Dilemma running Orals

[Omegasox]

It’s been controversial if HDL really even matters. As long as your LDL is within range and it is only your HDL being affected I wouldn’t be too concerned.

 

[RamboStallone]

The 500 mgs of test was just an example.

I was just using a hypothetical range. Let's say you have a reading of 40 on testosterone, you take anavar, it drops down to 15, and recovers back up to 25-30; that's still on the lower end.

But I really doubt it's as concrete as that... Some people might not even dip that low, and recover perfectly fine on injectables.

I have the tendency to overthink this stuff; that too is genetic I believe

I'll have to try this out on myself to see how my own physiology reacts.

Is your appetite affected by oral use too? Out of all of those, which one had the least effect?

Yes, var and tbol have messed with my stomach/appetite for sure. Seemed fine on dbol and winny. Sdrol I took sparingly so never really used too much or too often to know brother.

 

[brutus69]

what about orals in injectable form?

 

[heavyhitter]

Yes, var and tbol have messed with my stomach/appetite for sure. Seemed fine on dbol and winny. Sdrol I took sparingly so never really used too much or too often to know brother.

Pretty much all orals fuck with my guts. Tbol not as much.Everything else is pretty much a no go. Injectable anadrol definitely treated me better than oral though. Still some stomach issues but it took longer to hit me and wasn't as severe

 

[nothuman]

It’s been controversial if HDL really even matters. As long as your LDL is within range and it is only your HDL being affected I wouldn’t be too concerned.

Facts. I might as well copy and paste this post I saved from Rex Feral, that articulates it well.

"You guys really focus too much on HDL. The research doesn't substantiate your focus.

The first thing that makes low HDL virtually useless as a predictor in an androgen using population is upregulated reverse cholesterol transport. If the job of HDL that we we are primarily concerned with is reverse cholesterol transport and androgens upregulate reverse cholesterol transport then how can you argue that a low HDL for an androgen using exercising bodybuilder should be judged on the same scale as a natural sedentary person?

Example - "By lowering high density lipoprotein (HDL) cholesterol, testosterone contributes to the gender difference in HDL cholesterol and has been accused to be pro-atherogenic. The mechanism by which testosterone influences HDL cholesterol is little understood. We therefore investigated the effect of testosterone on the gene expression of apolipoprotein A-I (apoA-I), hepatic lipase (HL), scavenger receptor B1 (SR-BI), and the ATP binding cassette transporter A1 (ABCA1), all of which are important regulators of HDL metabolism. Testosterone led to a dose-dependent up-regulation of SR-BI, which was assessed on both the mRNA and the protein levels. As a functional consequence, we observed an increased HDL(3)-induced cholesterol efflux from macrophages. At supraphysiological dosages, testosterone also increased the expression of HL in HepG2 cells. These data suggest that testosterone, despite lowering HDL cholesterol, intensifies reverse cholesterol transport and thereby exerts an anti-atherogenic rather than a pro-atherogenic effect."

This also tells us what we should be concerned with. It is not HDL but rather cholesterol efflux capacity.

Example - "It is unclear whether high-density lipoprotein (HDL) cholesterol concentration plays a causal role in atherosclerosis. A more important factor may be HDL cholesterol efflux capacity, the ability of HDL to accept cholesterol from macrophages, which is a key step in reverse cholesterol transport. We investigated the epidemiology of cholesterol efflux capacity and its association with incident atherosclerotic cardiovascular disease outcomes in a large, multiethnic population cohort. We measured HDL cholesterol level, HDL particle concentration, and cholesterol efflux capacity at baseline in 2924 adults free from cardiovascular disease who were participants in the Dallas Heart Study. In contrast to HDL cholesterol level, which was associated with multiple traditional risk factors and metabolic variables, cholesterol efflux capacity had minimal association with these factors. Baseline HDL cholesterol level was not associated with cardiovascular events in an adjusted analysis. In a fully adjusted model that included traditional risk factors, HDL cholesterol level, and HDL particle concentration, there was a 67% reduction in cardiovascular risk in the highest quartile of cholesterol efflux capacity versus the lowest quartile. Cholesterol efflux capacity, a new biomarker that characterizes a key step in reverse cholesterol transport, was inversely associated with the incidence of cardiovascular events in a population-based cohort."

That all but proves, on some 3000 people, that HDL does not matter and cholesterol efflux capacity does. These are normal people also not using androgens with upregulated efflux.

One more time for those who find this hard to accept given their constant obsession with their HDL while on androgens. "Cholesterol-efflux capacity, which is a marker of HDL function that measures reverse cholesterol transport, is inversely associated with incident atherosclerotic cardiovascular disease in a large population of patients healthy at baseline. The findings, say researchers, support 'retiring' the HDL cholesterol hypothesis—the idea of simply raising HDL cholesterol to reduce the risk of cardiovascular disease—and instead should shift the focus to measures of HDL functionality."

HDL is low because you don't need as much of it. It's a biofeedback mechanism and not a reliable indicator of anything in an androgen using population and more and more evidence mounts to prove this is true for the general population as well. I think most people don't know this about androgens."

 

[concreter]

I found, I gained just as much taking my Orals pre-workout only as I did two to three times a day, daily.
So just three to four days a week, but 100 mgs drol, 10 mgs dbol, 10mgs halo and 1 anavar.
This while consuming my 3 shakes which total around 200gms of protein and 200 gms of carbs in that 3 hr Window.

 

[johnjuanb1]

what about orals in injectable form?

Injectable adrol didn’t negatively affect my appetite.

 

[RamboStallone]

Pretty much all orals fuck with my guts. Tbol not as much.Everything else is pretty much a no go. Injectable anadrol definitely treated me better than oral though. Still some stomach issues but it took longer to hit me and wasn't as severe

Speaking of injects, nothing wrecks my stomach worse then tren lol. I rather do the orals.

 

[RamboStallone]

I found, I gained just as much taking my Orals pre-workout only as I did two to three times a day, daily.
So just three to four days a week, but 100 mgs drol, 10 mgs dbol, 10mgs halo and 1 anavar.
This while consuming my 3 shakes which total around 200gms of protein and 200 gms of carbs in that 3 hr Window.

Do you time them some hrs preworkout? Or just take them when you can before heading to the gym? I've been a fan of the preworkout dosing as well.

 

[concreter]

I'll take my liquid Adrol 1hr pre and the rest on my way in my 1st shake.
Covers the entire workout window plus...

 

[Knight9]

Facts. I might as well copy and paste this post I saved from Rex Feral, that articulates it well.

"You guys really focus too much on HDL. The research doesn't substantiate your focus.

The first thing that makes low HDL virtually useless as a predictor in an androgen using population is upregulated reverse cholesterol transport. If the job of HDL that we we are primarily concerned with is reverse cholesterol transport and androgens upregulate reverse cholesterol transport then how can you argue that a low HDL for an androgen using exercising bodybuilder should be judged on the same scale as a natural sedentary person?

Example - "By lowering high density lipoprotein (HDL) cholesterol, testosterone contributes to the gender difference in HDL cholesterol and has been accused to be pro-atherogenic. The mechanism by which testosterone influences HDL cholesterol is little understood. We therefore investigated the effect of testosterone on the gene expression of apolipoprotein A-I (apoA-I), hepatic lipase (HL), scavenger receptor B1 (SR-BI), and the ATP binding cassette transporter A1 (ABCA1), all of which are important regulators of HDL metabolism. Testosterone led to a dose-dependent up-regulation of SR-BI, which was assessed on both the mRNA and the protein levels. As a functional consequence, we observed an increased HDL(3)-induced cholesterol efflux from macrophages. At supraphysiological dosages, testosterone also increased the expression of HL in HepG2 cells. These data suggest that testosterone, despite lowering HDL cholesterol, intensifies reverse cholesterol transport and thereby exerts an anti-atherogenic rather than a pro-atherogenic effect."

This also tells us what we should be concerned with. It is not HDL but rather cholesterol efflux capacity.

Example - "It is unclear whether high-density lipoprotein (HDL) cholesterol concentration plays a causal role in atherosclerosis. A more important factor may be HDL cholesterol efflux capacity, the ability of HDL to accept cholesterol from macrophages, which is a key step in reverse cholesterol transport. We investigated the epidemiology of cholesterol efflux capacity and its association with incident atherosclerotic cardiovascular disease outcomes in a large, multiethnic population cohort. We measured HDL cholesterol level, HDL particle concentration, and cholesterol efflux capacity at baseline in 2924 adults free from cardiovascular disease who were participants in the Dallas Heart Study. In contrast to HDL cholesterol level, which was associated with multiple traditional risk factors and metabolic variables, cholesterol efflux capacity had minimal association with these factors. Baseline HDL cholesterol level was not associated with cardiovascular events in an adjusted analysis. In a fully adjusted model that included traditional risk factors, HDL cholesterol level, and HDL particle concentration, there was a 67% reduction in cardiovascular risk in the highest quartile of cholesterol efflux capacity versus the lowest quartile. Cholesterol efflux capacity, a new biomarker that characterizes a key step in reverse cholesterol transport, was inversely associated with the incidence of cardiovascular events in a population-based cohort."

That all but proves, on some 3000 people, that HDL does not matter and cholesterol efflux capacity does. These are normal people also not using androgens with upregulated efflux.

One more time for those who find this hard to accept given their constant obsession with their HDL while on androgens. "Cholesterol-efflux capacity, which is a marker of HDL function that measures reverse cholesterol transport, is inversely associated with incident atherosclerotic cardiovascular disease in a large population of patients healthy at baseline. The findings, say researchers, support 'retiring' the HDL cholesterol hypothesis—the idea of simply raising HDL cholesterol to reduce the risk of cardiovascular disease—and instead should shift the focus to measures of HDL functionality."

HDL is low because you don't need as much of it. It's a biofeedback mechanism and not a reliable indicator of anything in an androgen using population and more and more evidence mounts to prove this is true for the general population as well. I think most people don't know this about androgens."

So optimally, we might want to concentrate on LDL and particle count and size?

Great suggestion prior...I think I will choose to do an NMR with my bloodwork next blast.


BTW, I believe bieberhole recently told me he saw an 8-10% jump in HDL from using metformin. Have you or anyone else heard of or noticed this before?

 

[danieltx]

Dave Palumbo was always big on LDL and particle size but in the last few months he found a new study where they showed particle size doesn't really matter. Forget which show of his it was on but maybe someone can go digging for it.

 

[nothuman]

So optimally, we might want to concentrate on LDL and particle count and size?

Great suggestion prior...I think I will choose to do an NMR with my bloodwork next blast.


BTW, I believe bieberhole recently told me he saw an 8-10% jump in HDL from using metformin. Have you or anyone else heard of or noticed this before?

Usually whenever I get blood test results, my eyes go to LDL and triglycerides before HDL. I definitely would choose an optimal LDL over HDL if I could only choose one. Obviously, we want everything to be good though.

I've been taking Metformin straight for a few years at this point so it's pretty much the new normal to me. Hard to say how much it boosts my HDL but I believe it does raise it a little. Generally, Metformin should improve a lipid panel to some degree. Only thing on bloodwork it could decrease is Vitamin B12.

 

[Knight9]

Usually whenever I get blood test results, my eyes go to LDL and triglycerides before HDL. I definitely would choose an optimal LDL over HDL if I could only choose one. Obviously, we want everything to be good though.

I've been taking Metformin straight for a few years at this point so it's pretty much the new normal to me. Hard to say how much it boosts my HDL but I believe it does raise it a little. Generally, Metformin should improve a lipid panel to some degree. Only thing on bloodwork it could decrease is Vitamin B12.

I ALWAYS focus on LDL and Triglycerides first as well...and then I move onto HDL which is always around 40-43. The only cycle I've run in the last 6yrs dipped me to 32 with Test and EQ. My last 6 lipid panels over 24mos have looked like:

39hdl/86ldl
31/81
32/88
38/73
43/92
42/87

I have personally found that neither Krill(viva labs) or Jarrow Citrus Bergamot(2 daily) do much of anything one way or another for my lipids.

 

[BIG1512]

I found, I gained just as much taking my Orals pre-workout only as I did two to three times a day, daily.
So just three to four days a week, but 100 mgs drol, 10 mgs dbol, 10mgs halo and 1 anavar.
This while consuming my 3 shakes which total around 200gms of protein and 200 gms of carbs in that 3 hr Window.

are you taking all those together? I do something similar

Sent from my SM-G920V using Professional Muscle mobile app

 

[pickapeck]

IDK.. Go back to the 60s, 70s, 80s. Those guys use to eat a lot of orals. Sergio is rumored to eat 100 mg/d of dianabol. Hated injecting mostly. Died of kidney disease at 71. Franco was rumored to eat Anavar like M &Ms. Still alive, working out and blowing up water bottles. Pretty sure Zane ate Winstrol and T3 all day every day when it came to contest prep. All those guys in the old Gold's Gym pics use to eat dianabol all day for a decade or more. Most of them are still around. Not sure of their heart health but you know any overall impact would have be be multivariate.

 

[nothuman]

I ALWAYS focus on LDL and Triglycerides first as well...and then I move onto HDL which is always around 40-43. The only cycle I've run in the last 6yrs dipped me to 32 with Test and EQ. My last 6 lipid panels over 24mos have looked like:

39hdl/86ldl
31/81
32/88
38/73
43/92
42/87

I have personally found that neither Krill(viva labs) or Jarrow Citrus Bergamot(2 daily) do much of anything one way or another for my lipids.

Wow those are some great LDL numbers. Mine are usually closer to 100 so I guess that is genetic for me since my mother is similar and she's a health freak with a larger supplement collection than us. Even if CB and krill oil don't affect those numbers much, I still feel they are beneficial overall. Honestly, I haven't used anything that would really tank my HDL that much in a while so it's hard for me to say what works and what doesn't for lipids.

 

[nothuman]

IDK.. Go back to the 60s, 70s, 80s. Those guys use to eat a lot of orals. Sergio is rumored to eat 100 mg/d of dianabol. Hated injecting mostly. Died of kidney disease at 71. Franco was rumored to eat Anavar like M &Ms. Still alive, working out and blowing up water bottles. Pretty sure Zane ate Winstrol and T3 all day every day when it came to contest prep. All those guys in the old Gold's Gym pics use to eat dianabol all day for a decade or more. Most of them are still around. Not sure of their heart health but you know any overall impact would have be be multivariate.

I assume they mostly cycled off for a while. It's the always being on all the time that is most deadly.

 

[Hastur]

BTW, I believe bieberhole recently told me he saw an 8-10% jump in HDL from using metformin. Have you or anyone else heard of or noticed this before?

It's actually one of the main reasons why I started using Meformin. There's quite a bit of information out there regarding it, here are some numbers I've seen:

--Metformin is known to:
Reduce triglycerides (TG) by about 10%
Reduce low density lipoprotein cholesterol (LDL-C) by 10 to 15%
Increase high density lipoprotein cholesterol (HDL-C) up to 7%

--With citations for those numbers coming from:

DeFronzo RA. Pharmacologic therapy for type 2 diabetes mellitus. Ann Intern Med 1999;131(4):281-303.

Bristol-Myers Squibb Co. Glucophage (metformin hydrochloride) package insert. Princeton, NJ; August 2008. Link obtained on 11/24/2008.

DeFronzo RA, Goodman AM. Efficacy of metformin in patients with non-insulin-dependent diabetes mellitus. The Multicenter Metformin Study Group. N Engl J Med 1995;333:541-9.

Cusi K, Consoli A, DeFronzo RA. Metabolic effects of metformin on glucose and lactate metabolism in noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab 1996;81:4059-4067.

DeFronzo RA, Barzilai N, Simonson DC. Mechanism of metformin action in obese and lean noninsulin-dependent diabetics subjects. J Clin Endocrinol Metab 1991;73(6):1294-301.

Jeppesen J, Zhou MY et al. Effect of metformin on postprandial lipemia in patients with fairly to poorly controlled NIDDM. Diabetes Care 1994;17(10):1093-9.

 

[heavyhitter]

Speaking of injects, nothing wrecks my stomach worse then tren lol. I rather do the orals.

Oh my god me too! I cant even use it anymore. It makes me absolutely sick. My appetite gets crushed and after about 2 weeks I start having diarrhea and vomiting. E affects me way worse than A.