RockyP
Member
30 mg daily?
MESO-Rx
Anabolic Steroids
Had a Heart Attack today at age ~30. Be safe guys.
- Thread starter ChemBB
- Start date
RockyP
Member
This is interesting. Certainly there are some differences between humans and rats but I always wondered why i tolerated tren so well, perhaps it was because I ran it with low / HRT levels of test. Anecdotally, it seems many folks get worse "nandrolone" sides when used with higher dosages of test. Many guys report running deca / nandrolone only cycles were side effect-free.Believe it or not, medical literature demonstrates Tren is less harmful in terms of cardiac health than Test, mg-for-mg.
See my post here:
Research Evidence:
17β-Hydroxyestra-4,9,11-trien-3-one (trenbolone) exhibits tissue selective anabolic activity: effects on muscle, bone, adiposity, hemoglobin, and prostate
Improvements in body composition, cardiometabolic risk factors and insulin sensitivity with trenbolone in normogonadic rats
- Trenbolone decreased fat mass by 37% and increased lean mass by 11%
- No evidence of adverse cardiac (e.g., no fibrosis or impaired ischemia tolerance) or hepatic effects
Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome
- Reduced subcutaneous and visceral fat accumulation, hypertriglyceridemia, hypercholesterolemia, hyperinsulinemia, and myocardial damage compared to untreated deficient rats
- Improved myocardial tolerance to ischemia-reperfusion injury, suggesting cardioprotective effects
- Metabolic benefits included better insulin sensitivity and lipid profiles
When I finish my current test / primo regimen I plan to drop back to HRT test for 8 weeks and then add some tren 10 - 20 mg daily
Banana Joe
Member
My bad, I meant to write weekly.
I actually do that and feel it is working great for me. My lipids are still bad, but actually not any worse than they were before.
RockyP
Member
What effects are you getting form 30 mg weekly? Fat loss? Anti-catabolism?
Type-IIx
Member
Tren's waaay worse per-mg than testosterone for cardiovascular-thrombotic risk bro! Effects on electrolytes, MR antagonism, it's actually real ugly in that regard.Believe it or not, medical literature demonstrates Tren is less harmful in terms of cardiac health than Test, mg-for-mg.
See my post here:
Research Evidence:
17β-Hydroxyestra-4,9,11-trien-3-one (trenbolone) exhibits tissue selective anabolic activity: effects on muscle, bone, adiposity, hemoglobin, and prostate
Improvements in body composition, cardiometabolic risk factors and insulin sensitivity with trenbolone in normogonadic rats
- Trenbolone decreased fat mass by 37% and increased lean mass by 11%
- No evidence of adverse cardiac (e.g., no fibrosis or impaired ischemia tolerance) or hepatic effects
Trenbolone Improves Cardiometabolic Risk Factors and Myocardial Tolerance to Ischemia-Reperfusion in Male Rats With Testosterone-Deficient Metabolic Syndrome
- Reduced subcutaneous and visceral fat accumulation, hypertriglyceridemia, hypercholesterolemia, hyperinsulinemia, and myocardial damage compared to untreated deficient rats
- Improved myocardial tolerance to ischemia-reperfusion injury, suggesting cardioprotective effects
- Metabolic benefits included better insulin sensitivity and lipid profiles
Where trenbolone can be argued to be relatively beneficial is metabolic health, insulin sensitivity, decreasing insulin /and/ glucose for example, as shown in this study
Recover soon!
RockyP
Member
Can you estimate how much worse mg per mg? I ask because I get plenty of benefit from 70 mg tren weekly, and if it is not 5x worse than test in that regard it would actually be worth it (for me) to run it since I usually run my test at / just above HRT levels (225 ish).
Type-IIx
Member
Gentleman's threefold, at least? The way I talk about tren synergistically benefiting muscle gain; recomp, strength/power… in many ways tren is greater than additive in its mechanisms of cardiovascular disease risk
RockyP
Member
guess it's true what they say - there's no safe dosage of tren
Type-IIx
Member
Everyone should be doing an annual echocardiogram and abdominal ultrasound, anyway. I've seen some nightmare fuel threads, one that stands out was a guy who survived a widow maker, only detected by a stress test, and he came back after years of rehab to say he had believed his low dose, long term (continuous, years) trenbolone was beneficial. It always deterred me.
RockyP
Member
Area under the curve can be a tricky concept for some…more and more competitors / retired pros are coming out warning recreational ped users to skip the tren.
Type-IIx
Member
I think assuming that "the dose makes the poison" is a major blind spot in bodybuilding because it's not true, there are drug effects and time effects too. Drug effect: tren's decreasing IGF-1, any dose. Time effect: GH doesn't affect bone/spine density for the first 6 months of use, then it kicks, bi-phasic/modal.
IndividualMan
Member
how is spine density different from bone density? ain't it just the density of the bones that make up your spine or am I misunderstanding something?
Wizbang
Member
Do not trust this.
Ghoul
Member
Correct. Plaque buildup doesn't move inwards, like buildup clogging a pipe in your house plumbing It infiltrates the arterial wall, growing *outwards*, and undetectable (in people under 45 especially since it hasn't calcified so 0 CAC score) for a long time. This keeps the "lumen" open so flow isn't blocked. Eventually it crosses a threshold where continuing plaque buildup starts to block the artery fairly quickly.
The biggest problem with this undetectable soft plaque, even in an artery that's 99% open, is that a piece can break off at any time causing a sudden blockage. This is where inflammation becomes a major factor, since, like a "pimple" forming under the plaque, it can push a chunk off.
Like they say about a business going broke. It happens very slowly over a long period of time and then all at once.
Photon
Member
Soft plaque can be detected via cleerly CCTA.
RockyP
Member
Is there any validity to the claims that the anti inflammatory effects of compounds like Lovaza and Vascepa (and statins) can help stabilize these plaques?
Wizbang
Member
I am trying to get my doc to get me one.
Wizbang
Member
After 18 months of treatment, the EVAPORATE trial showed a significant decrease in total noncalcified plaque and total plaque volume with icosapent ethyl, compared to an increase in the placebo group. (I believe this was in conjunction with a statin)
RockyP
Member
Can be tough if you’re mostly healthy. I had one a few years ago due to “symptomatic chest pain on exertion” though it turned not to be panic / anxiety. I was still glad to get it as a baseline. Will be getting more in the future.
Wizbang
Member
@RockyP
Reduction of remnant lipoproteins
In addition to triglyceride values, great attention has recently been paid to remnant lipoproteins (RLP-C), recognized as highly atherogenic. In fact, these particles contain up to four times the concentration of cholesterol compared to LDL, thus potentially resulting much more atherogenic. Indeed, in the ANCHOR and MARINE studies, IPE therapy was shown to result in a reduction in RLP-C of up to 30% compared to placebo (by—25.8%, P = 0.0001 and—29.8%, P = 0.004, respectively), being able to partially explain the beneficial effects of this therapy that go beyond the reduction of triglyceride values.
Stabilizing effect on atheromatous plaque
The EVAPORATE study provides important mechanistic information regarding the therapeutic effect that IPE exerts on the characteristics of vulnerable atheromatous plaques, from growth reduction to the induction of true plaque regression. In particular, it was also observed that the total volumetric progression rates of fibroadipose component plaques were −34% in the IPE group compared to a progression of 32% in the placebo group (P = 0.0002). Furthermore, this reduction in plaque volume progression was not accompanied by a significant reduction in LDL cholesterol and triglycerides from baseline10. It is interesting to note how, compared to the data existing in the literature regarding the effects of statins on the volume of coronary plaques, the data emerging from the EVAPORATE study are surprising, since the effect of IPE would appear to be more effective than an intensive therapy with statins on the stabilization and regression of atheromatous plaque.11,12
Reduction of remnant lipoproteins
In addition to triglyceride values, great attention has recently been paid to remnant lipoproteins (RLP-C), recognized as highly atherogenic. In fact, these particles contain up to four times the concentration of cholesterol compared to LDL, thus potentially resulting much more atherogenic. Indeed, in the ANCHOR and MARINE studies, IPE therapy was shown to result in a reduction in RLP-C of up to 30% compared to placebo (by—25.8%, P = 0.0001 and—29.8%, P = 0.004, respectively), being able to partially explain the beneficial effects of this therapy that go beyond the reduction of triglyceride values.
Stabilizing effect on atheromatous plaque
The EVAPORATE study provides important mechanistic information regarding the therapeutic effect that IPE exerts on the characteristics of vulnerable atheromatous plaques, from growth reduction to the induction of true plaque regression. In particular, it was also observed that the total volumetric progression rates of fibroadipose component plaques were −34% in the IPE group compared to a progression of 32% in the placebo group (P = 0.0002). Furthermore, this reduction in plaque volume progression was not accompanied by a significant reduction in LDL cholesterol and triglycerides from baseline10. It is interesting to note how, compared to the data existing in the literature regarding the effects of statins on the volume of coronary plaques, the data emerging from the EVAPORATE study are surprising, since the effect of IPE would appear to be more effective than an intensive therapy with statins on the stabilization and regression of atheromatous plaque.11,12
