T Nation

Testosterone + Nandrolone + Drostanolone is a Good Lean-Bulk Stack


#61

I know someone who’s running 500 mg continually, so I’d agree with @chemania that it’s typical in some circles.

I’m not sure that I’d want to risk it.


#62

Are you referring to not being able to sleep (legitimately) or you’re scratching you’re head as to why oxymetholone has supposed estrogenic activity. I personally believe oxymetholone is more androgenic than its rating implies due to the fact that it is partially metabolized to mestanolone when Ingested (remove the C2 hydromethylene group and it’s mestanolone). Very little is known about the pharmokinetics of oxymetholone (more research should be conducted actually, since it still is used as adjunct therapy for aplastic anaemia, fanconis anaemia and severe HIV related wasting)… Hell even the HL is unknown STILL! For a drug that’s been around since 59 that’s pathetic…

You’re PR antagonist theory makes sense, as the 11 HSD inhibition would cause water/sodium retention and the PR antagonism could cause gyno, thus the “estrogenicity” of the drug would actually be estrogen related at all… However due to the androgenic and non aromatisable nature of the drug I find it hard to believe such EXTREME water retention could occur in the absence of ER binding, there hasn’t been any research on the compounds “estrogenic” activity

Oxymetholone itself actually has a relatively low binding affinity to SHBG ( https://academic.oup.com/endo/article-abstract/114/6/2100/2538442?redirectedFrom=fulltext ) however mestanolone has a very high binding affinity to SHBG, mestanolone doesn’t tend to cause gyno or estrogenic effects, unless one was taking a massive dose of test/ aromatising AAS, a shbg decrease shouldn’t spell a significant increase in estrogenic sides (say 100mg test/wk + 25-50mg oxymetholone/day) I don’t think there’d be much of a noticeable increase in direct shbg mediated estrogenicity, 500mg+ test + oxymethomone and I’d agree there could be a difference.

If the issue is increased estrogen itself causing the sides, an AI would help (although I dislike AI’s), if it’s ER antagonism you’d need a serm, an AI will lower estrogen, but estrogenic activity related to ER binding would require a serm (which I believe have their own set of risks), however why jump the gun, first make sure you get estro sides before adding more drugs.

Need more sleep lol, I get 10-12hrs a day, sometimes more (there’s something wrong with me as to why I sleep so much, it’s been an issue for years, potentially chronic fatigue or something, not a big deal tho). Why are you getting up at 4am… Holy shit that’s so early, it’s still DARK out!!!

My E2 is less than half what yours is, however I’m just on trt + dhea, and soon 1-dhea as an experiment (gonna trrraaaassh my lipids)

https://www.physiology.org/doi/full/10.1152/japplphysiol.00616.2013

Gonna take a third of the dose in this study to see what it does to my HR and BP. I’m aware my health isn’t great but I don’t think I’ve got that long anyway, a LOT of my issues are anxiety related, I get these massive spikes in adrenaline sometimes for no God damn reason, esp when I socialise, I probs need to be medicated for the anxiety… it’s pretty bad.


#63

Let’s ask the super expert resident endocrinologist bodybuilding competitor Dr Mr Sir

@physioLojik why does oxymetholone (anadrol) have estrogenic side effects?


#64

What was the name/brand of those spring rolls


#65

I’m going to sleep now, I’ll check tommorow (still got some of em) will update tommorow morning.


#66

Liver support during oral AAS - the most reliable solutions.

Mechanism of liver damage induced by xenobiotics - a fast overview:


“Detoxification of drugs and xenobiotics in the liver by drug metabolizing enzymes (DMEs) is an important phenomenon in the acquisition of homeostasis. Alteration in homeostatic status leads to a shift in the dynamic equilibrium of metabolism toward the ROS generation thereby oxidative stress leading to organ malfunction.”.

“Phase I and phase II enzymes play a crucial role in the metabolism and detoxification of various drugs and xenobiotics. For the acquisition of dynamic homeostasis, highly tuned metabolic control of drugs or xenobiotics by xenobiotic metabolizing enzymes is needed. Any imbalance in the activity of these enzymes ultimately leads to the shifting of equilibrium toward free radical generation that could finally bind to macromolecules such as DNA to cause mutation, lipid to cause membrane damage, or proteins to alter their activities”.

“The hepatotoxic reactions caused by drugs may be summarized as acute reactions (which consist of hepatocellular necrosis), cholestasis (with or without inflammation), and miscellaneous reactions; however, some drugs can cause chronic damage and may even lead to tumor growth”.

“There are several studies that suggest the generation of reactive metabolites and free radicals from hepatotoxic drugs. (…) Membrane lipid peroxidation is directly related to the depletion of tissue GSH (an intracellular antioxidant) leading to the altered functional integrity of these structures and if the damage is sever, it could be fatal. (…) Membrane lipid peroxidation may lead to alteration in membrane fluidity and permeability, enhanced rates of protein degradation, and ultimately cell death. (…) The concentration of intracellular GSH, therefore, is the key determinant of membrane integrity and the extent of toxicant-induced hepatic cell injury.”.

“CYP-mediated reduction of halogenated hydrocarbons, for example, carbon tetrachloride or halothane, can likewise create free radical intermediates, which can straightforwardly harm cell layers through lipid peroxidation, or can target nucleophilic DNA deposits”

“Glutathione- S -transferases (GST), a crucial Phase II enzyme, initiates the detoxification process by catalyzing the conjugation of –SH moiety of glutathione to xenobiotics, thereby neutralizing the electrophilic sites and rendering the products more water-soluble.”

“In addition to the dynamic equilibrium of Phase I and Phase II enzymes, reduced GSH, glutathione peroxidase (GPx) and catalase (CAT) are also critical in acquisition of normal cellular physiology as these are involved in the elimination of lipid peroxides and toxic oxygen radicals formed during the cellular metabolism”

Conclusion: to limit toxic influence of oral SAA on hepatic cell, membrane integrity, DNA & proteins structure must be upheld with the help of antioxidant power and by mechanisms allowing membrane to recuperate faster/limit disintegration (obviously, elevated liver markers results from spilling of the cell).

SILYMARIN (mixture)


“Its hepatoprotective activity is unique and acts in different ways, including antioxidant and anti-inflammatory activities, cell permeability regulator and membrane stabilizer, stimulation of liver regeneration and inhibition of deposition in collagen fibers, which may lead to cirrhosis”


decreased lipotoxicity


“Silibinin administration decreased serum alanine aminotransferase and improved liver steatosis, hepatocyte ballooning, and lobular inflammation in db/db mice fed an MCD diet” (~250 mg HED injection)


“In alcoholic liver disease, comparing with placebo, aspartate aminotransferase was reduced in the silymarin-treated groups (p = 0.01) while alkaline phosphatase was not” (400-600 mg, oral administration)


“exacerbated the promotional effects of ethanol in HCC bearing mice, but only in males”


“The results showed that SIL reduced the AST and ALT levels more significantly than the control group” (200-1200 mg/d, was not dose-dependent)

“Based on our clinical experience and the results in this meta-analysis, the regimen in Han et al (silymarin 70 mg/tid 12 weeks + simvastatin) and Masoodi et al (silymarin 140 mg/bid 12 weeks) were strongly recommended because of their robust therapeutic effect and less side effect events.”


“In a systematic review and meta-analysis including five randomized controlled trials and 270 patients, routine silymarin administration determines a significant reduction in fasting blood glucose levels and has no effect on lipid profil” (200-600 mg/d)


~1% of BV (there are some innovative solutions to enhance this, not in my country)

More about this later.


#67

Still waiting on the egg roll brand… I love Chinese food but can never seem to find a good frozen egg roll… IV been buying these “takhi” stick egg rolls but there not cutting it. Would love to try something new


#68

Asiana selection cocktail spring rolls. They come frozen and you can pan fry or oven bake them. They’re unhealthy tho


#69

Thanks! Did some research don’t think they sell them by me so I ordered some. I eat healthy 85% of the time the other 15% I eat egg rolls and cheesecake


#70

So with the 1% oral bioavailability do you bother taking this supplement (you mention there isn’t a way to enhance the BV in you’re country), I mean… you could take a loooooooooooooooooooooooooooooooooooooooooot, kinda like oral test undecanoate, super low oral bioavailability due to the lack of C-17 methylation (Oral Test U is absorbed via lympatic system)


#71

At first I wanted to describe each compound I use directed to liver health, but then I’ve realized it’d take too much time which I have less and less… All antioxidants with confirmed hepato-protective properties will fit here, as well as GSH substrates. Vitamins E & C, selenium, choline, cysteine, sylimarol, cynarine, PC with Pgp inhibitors (coumarines, black pepper) to enhance sylimarol and cynarine BV would help for sure. Diet is no less important (should be rich in flavonoids, carotenes).

It’s 3rd day of oxymetholone @ 75 mg. Massive bloat as people describe (I’ve gained 2 kg after just 3 days!), immediately increase in strenght (+3 kg in bench press per set). Feeling great, administering oxy with food so no GI tract disturbances (maybe a little). Despite water retention, BP & HR are in check (120/80, 70 BPM). No change in libido or perception in any way. What’s interesting, I need more sleep (from 6 h to 8 h for sure). I don’t feel “unwell” or something, like people say. We’ll see what happens next. The last thing I want is to cumulate body fat, It’d be just 4 weeks on this wet compound then switching to trenbolone for another 3-4 weeks if health allows.


#72

May I ask why you’re using this much gear (just curious). Oxymetholone doesn’t have the greatest track record for safety, while it’s hepatotoxic nature is vastly overstated. It’s use has many reported case of adverse effects (granted mostly in sick people and high doses for prolonged periods of time). Do you intend to get an EKG or ECG post cycle to check cardiac function? I’d use mestanolone though (If I had a clean bill of health, which I most certainly don’t). I’d choose metandienone any day over oxymetholone… However what I really want to use one day (if my health ever goes back to normal) is methyltestosterone, however there’s no way to get it domestically in Australia, probably due to low demand (hepatotoxicity, highly estrogenic yet moderately anabolic, fairly low oral bioavailability (around 50 percent orally)) make it impractical for bulking up, and this isn’t why I’d use methyltestosterone, I’d take it at the higher end of the prescription spectrum (so 40/day, equiv to about 20mg of testosterone being absorbed thus being equiv to around 200mgs of test/wk). I’m curious to see the effect it would have on my lipids, blood pressure, liver function and sense of well-being compared to regular testosterone, plus it’d give me a break from the primoteston that I have bad reactions to, I’ve already got a fair bit of scar tissue. it’d be more like an experiment in which i’d be using myself as a guini pig. Currently can’t do that though, just got some bloods done to determine if there’s any endocrine reason for my heart problems (recent bloods hinted at me becoming anaemic), I’ve been having PVC’s over the past few days, fairly frequently, they suck. Potentially I’m very sensitive to beta adrenergic receptor upregulation, that being said I also appear to have serious orthostatic intolerance (think POTS). might be prescribed beta blockers in the near future :/. I highy, highly doubt my very low doses of AAS for short periods of time have caused cardiomyopathy or some other cardiac manifestation, I think it’s coincidence and bad luck.