Anyone taking Statins ( Crestor )

[mooseman109]

Had an MI in April, been on crestor since, not side effects for me. Total chocolate is 100 give or take and ldl is mid 30’s. Was right at upper limit before

 

[broker]

A good option is taking crestor at a low dose ( 5 mgs ) every other day. It has a rather long half life.

 

[Vince]

Its not nonsense. Its the truth. I have a genetic mutation of the 13 gene, giving me abolition of ldl receptor activity on the y chromosome. (HeFh)

The consequence of this is massively raised LDL-c.
The hypothesis that high LDL is causative towards heart disease was utterly ruined once many individuals with the same familial hypercholesterolemia gene mutation as myself, which causes very high levels of LDL-c were found to have no incidence of CVD, nor evidence of atherosclerosis of any kind under examination.

In short, some people with hypercholesterolemia have heart disease, some dont. Proving that LDL-c isnt, and never was the cause of CVD.

The ‘theory’ or hypothesis that high ldl-c is a marker for CVD is dead in the water. All current evidence points towards clotting, thrombus, endothelial inflammation and intestinal issues.

The majority of cvd patients have ldl-c well within the ‘recommended’ parameters. The same for those dying from myocardial infarctions. (LDL-c within the guideline range)

Statins are actually dangerous from the pov of cvd as they ‘encourage’ the calcium levels within arterial plaque to rise. The idea being that this promotes stability within the lesion.
If anything, they are causative towards angina and other coronary calcification issues such as aortic stenosis and heart valve issues.

The use of statin therapy for cvd is one of the biggest lies in the history of medicine.

Novartis to acquire The Medicines Company for USD 9.7 bn, adding inclisiran, a potentially transformational investigational cholesterol-lowering therapy to address leading global cause of death
Nov 24, 2019

Over 50 million secondary prevention patients worldwide with atherosclerotic cardiovascular disease (ASCVD) or familial hypercholesterolemia (FH) on current standard of care do not achieve LDL cholesterol (LDL-C) goal and remain at increased risk of cardiovascular events1
Novartis to acquire The Medicines Company for USD 9.7 bn, adding inclisiran, a potentially transformational investigational cholesterol-lowering therapy to address leading global cause of death | Novartis

 

[xqfq]

Novartis to acquire The Medicines Company for USD 9.7 bn, adding inclisiran, a potentially transformational investigational cholesterol-lowering therapy to address leading global cause of death
Nov 24, 2019

Over 50 million secondary prevention patients worldwide with atherosclerotic cardiovascular disease (ASCVD) or familial hypercholesterolemia (FH) on current standard of care do not achieve LDL cholesterol (LDL-C) goal and remain at increased risk of cardiovascular events1
Novartis to acquire The Medicines Company for USD 9.7 bn, adding inclisiran, a potentially transformational investigational cholesterol-lowering therapy to address leading global cause of death | Novartis

These drugs are going to change the world (once they're cheap enough for normal people to use!) Inclisiran is a PCSK9 inhibitor (NOT a statin!), but works differently than existing PCSK9 inhibitors and only needs to be injected twice a year:

“If the outcomes trials validate what most of us think it will or hope it will, [inclisiran] will be more broadly used than just a niche, I think, because there is so much of a burden of atherosclerosis that remains that we’re not addressing that this could be a powerful tool,” according to Watson.

“If this drug is approved, it will be nice to have a second option to lower LDL in the PCSK9 pathway,” Wright said. “Then the question becomes: is it more convenient to take a drug twice a year versus 26 times a year and what's the value to patients?” He acknowledged not knowing how inclisiran will be priced but said “those are issues to be considered.”

“Inclisiran is the first cholesterol-lowering agent in the siRNA class that opens up a whole host of new and exciting possibilities, and definitely increasing the number and types of effective therapeutic options that our patients have available to them is good medicine,” Watson concluded.

PCSK9 inhibitors are incredible. They aren't statins - they don't inhibit cholesterol synthesis inside of cells. They create more LDL receptors, increasing the clearance of LDL.

Because of this, LDL can be driven very, very low without the same side effects you see with statins. With a high dose of statins, side effects may appear because you increasingly inhibit cholesterol synthesis in cells.

 

[bp]

Novartis to acquire The Medicines Company for USD 9.7 bn, adding inclisiran, a potentially transformational investigational cholesterol-lowering therapy to address leading global cause of death
Nov 24, 2019

Over 50 million secondary prevention patients worldwide with atherosclerotic cardiovascular disease (ASCVD) or familial hypercholesterolemia (FH) on current standard of care do not achieve LDL cholesterol (LDL-C) goal and remain at increased risk of cardiovascular events1
Novartis to acquire The Medicines Company for USD 9.7 bn, adding inclisiran, a potentially transformational investigational cholesterol-lowering therapy to address leading global cause of death | Novartis

I use a pcsk9 inhibitor Vince. 1 year in so far. They have a terrific effect on the endothelial function, and so far, no major side effects.

 

[bp]

These drugs are going to change the world (once they're cheap enough for normal people to use!) Inclisiran is a PCSK9 inhibitor (NOT a statin!), but works differently than existing PCSK9 inhibitors and only needs to be injected twice a year:



PCSK9 inhibitors are incredible. They aren't statins - they don't inhibit cholesterol synthesis inside of cells. They create more LDL receptors, increasing the clearance of LDL.

Because of this, LDL can be driven very, very low without the same side effects you see with statins. With a high dose of statins, side effects may appear because you increasingly inhibit cholesterol synthesis in cells.

Im on one. (PCSK9 INHIBITOR) 2/month
The effect on intima inflammation appears to be profound. Which is the no.1 reason i use them TBH.

 

[xqfq]

Im on one. (PCSK9 INHIBITOR) 2/month
The effect on intima inflammation appears to be profound. Which is the no.1 reason i use them TBH.

Does your insurance cover it or do you pay out of pocket? I’ve read they are around $15k/year— maybe yours is cheaper? What does it have your particle count and LDL-C at?

I have read some people can get insurance coverage with proof of statin intolerance but I’m not sure.

 

[Will Brink]

This is complete and utter nonsense. I’ve been researching CVD for 10 years (since my father got sick).

This forum, like many places on the Internet, is extremely biased against statins and in general the idea of fixing your poor blood lipids. Please be careful taking advice here.

I agree with that assessment. Statins have a place and are of value for some. Over prescribed? Yes. But, few willing to do what's needed to improve their lipid profiles, and for some, there's a genetic component damn near impossible to improve. Docs, etc I trust feel statins are of value, but don't paint them as wonder drugs either of course. I tend to think it's best to start with mid statin and low dose and work up if needed, and even a low dose every other day appears a benefit with no side effects. As far as particle sizes, etc, and excellent article by Monica Mollica:

Why you need to look beyond your LDL - “bad cholesterol” - level | BrinkZone.com

 

[Will Brink]

My LDL particle number is very high. The overall cholesterol is 199 but LDL is 123. That said, the particle number is extremely high.
1)Can diet alone lower particle number?
2) i also read about taking low dose cestor ( 5 mgs) every other day to reduce potential side effects. I even see studies where people take it once per week.

1, maybe, and worth trying, but genetic component rules all

2, try it and see what it does for your lipids, and proceed from there.

Obviously, make sure to supplement CoQ10.

 

[Will Brink]

In short, some people with hypercholesterolemia have heart disease, some dont. Proving that LDL-c isnt, and never was the cause of CVD.

In short, lipid levels still correlate to CVD. The moving target is which lipids, trg/LDL ratios, particle sizes and ratios, various confounders, etc. There's obviously other risk factors unrelated to lipid levels that dictate CVD or not, some of which we have control over, some of which we don't. For sure, the old models are of minimal value, but saying hypercholesterolemia is unrelated to CVD is simple false. It's a generalization no better than saying everone with hypercholesterolemia will get CVD.

 

[Golfboy307]

Thanks Will and xq for providing a more nuanced and proper understanding of lipids role in CVD. It shouldn't be labeled "the cause" as CVD is multi-factoral, beginning with damage to the lining of artery walls. But there is a lipid correlation in many people. That is what modern medicine is based on. Treat the percentages.

One doctor explained CVD to me with an interesting analogy: picture your coronary arteries as a hallway in your house. Over time the walls get nicked up and dented. You can spackle them to repair the holes. Cholesterol is the body's spackle, that will then harden into plaque to fix the damage. When the damage keeps happening or you have too much spackle, the "hallway" can be narrowed too much. You have two options: figure out why the damage is happening (multi-faceted in the body) or reduce the amount of spackle available. Statins do the latter. Pretty simplistic model, but it helps explain its not just cholesterol.

 

[bp]

In short, lipid levels still correlate to CVD. The moving target is which lipids, trg/LDL ratios, particle sizes and ratios, various confounders, etc. There's obviously other risk factors unrelated to lipid levels that dictate CVD or not, some of which we have control over, some of which we don't. For sure, the old models are of minimal value, but saying hypercholesterolemia is unrelated to CVD is simple false. It's a generalization no better than saying everone with hypercholesterolemia will get CVD.

Correlation isn’t causation, and that’s my point.
If only one person with heFH doesn’t have CVD, then this is definitive proof that LDL isn’t the cause, and merely has a correlation to CVD.

Focus needs to be on causation factors, not shitty correlations.
There are elephants in the room with ‘causation’ tattooed onto their foreheads, which outway correlations by 1000’s of percentages in terms of risk factors for CVD, yet much attention is still focused on LDL, when energy and effort would have been best spent elsewhere.
It’s cost the lives of millions.

 

[Vince]

If you are on statins, have gingivitis and reduced heart ejection fraction, take this supplement. The speaker recommends 150 mg three times per day. I take it for protection.


Peter Langsjoen, MD discusses why we should take Coenzyme Q10

 

[xqfq]

If you are on statins, have gingivitis and reduced heart ejection fraction, take this supplement. The speaker recommends 150 mg three times per day. I take it for protection.


Peter Langsjoen, MD discusses why we should take Coenzyme Q10

Do you take 150mg three times a day? I’ve been taking 100mg twice a day. It’s fairly expensive in supplement terms and I worry about using too much?

 

[madman]

Do you take 150mg three times a day? I’ve been taking 100mg twice a day. It’s fairly expensive in supplement terms and I worry about using too much?

How to Choose the Right CoQ10 Supplement


The “magic number” used in the vast majority of the research is 200 mg. Studies show that 200 mg daily keeps your arteries relaxed and flexible, allowing blood to move freely through them. CoQ10 shields the endothelial cells that line the walls of your blood vessels, protecting them from free radicals and keeping them fueled and strong. This in turn has a significantly positive impact on your blood pressure.



Which Form of CoQ10 Is Best, Ubiquinol or Ubiquinone?

How Much CoQ10 Should You Take Daily?

• Healthy people under age 60 should take 50 to 100 mg
• If you’re over 60 or on a statin drug, I recommend 100 to 200 mg
• If you had recent heart surgery, a heart attack, or congestive heart failure, I recommend 200 to 300 mg

A general rule of thumb with coenzyme Q10 is the sicker the individual, the more CoQ10 is required. One of the mysteries, and highly beneficial qualities of this nutrient, is that it will help to “rescue” any tissue in need.

 

[Will Brink]

Correlation isn’t causation, and that’s my point.
If only one person with heFH doesn’t have CVD, then this is definitive proof that LDL isn’t the cause, and merely has a correlation to CVD.

Focus needs to be on causation factors, not shitty correlations.
There are elephants in the room with ‘causation’ tattooed onto their foreheads, which outway correlations by 1000’s of percentages in terms of risk factors for CVD, yet much attention is still focused on LDL, when energy and effort would have been best spent elsewhere.
It’s cost the lives of millions.

Correlations are almost always what leads to understanding/discovery of mechanistisc pathaways and causation factors. All of the risk factors you're aware of were discovered via epi/correlational data. It's very difficult to do meaningful tghtly controlled RCTs in free living humans and CVD for obvious reasons. Hence, we are left with what he have to work with, understanding the value of epi data, while always understanding cause/effect is tenous at best with such data.

The reason we know particle sizes vs simple LDL appears to be a much more important risk factor for CVD is due to correlational data....

Everyone knows smoking causes cancer, yet not a single human RCT ever done for obvious reasons.

So, when one has a large body of epi research, prospective and retrospective, with large data sets, accounting for confounders, etc, is often the best we are going to have coming to some cause/effect conclusions RE, major human diseases and killers.

 

[Vince]

Do you take 150mg three times a day? I’ve been taking 100mg twice a day. It’s fairly expensive in supplement terms and I worry about using too much?

Don't worry about taking too much. I'm presently taking 400 mg twice a day. I've had my levels checked and they are way over range. I am told by my doctor, high levels will not harm me. I also think it's not necessary to have levels as high as mine.

 

[Jayyy]

My wife uses crestor. The generic brand, very inexpensive. She has no issues from using it. Her LDL cholesterol is now very good. It also helped her particle count. Her bad particle count did go lower and her good protocol number increased.

Can people use it for long term? What about fenofibrate?

 

[Jayyy]

I was prescribed Lipitor in 2008. It initially gave me severe muscle cramping in my lower back. I discovered that supplementing with COQ10 helped a lot with the cramping. Recently with TRT and thyroid meds, my cholesterol levels dropped back into the normal range, and I've been without the Lipitor for about 6 months.

Does TRT decreasd your LDL cholestrol?

 

[Jayyy]

So does testosterone therapy increases or decreases LDL or it shouldnt matter at all.