Pita / Zetia / Vascepa vs test / tren / mast / var (bloodwork)

RockyP

Member
Will get straight to it. As promised the battle royale between the lipid destroying DHT’s and Tren and pita / Zetia.

Sustanon 150 eod
Mast P 140 eod
Tren ace 60 eod
Anavar 40-50 daily (for last 10 days prior to labs)

Cardiac regimen
Pita 4 mg
Zetia 10 mg
Vascepa 4 g
Nattokinase 4000 FU
Reta 5 mg (not cardiac but plays a role in metabolism)

LDL 33
Hgb 16
HCT 48
triglycerides 57
HDL 11 (thanks anavar)
Lp(a) < 9
ApoB 53
Sensitive E2 was 43 with no AI

All other parameters normal including CRP, GGT, AST, ALT, and cystatin C.

Other support Supps are the usual berberine, astragalus, ALA, K2 D3, ubiquinol CoQ10, and I’m prob forgetting some.

Will be running these labs again off of the tren and anavar. Want to see where the HDL sits on just test / mast. But with an LDL of 33, it’s not such an issue. Today is the last day of anavar and I’ve got maybe 3 days left on tren.

Thank you to @Ghoul for sharing all the cardiac information.

Also, all of those cardiac parameters IMPROVED (not the HDL, that was 23 on test / primo) since the last draw WHILE adding Tren, mast, and var.
 
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Will get straight to it. As promised the battle royale between the lipid destroying DHT’s and Tren and pita / Zetia.

Sustanon 150 eod
Mast P 140 eod
Tren ace 60 eod
Anavar 40-50 daily (for last 10 days prior to labs)

Cardiac regimen
Pita 4 mg
Zetia 10 mg
Vascepa 4 g
Nattokinase 4000 FU
Reta 5 mg (not cardiac but plays a role in metabolism)

LDL 33
Hgb 16
HCT 48
triglycerides 57
HDL 11 (thanks anavar)
Lp(a) < 9
ApoB 53
Sensitive E2 was 43 with no AI

All other parameters normal including CRP, GGT, AST, ALT, and cystatin C.

Other support Supps are the usual berberine, astragalus, ALA, K2 D3, ubiquinol CoQ10, and I’m prob forgetting some.

Will be running these labs again off of the tren and anavar. Want to see where the HDL sits on just test / mast. But with an LDL of 33, it’s not such an issue. Today is the last day of anavar and I’ve got maybe 3 days left on tren.

Thank you to @Ghoul for sharing all the cardiac information.

Also, all of those cardiac parameters IMPROVED (not the HDL, that was 23 on test / primo) since the last draw WHILE adding Tren, mast, and var.

So you’ve essentially turned off the flow of incoming plaque, the most important factor.

Obviously HDL-C is well below guideline “healthy” levels. So this would suggest that the main problem now is plaque regression that might otherwise be happening is impaired. After all, it’s HDL that “reverse transports” cholesterol out of the arteries for disposal by the liver.

But HDL-C doesn’t really tell us much when LDL-C is so low.

That’s because it’s a measurement of the cholesterol “load” within HDL, not how many HDL “dump trucks” you have or how well they’re functioning. You might just have a low amount of arterial plaque available to be reversed, so not much cholesterol for HDL to remove, resulting in a low HDL-C.

If you want to measure how well your plaque removal mechanism is functioning HDL-C isn’t the marker.

Checking HDL-P (particle count) will tell you how many HDL “trucks” are available to carry cholesterol out of your arteries, and APO-I will tell you whether they’re working well or broken down.

Not absolutely necessary, but you might be pleasantly surprised to find HDL-P is high and APO-I is adequate, and plaque is regressing, or not. More out of curiosity than anything else, always nice to know what’s going on.
 
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So you’ve essentially turned off the flow of incoming plaque, the most important factor.

Obviously HDL-C is well below guideline “healthy” levels. So this would suggest that the main problem now is plaque regression that might otherwise be happening is impaired. After all, it’s HDL that “reverse transports” cholesterol out of the arteries for disposal by the liver.

But HDL-C doesn’t really tell us much when LDL-C is so low.

That’s because it’s a measurement of the cholesterol “load” within HDL, not how many HDL “dump trucks” you have or how well they’re functioning. You might just have a low amount of arterial plaque available to be reversed, so not much cholesterol for HDL to remove, resulting in a low HDL-C.

If you’re you want to measure how well your plaque removal mechanism is functioning HDL-C isn’t the marker.

Checking HDL-P (particle count) will tell you how many HDL “trucks” are available to carry cholesterol out of your arteries, and APO-I will tell you whether they’re working well or broken down.

Not absolutely necessary, but you might be pleasantly surprised to find HDL-P is high and APO-I is adequate, and plaque is regressing, or not. Still, always nice to know what’s going on.
Thank you sir. I’ve always had low HDL even on TRT. I do want to see where I sit on test / mast and then just test cruise. But I’m very pleased with these LDL, ApoB, and Lp(a) numbers. And this is without nexletol. I still have it on deck if needed. This is about as harsh a cycle as I’ll ever run.
 
Thank you sir. I’ve always had low HDL even on TRT. I do want to see where I sit on test / mast and then just test cruise. But I’m very pleased with these LDL, ApoB, and Lp(a) numbers. And this is without nexletol. I still have it on deck if needed. This is about as harsh a cycle as I’ll ever run.

Despite driving “LDL lower regardless of how” is better, the one caveat with Bemp long term is that tendon risk. It’s very low, and only seen in older ages so far, but it’s definately there. With my LDL @ 24 it would only get me a few points lower so not worth even a tiny added risk for unmeasurable gain.

But if I wasn’t using a statin for whatever reason, or didn’t have Repatha in my stack, Bemp could lower LDL much more and tip the balance in its favor. I just have nothing to gain from it with current levels.
 
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Despite driving “LDL lower regardless of how” is better, the one caveat with Bemp long term is that tendon risk. It’s very low, and only seen in older ages so far, but it’s definately there. With LDL it would only get me a few points lower so not worth even a tiny added risk for unmeasurable gain.

But if I wasn’t using a statin for whatever reason, or didn’t have Repatha in my stack, Bemp could lower LDL much more and tip the balance in its favor. I just have nothing to gain from it with current levels.
That’s how I feel also, especially given these labs on a stack known to cause harsh dyslipidemia. I purposely tested labs on mast / tren / anavar to see how the pita and zetia would handle it and I’m impressed.
 
That’s how I feel also, especially given these labs on a stack known to cause harsh dyslipidemia. I purposely tested labs on mast / tren / anavar to see how the pita and zetia would handle it and I’m impressed.

For anyone reading this I want to be clear that I’m not advising against Bemp, it has a very good safety record with no sides ever developing for most people even after decades of use.

It’s just that once LDL is in the 30s, Bemp won’t bring it down very much (or at all). So I’d reserve it as the last add on if you’re >40 after using everything else that will be in your lipid stack.
 
Just wanted to add that my IGF-1 was 145 on 5 iu of GH. The GH is tested / real. Cactus hands and all. But this is what happens to IGF-1 levels when you diet hard in a big deficit for a long time. I had ben on 4 iu for a long time and i do notice much better sleep quality and improved recovery from the higher dosage. If it were more expensive I would prob run it at 3-4 on a cut but we lived in blessed times.
 
Just wanted to add that my IGF-1 was 145 on 5 iu of GH. The GH is tested / real. Cactus hands and all. But this is what happens to IGF-1 levels when you diet hard in a big deficit for a long time. I had ben on 4 iu for a long time and i do notice much better sleep quality and improved recovery from the higher dosage. If it were more expensive I would prob run it at 3-4 on a cut but we lived in blessed times.
How hard of a cut and for how long?

My IGF-1 was just measured at 141 on 2.5iu's - and was disappointing me. Don't know if I'm underdosed or a poor responder. But I also started cutting prior to the labs....
 
How hard of a cut and for how long?

My IGF-1 was just measured at 141 on 2.5iu's - and was disappointing me. Don't know if I'm underdosed or a poor responder. But I also started cutting prior to the labs....
About 700-1000 cals per day for the last 6 months. Also was on a 14 hour fast prior to labs being drawn.
 
For anyone reading this I want to be clear that I’m not advising against Bemp, it has a very good safety record with no sides ever developing for most people even after decades of use.

It’s just that once LDL is in the 30s, Bemp won’t bring it down very much (or at all). So I’d reserve it as the last add on if you’re >40 after using everything else that will be in your lipid stack.
I see my dr in January to get my repatha script. Would you still stay on a statin as well?
 
So what's the lipid stack now @Ghoul I only know of the pitavastatin and ezetembe combo? (With citrus bergamot thrown ontop)

That’s about all I recommend under normal circumstances. Its very potent, exceptionally effective against AAS induced high lipids, cheap (ish), easily accessible, no sides (overwhelmingly).

If you’re still >70, or aiming for regression and >40 add Bempadoic Acid.

For those with high lipids, absolutely can’t / won’t take a statin, or have years of untreated high cholesterol and want maximum possible regression + stabilization, or just willing to spend the cash for the very best cardiovascular protection, Repatha is an incredible 1 or 2x a month injection that’s ultra powerful. It has a very strong reputation for stopping future heart attacks and strokes.

It’s the only lipid med that reduces Lp(a), and it’s basically side effect free for the vast majority. It’s best combined with a statin if you can, to get the anti inflammatory effects only statins provide.

If you combine Pitavastatin 4, Ezetimibe, and Repatha, you’re using the most potent anti-cardiovascular disease combination science has available. 90%+ APO-b, LDL-C, 30% Lp(a), 60% HS-CRP (inflammation) reduction. Plaque will strongly regress over 18 months or so, whatever’s left will dry out and stabilize reducing risk even more over time.

I spoke to a cardiologist who told me if a patient has no symptoms, and they’re on this combo, he doesn’t even see a need for imaging, regardless of risk factors or 30 years of sky high cholesterol. “What difference would it make? This is the strongest risk reduction treatment a patient could be on, no matter how much plaque they have”. *

After a couple of years of this, even with a history of high cholesterol, if you also keep BP controlled, HS-CRP <1, and avoid diabetes, it’s plausible to have a 70%+ lower risk of heart attack, stroke, need a stent or bypass, vs a same age average peer.

*there is one other thing, anti-clot measures like asprin or other meds, that significantly adds to risk reduction, but this a complicated topic for a separate discussion
 
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I see my dr in January to get my repatha script. Would you still stay on a statin as well?

Absolutely.* The additional LDL reduction is useful, but the main benefit is the huge drop in systemic (especially within artery) inflammation.

After you’ve crushed ApoB/LDL and you’re no longer adding to plaque, the next biggest risk is a piece of soft plaque breaking off (which leaves a wound, and the clot that forms is the most common cause of heart attacks), Inflammation is the main driver of that risk. High inflammation causes “pimples” to form under the plaque destabilizing it. By lowering HS-CRP <1 you minimize that risk.

Over time, as you maintain very low ApoB/LDL, whatever soft plaque hasn’t been removed hardens, eventually turns into a sheet of calcium, and very unlikely to ever break off. It’s the fresh soft plaque that’s highly inflammatory and at risk of breaking off.

*often the lowest friction path to Repatha insurance coverage is pretending you can’t tolerate statins. Once you’re approved, you can always go back on a statin and you won’t lose Repatha coverage.
 
That’s about all I recommend under normal circumstances. Its very potent, exceptionally effective against AAS induced high lipids, cheap (ish), easily accessible, no sides (overwhelmingly).

If you’re still >70, or aiming for regression and >40 add Bempadoic Acid.

For those with high lipids, absolutely can’t / won’t take a statin, or have years of untreated high cholesterol and want maximum possible regression + stabilization, or just willing to spend the cash for the very best cardiovascular protection, Repatha is an incredible 1 or 2x a month injection that’s ultra powerful. It has a very strong reputation for stopping future heart attacks and strokes.

It’s the only lipid med that reduces Lp(a), and it’s basically side effect free for the vast majority. It’s best combined with a statin if you can, to get the anti inflammatory effects only statins provide.

If you combine Pitavastatin 4, Ezetimibe, and Repatha, you’re using the most potent anti-cardiovascular disease combination science has available. 90%+ APO-b, LDL-C, 30% Lp(a), 60% HS-CRP (inflammation) reduction. Plaque will strongly regress over 18 months or so, whatever’s left will dry out and stabilize reducing risk even more over time.

I spoke to a cardiologist who told me if a patient has no symptoms, and they’re on this combo, he doesn’t even see a need for imaging, regardless of risk factors or 30 years of sky high cholesterol. “What difference would it make? This is the strongest risk reduction treatment a patient could be on, no matter how much plaque they have”. *

After a couple of years of this, even with a history of high cholesterol, if you also keep BP controlled, HS-CRP <1, and avoid diabetes, it’s plausible to have a 70%+ lower risk of heart attack, stroke, need a stent or bypass, vs a same age average peer.

*there is one other thing, anti-clot measures like asprin or other meds, that significantly adds to risk reduction, but this a complicated topic for a separate discussion
Time for the stupid question again…

For someone like me with An LDL of 33 even on a dyslipidemia promoting stack, is repatha overkill? Aka make my lipids “too low”
 
Time for the stupid question again…

For someone like me with An LDL of 33 even on a dyslipidemia promoting stack, is repatha overkill? Aka make my lipids “too low”

ApoB / LDL can’t be too low. Science has largely put that concern to rest. (Certain conditions are associated with low lipids, but the disease, cancer, Alzheimer’s, etc, are the cause of it, not caused by it).

That said given the expense of Repatha, and you’re already so far into risk reduction territory I’d only use it if I had elevated Lp(A).

Have you had Lipoprotein A checked?
 
ApoB / LDL can’t be too low. Science has largely put that concern to rest. (Certain conditions are associated with low lipids, but the disease, cancer, Alzheimer’s, etc, are the cause of it, not caused by it).

That said given the expense of Repatha, and you’re already so far into risk reduction territory I’d only use it if I had elevated Lp(A).

Have you had Lipoprotein A checked?
Was undetectable. They even had to repeat the assay.
 
Was undetectable. They even had to repeat the assay.

I’m all for maximizing risk reduction of the #1 cause of death, but unless your situation changes in the future, you’re good to go.

Repatha doesn’t really even have any pleiotropic “bonus” effects like inflammation reduction that would make it worthwhile in your case.
 
Fhanks
That’s about all I recommend under normal circumstances. Its very potent, exceptionally effective against AAS induced high lipids, cheap (ish), easily accessible, no sides (overwhelmingly).

If you’re still >70, or aiming for regression and >40 add Bempadoic Acid.

For those with high lipids, absolutely can’t / won’t take a statin, or have years of untreated high cholesterol and want maximum possible regression + stabilization, or just willing to spend the cash for the very best cardiovascular protection, Repatha is an incredible 1 or 2x a month injection that’s ultra powerful. It has a very strong reputation for stopping future heart attacks and strokes.

It’s the only lipid med that reduces Lp(a), and it’s basically side effect free for the vast majority. It’s best combined with a statin if you can, to get the anti inflammatory effects only statins provide.

If you combine Pitavastatin 4, Ezetimibe, and Repatha, you’re using the most potent anti-cardiovascular disease combination science has available. 90%+ APO-b, LDL-C, 30% Lp(a), 60% HS-CRP (inflammation) reduction. Plaque will strongly regress over 18 months or so, whatever’s left will dry out and stabilize reducing risk even more over time.

I spoke to a cardiologist who told me if a patient has no symptoms, and they’re on this combo, he doesn’t even see a need for imaging, regardless of risk factors or 30 years of sky high cholesterol. “What difference would it make? This is the strongest risk reduction treatment a patient could be on, no matter how much plaque they have”. *

After a couple of years of this, even with a history of high cholesterol, if you also keep BP controlled, HS-CRP <1, and avoid diabetes, it’s plausible to have a 70%+ lower risk of heart attack, stroke, need a stent or bypass, vs a same age average peer.

*there is one other thing, anti-clot measures like asprin or other meds, that significantly adds to risk reduction, but this a complicated topic for a separate discussion
Thanks for the reply Ghoul, I'm surprised to learn it's the inflammation reduction that the drugs provide more than the raw lipoprotein reduction that makes a difference.

Is the bempadoic acid instead of or in conjunction with the statin? When I was reading about it, it was mostly used in place of the statin.
 
Fhanks

Thanks for the reply Ghoul, I'm surprised to learn it's the inflammation reduction that the drugs provide more than the raw lipoprotein reduction that makes a difference.

Is the bempadoic acid instead of or in conjunction with the statin? When I was reading about it, it was mostly used in place of the statin.

There’s so much anti-statin paranoia out there (including me for a long time), getting people to take anything to lower LDL has been a huge battle, so non-statin meds like Eze, Bemp, and PCSK9 (like Repatha) have been thought to be “the holy grail” of cardiology to finally get people to treat ldl down into a safe range.

The problem is all the studies show statins used as a base with any of those other meds do significantly more to lower risk than just the ldl reduction accounts for. It’s down to the anti-inflammatory effect. (It may be the cholesterol crystal dissolving property of statins responsible for much of that, less injury to the arteries from all that stabbing).

Without a statin, Eze and Bemp look weak on their own. (Better than nothing, just much much more effective as add ons to statins).
 
Absolutely.* The additional LDL reduction is useful, but the main benefit is the huge drop in systemic (especially within artery) inflammation.

After you’ve crushed ApoB/LDL and you’re no longer adding to plaque, the next biggest risk is a piece of soft plaque breaking off (which leaves a wound, and the clot that forms is the most common cause of heart attacks), Inflammation is the main driver of that risk. High inflammation causes “pimples” to form under the plaque destabilizing it. By lowering HS-CRP <1 you minimize that risk.

Over time, as you maintain very low ApoB/LDL, whatever soft plaque hasn’t been removed hardens, eventually turns into a sheet of calcium, and very unlikely to ever break off. It’s the fresh soft plaque that’s highly inflammatory and at risk of breaking off.

*often the lowest friction path to Repatha insurance coverage is pretending you can’t tolerate statins. Once you’re approved, you can always go back on a statin and you won’t lose Repatha coverage.
Thanks my friend. Yes lipo a was <10 , apo b high at 1.14 though with total and ldl fairly elevated. Plan is to stick on simvastatin and repatha (no pitavastatin approval in Canada yet)
 
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