolism in diabetic rats

Some of the "hrt" products using DHEA were transdermal, which resulted in conversion to different compounds. For example if you applied transdermal DHEA to your scrotum you would get very high conversion to DHT. Go figure. Just keep the form of administration in mind when you are looking at those studies.
 
Some of the "hrt" products using DHEA were transdermal, which resulted in conversion to different compounds. For example if you applied transdermal DHEA to your scrotum you would get very high conversion to DHT. Go figure. Just keep the form of administration in mind when you are looking at those studies.
You mean like the old Dermacrine transdermal?
 
You mean like the old Dermacrine transdermal?

Exactly. The conversion (and not just absorption) is why you can't really equate oral doses to transdermal or parenteral dosing.
 
There's nothing unique to boldenone that makes it particularly hepato- nor nephro- toxic, other than its being relatively less estrogenic than T (in vitro data suggests that podocyte cells [part of the glomerulus in the kidneys] express AR & ER; androgens promote apoptosis, whereas estrogens oppose) and, perhaps, the undecylenate ester (trivially in man, perhaps less so in rodent) increases resistance to hepatic breakdown.

On a continuum of toxicity in liver (described by the formula: potency to activate AR * resistance to hepatic breakdown) and kidneys, EQ lies closer to testosterone than trenbolone and rather far from the extreme end of the commercially available androgens, Superdrol and methyltren.

In both instances of liver & kidney toxicity, ascorbate (Vitamin C) acts as a free radical scavenger, decreasing ROS (and increasing NO). Ascorbate thereby ameliorates the ROS production that causes mitochondrial swelling and subsequent apoptosis.

This does not call for you, a human, to take megadoses of Vitamin C because EQ is kidney and liver toxic in rats.

I cannot say it enough: rats are not humans. While we can make some (mechanistic mostly) extrapolations from rodent data to man, talking about any sort of dose-response is folly. Rats are clearly more impacted by parenterally-administered androgens (injected AAS) than man at these doses with respect to hepatotoxicity/liver membrane and cell damage.

Moreover, megadoses of antioxidants blunt the adaptive response to resistance training, essentially blocking this primary stimulus for growth/hypertrophy outright. They likewise blunt many adaptations to endurance training, including endurance training enhancements to antioxidant capacity, mitochondrial biogenesis, cellular defence mechanisms and insulin sensitivity.

Guys that blast more than 16 weeks 1x yearly for a few (3+, arbitrarily) consecutive years should be getting annual liver & kidney ultrasounds in addition to echocardiograms, and doing regular (3-6 mo intervals) 24-hr creatinine clearance testing, C-reactive protein, in addition to the standard bloodwork parameters everyone does.
I wonder if the AR theory and protective effects of renal ER-activation on excessive AR renal activation-induced renal damage might be the main or only explanation to the deleterious observe effects of Boldenone (and other AAS to a lesser degree) on Kidney health and markers (at least in rats).
 
Has anyone here ever had kidney issues that blood work and urinalysis did not detect? Meaning your creatinine was good, urine was free of protein, yet you had a kidney issue?
so if you cannot prove you have kidney damage neither by means of a range of available blood and urine test panels, what can you do other than assume you have, or don't have kidney damage?

But that's not a solution, to "hope for the best" because the tests one has done come out ok (and were repeated over a period of time).

Maybe it's different for others, but now my personal stance on the state of my current kidney health at 30 years old is:

I have done lots of tests, what was available to me, blood and urine, repeated over a period of time as well, and all resulting indicators and values seem to be pointing out at my kidney health being fine.

So I could stop here; but since I assume and am personally positive I have done some good damage to my kidneys over the years, I persisted and have an appointment with a Nephrologist soon, goal is to know if there's a possibility of doing more advanced tests somewhere in my country, because I know from research there have been novel, more accurate, test markers for kidney health (blood/urine/ultrasound) developed over the last few years,

such tests are just not yet practically practiced often and everywhere (such as test for Urinary KIM-1, marker of tubular damage).
 
That first study (the relevant one) shows that UDCA is efficacious for (chemotherapy-induced) cholestasis with (complete) biliary obstruction in man.

There is some hypothetical risk that hasn't been borne out that it may disrupt biliary integrity.

Again, in my view it's a potent drug usually unnecessary, but seems most appropriate with Superdrol & methyltrienolone use.
Speaking of liver support, would you still recommend the "Essentiale Forte" PPC liver aid on cycle (or equivalent PPC supplement, polyenylphosphatidylcholine) along with the likes of TUDCA (500-750mg) and NAC (that I used to be taking at higher 2000mg+ doses anyway daily for a while for cognitive and mental issues)? Seems like there's a lot of biased science surrounding the Essentiale Forte product though.
 
I wonder if the AR theory and protective effects of renal ER-activation on excessive AR renal activation-induced renal damage might be the main or only explanation to the deleterious observe effects of Boldenone (and other AAS to a lesser degree) on Kidney health and markers (at least in rats).
I think so, yes. Essentially, it's due to AR activation ⇒ ⇑mitochondrial FA β-oxidation [⇑CPT1 mRNA, rate-limiting enzyme in mitochondrial FA oxidation].
Speaking of liver support, would you still recommend the "Essentiale Forte" PPC liver aid on cycle (or equivalent PPC supplement, polyenylphosphatidylcholine) along with the likes of TUDCA (500-750mg) and NAC (that I used to be taking at higher 2000mg+ doses anyway daily for a while for cognitive and mental issues)? Seems like there's a lot of biased science surrounding the Essentiale Forte product though.
Yes, I think that Essentiale Forte is a fine supplement. The data I've seen demonstrates that polyunsaturated phosphatidylcholine in combination with mitochondrial antioxidants (e.g., vitamins B1, B2, B6, etc.) is effective in preventing 17AA-induced hepatotoxicity.

I think that using TUDCA/UDCA (which serves to prevent absorption and saturation of cholesterol, a C-27 3β-hydroxy-Δ₅-steroid, parent to androgen, and may conceivable reduce 17AA anabolism) & NAC (which can reduce hypertrophic signaling) are overkill. I think that dose/duration and compound selection should be controlling, rather than throwing the kitchen sink of various hepatotoprotective agents at a largely nonexistent problem (most 17AAs in popular use are not particularly hepatotoxic at optimal doses and toxicity is rapidly reversible).
 
Really love your posts @Type-IIx

Kinda goes for everyone but not sure why we cannot talk like adults. Hey what do you think of this or that? Instead of getting hyper defensive and downright rude online. I get it, your all proper gangsters. But maybe we all just chill the fuck out?
 

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