Statin Wars?

RAE, the diet/heart hypothesis, whether flawed or not, does not appear particularly relevant to whether statins are efficacious for primary prevention of CVD.


I think it is very relevant, because:


- if the diet/heart hypothesis is wrong (and cholesterol is not the cause of heart disease), then prescribing drugs to lower total cholesterol to people that do not have existing CVD is either ineffective (at best), or potentially harmful (due to potential side effects from statins, as well as studies showing that people above age 60 or so with higher total cholesterol generally live longer than those with lower cholesterol). As the paper I cited above made pretty clear, there may be an "association" between serum cholesterol and CVD, but there has never been any strong evidence that association is "causative". So, high serum cholesterol may actually be just a marker for CVD, rather than something that causes CVD. Remember, over half of the people that have major heart attacks actually have "normal" cholesterol levels. If cholesterol was a primary cause of CVD/CVD events, one would expect that the risk for having a CVD would rise linearly as serum cholesterol rises. But that is not generally the case.


So, as the paper I cited said, it could very well be that there are other causes for heart disease, and that using drugs to lower cholesterol simply does not address those causes. Perhaps heart disease is actually rooted in metabolic syndrome (that is one current theory, anyway), and if so, then doing things to address insulin resistance (such as diet/lifestyle changes that lower blood glucose) would be much more effective.
 
Sounds like from reading above, I should get off 81 mg/day aspirin that I have been taking for a decade or so (I'm 75). Next year, when I have my annual doctor visit, I'll see what she says.

I think I got told to take one daily when I was put on BP meds years ago. I'm off BP meds (cardiologist told me I probably never needed them in the first place in 2018) so maybe I don't need the aspirin too.
The thinking has changed, for sure, so if your doc has kept up, you may get a recommendation to come off the aspirin. Back when the aspirin thing proved effective, the population wasn't as highly monitored for risk factors associated with platelet clumping. So since we are generally healthier now, the effect of aspirin is not as great.
 
"You'd be surprised at the information that is out there on things like iron overload (much of it written by doctors and medical researchers, by the way), if you just do a little searching of your own."

I do plenty of research. In fact, DW complains I do far too much research prior to making decisions. I'm not sure why I would do said research on topics I'm not aware of or affected by (at the moment) such as iron overload. I'm glad that you had good results from your research. What I don't understand is how that has anything to do with trusting Drs on things like statins. My results with Crestor have been very good. Factors that should go up, went up. Those that should go down, went down.

Making an informed decision based on professional advice and our own research is what we should all be doing. I see no indication that you ever asked a Dr if blood letting was a good idea to solve your problem - which is what my sarcastic reference to leeches was. Have you since discussed it with a Dr? My total lack of medical training leads me to believe your conversation would not go well. Do you plan to do this again if your ferritin levels go back up? I suppose the Red Cross is grateful, but I can't see blood letting as a permanent solution, let alone a suggested medical one.
 
Dr. Put me on Ezetimibe - YES IT IS A STATIN ALSO!!! We decided to take me off for >6 months, see how my head felt, it felt much less stupid! We had cognitive tests, CAT or MRI SCANS on head all come back as normal for a 58yr old... During that time, my cholesterol when back up to >250 from ~ 155. We eat health, not a lot a meat, no beef really and lots of veggies and salads with minimal oils. not a lot of exercise for me, but get my >10000 step a day weight about 175.... So i reluctantly when back on knowing first sign of getting stupid, off i came.... Been feeling fine, will continue to watch.....

Ezetimibe is not a statin.
 
"You'd be surprised at the information that is out there on things like iron overload (much of it written by doctors and medical researchers, by the way), if you just do a little searching of your own."

I do plenty of research. In fact, DW complains I do far too much research prior to making decisions. I'm not sure why I would do said research on topics I'm not aware of or affected by (at the moment) such as iron overload. I'm glad that you had good results from your research. What I don't understand is how that has anything to do with trusting Drs on things like statins. My results with Crestor have been very good. Factors that should go up, went up. Those that should go down, went down.

Making an informed decision based on professional advice and our own research is what we should all be doing. I see no indication that you ever asked a Dr if blood letting was a good idea to solve your problem - which is what my sarcastic reference to leeches was. Have you since discussed it with a Dr? My total lack of medical training leads me to believe your conversation would not go well. Do you plan to do this again if your ferritin levels go back up? I suppose the Red Cross is grateful, but I can't see blood letting as a permanent solution, let alone a suggested medical one.

http://www.irondisorders.org/phlebotomy


"Iron is removed therapeutically from the body in two ways, by blood donation (phlebotomy) or chelation therapy (pharmacological removal). The therapeutic approach used, the amount of iron removed, follow-up testing of iron levels, dietary and behavioral changes made will all differ according to the patient’s iron levels, general health, age and ability to tolerate the chosen approach"
 
I do plenty of research. In fact, DW complains I do far too much research prior to making decisions. I'm not sure why I would do said research on topics I'm not aware of or affected by (at the moment) such as iron overload. I'm glad that you had good results from your research. What I don't understand is how that has anything to do with trusting Drs on things like statins. My results with Crestor have been very good. Factors that should go up, went up. Those that should go down, went down.

Making an informed decision based on professional advice and our own research is what we should all be doing. I see no indication that you ever asked a Dr if blood letting was a good idea to solve your problem - which is what my sarcastic reference to leeches was. Have you since discussed it with a Dr? My total lack of medical training leads me to believe your conversation would not go well. Do you plan to do this again if your ferritin levels go back up? I suppose the Red Cross is grateful, but I can't see blood letting as a permanent solution, let alone a suggested medical one.

Beowulf, my opinion on statins is based almost entirely on the research I have done on CVD and statin use. The lack of help I got from doctors re. my iron overload problem is only relevant here because it reinforced my general belief that doctors don't know everything, and can sometimes be misinformed/wrong (just like anyone can). And I definitely did ask my PCP if he thought it would be a good idea to have a therapeutic phlebotamy done to reduce my ferritin level, after I discovered that a ferritin level of 400 was likely a problem. The response was as I said in an earlier post about this - the PCP simply refused to acknowledge that a ferritin level of 400 ng/mL could be the source of my issues, so he refused to order the phlebotamy. He said that a ferritin level of 400 is within the reference range (which was about 25-500), and that since my level did not exceed 500, there was nothing wrong with my ferritin level. I found out later, on my own, that many countries in the world use a reference range for ferritin that tops out around 200-250, which is when I started to realize that my ferritin level could indeed be the source of my issues (despite what my PCP said). So, my only alternative was to go and donate blood myself to the blood bank, which I did several times, after which I felt a whole lot better (and I continue to feel good to this day).

And I thought I made this clear already, but I check my ferritin level at least annually now, to make sure it is where I want it to be (around 60-80). I have found that by donating blood about 2X each year, I can keep it there. Many other people with iron overload have to donate blood a few times each year for the rest of their lives, which is all that is needed to keep the ferritin from getting too high again. So.........I do consider periodic donation of blood a "permanent" solution, and it's easy........takes roughly 45 minutes total, twice yearly. Why do you find that to be so strange?

I'm glad your results with Crestor have been good.........that's great. I am not questioning your decision to follow your doctor's advice, and I never said that I don't intend to ever follow my doctor's advice again. I do know that unless I am convinced otherwise, I don't plan to go on a statin drug in the foreseeable future, based on what I know about statins.
I guess you find that to be a mistake on my part, but that's your opinion, and that's ok!
 
Iron Disorders Institute:: Phlebotomy


"Iron is removed therapeutically from the body in two ways, by blood donation (phlebotomy) or chelation therapy (pharmacological removal). The therapeutic approach used, the amount of iron removed, follow-up testing of iron levels, dietary and behavioral changes made will all differ according to the patient’s iron levels, general health, age and ability to tolerate the chosen approach"


Yep, that is all correct. Chelation can help slowly remove some iron, but donating blood is a much quicker way to do it. Each time you donate blood, you reduce your ferritin level by approx. 30 ng/mL. The optimum serum ferritin level based on everything I've read is about 60-80 ng/mL.

Many people have ferritin levels much higher than that and remain asymptomatic, but that doesn't necessarily mean that no damage is occurring in your body. Excess iron can damage virtually all bodily organs, including the heart and liver. I would highly recommend that most people age 50 or over (especially males) get their ferritin tested, just to see where they are at. It is an inexpensive test, and covered by most insurance.
 
Ezetimibe is not a statin.

It's not a statin itself, but I found out there is a pill that combines it with a statin to increase effectiveness. The way sulpha and amoxcilan are a "two-fer" in Bactrim. That might be what f35phixer is referring to. And the symptoms listed are consistent with statins.

f35phixer View Post
Dr. Put me on Ezetimibe - YES IT IS A STATIN ALSO!!! We decided to take me off for >6 months, see how my head felt, it felt much less stupid! We had cognitive tests, CAT or MRI SCANS on head all come back as normal for a 58yr old... During that time, my cholesterol when back up to >250 from ~ 155.
Did the doctor say just what the risk difference is between 250 and 155 for the remaining 25-30-ish yrs of your life? I always ask that and they can never give me a good answer.
 
An analogy in medicine

A calculator which "determines" if you should be on a statin or not is just codifying the recommendations arrived at by the organizations that make such recommendations, of course. Leaving aside whether these organizations have a bias toward higher usage, these recommendations are based on "established thinking". Again, leaving aside whether this thinking is biased toward higher effectiveness and/or reduced negative consequences, they are not based on the latest thinking, simply because it takes time for data, whether gathered in a research or clinical settings, to become integrated into the recommendations.

I believe there is a role for participants (doctors and patients) to explore beyond the established recommendations. Not all doctors and not all patients are candidates for this path, and one of the reasons why threads like this get so much attention.

As an illustration for this exploration beyond the established recommendations, the history of diabetes (type 2) might be examined. For a long time, doctors were advised to give ever increasing doses of insulin to push sugar out of the blood and into the cells. Decades ago, maybe because they noticed that diabetic gastric bypass patients suddenly became non-diabetic, a few clinicians risked their license by having their patients undergo various levels of fasting. There were no studies at the time "proving" this worked, but some clinicians trusted what they saw, and moved in a direction not prescribed by the current, at the time, official recommendations. More recently, the idea of draining glucose from cells of the body through fasting has taken an official role in the recommendations for diabetes treatment. Doctors who, years ago, were on the leading edge, realized that by not trying to force glucose out of the blood into cells that couldn't take any more glucose, probably saved a lot of lives (and suffering and amputations). But on the other side, there are doctors who suffer the cognitive dissonance of knowing that it turns out that what they were doing all those years wasn't the best thing for patients. And you will almost certainly find clinicians that have never prescribed a fast; people are often very slow to change their ways.

So coming back to the statin situation with the history of the diabetes situation in mind, I wonder how the statin thing will turn out. I'm sure there are people that will think that treating diabetes and preventing CVD are apples and oranges. I agree that many aspects are hugely different. The point is to illustrate how the wheels of the health industrial complex have progressed through one big revenue disease to see if any knowledge gleaned there can be applied to another big revenue thing, in this case, a CVD prevention effort using statins. One could argue a survivor bias, where the suggested non-accepted diabetes treatments that didn't work are not getting any press?

More differences abound. When you look at diabetes treatment, the up-side potential was huge (i.e. if it works, you won't cut off my foot). The upside potential for a statin might be maybe I might put-off a CVD event that may or may not happen anyway. Then there's the down-side. I can choose to not eat for a few days and see what happens. That's not exactly stopping to pick up a penny in front of a Mack truck barreling down on you...more like stopping to pick up $10 in front of a kid on a trike. I'll leave it up to the reader to come up with an analogy like that for starting on a statin, and continuing on a statin if you tolerate it well.
 
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Saw this the other day, thought it was a good discussion, passing it on. It's David Diamond, PhD and Bret Scher, MD in conversation about statins. Diamond is a cognitive scientist who also analyzes and publishes in the area of cholesterol and stain research. Scher is a low-carb cardiologist. I found it illuminating.

https://youtu.be/YaEmiUfL7ts?list=LLT81zbRgudFSf6HmVxotDVw
 
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It's not a statin itself, but I found out there is a pill that combines it with a statin to increase effectiveness. The way sulpha and amoxcilan are a "two-fer" in Bactrim. That might be what f35phixer is referring to. And the symptoms listed are consistent with statins.

f35phixer View Post
Dr. Put me on Ezetimibe - YES IT IS A STATIN ALSO!!! We decided to take me off for >6 months, see how my head felt, it felt much less stupid! We had cognitive tests, CAT or MRI SCANS on head all come back as normal for a 58yr old... During that time, my cholesterol when back up to >250 from ~ 155.
Did the doctor say just what the risk difference is between 250 and 155 for the remaining 25-30-ish yrs of your life? I always ask that and they can never give me a good answer.

My mistake , I goggle and it said can be combined statin pill, misread it..... that just confirms more how well my brain feels... ill go back in nov and see what blood shows, if it’s lower and brain isn’t stupid I say win win....
 
This should be fun:


"Boris Johnson’s*new Chief Medical Adviser*should carry out an immediate review into*statins*to help clarify whether millions of patients are actually benefiting from the cholesterol lowering*drug, according to the chair of the science and technology committee.

Norman Lamb said the move was necessary due to*the number of neverending contradictory claims being made about the drug*– by far the most common in the UK with more than eight million people prescribed them.
.
.
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The group’s central argument is a lack of transparency over the raw data in statins trials dating back several years has prevented a clear picture emerging for the public over the benefits of the drug compared to any side effects, which they argue have been “underplayed""



https://inews.co.uk/news/health/statins-review-nhs-government-chief-medical-adviser-norman-lamb/
 
I find this conversation very interesting, and would like to ask a simple question: For primary prevention, how much will taking a statin reduce my chance of having a CVD event?

In the linked video, Dr. David Diamond analyzes some of the most influential statin papers and explains that the absolute risk reduction is about 1%. The rates of reduction touted by drug companies and others of 36% or more are usually referring to relative risk, which in my opinion is very deceptive.

I would appreciate any criticisms of the points raised in the video.

https://youtu.be/psnkNqLA4Os
 
The real question is whether high cholesterol increases the chances of a CVD event. If it doesn’t, then reducing cholesterol is a waste of money. If high cholesterol increases your chance of a CVD, then reducing it makes sense.
 
The real question is whether high cholesterol increases the chances of a CVD event. If it doesn’t, then reducing cholesterol is a waste of money. If high cholesterol increases your chance of a CVD, then reducing it makes sense.

I totally agree. I was trying to make the point that if significantly lowering LDL yields at best a 1% in event reduction, that maybe LDL is not the correct target.

Mark
 
The real question is whether high cholesterol increases the chances of a CVD event. If it doesn’t, then reducing cholesterol is a waste of money. If high cholesterol increases your chance of a CVD, then reducing it makes sense.
Well, as I think through this, I'm not sure that it's a waste of money in all cases. If we're talking about otherwise healthy people who have very few risk factors that would be taking a statin because when their age and LDL-C is plugged into a calculator (which itself is based on a protocol derived through this opaque processing of studies, referenced above), then yes, probably a waste of money. But there are so many other things to consider besides "high cholesterol".


Let's try this analogy, just for fun...


A long time ago the cops went out and saw a lot of crime (CVD) (picture Chicago gangsters). They suspected the Cholesterol Crime Family (CCF). Although some of them ran legit businesses (HDL-C), some looked more shady (LDL-C). The papers, at first, ignored the details and had headlines about how the CCF was getting away with a lot of crime (CVD). The cops turned over the evidence to the DA's office (pharma). The DA's office had techniques to prosecute these kinds of cases where there wasn't quite enough evidence to indite (compounds randomly arrived at that needed to be matched with a health issue). The DA's office came up with the theory of the crime: LDL-C causes CVD. Meanwhile, the papers ran headlines about how how the entire bunch of immigrants from the country of "FatLanders" were ruining everything. The stories of the FatLanders and the Cholesterol Crime Family sold a lot of papers, but it turns out all of this was just wrong. But now the DA's office was invested. They don't want to look incompetent, so they keep pounding. The cops keep digging and realize that the CCF isn't really a crime family after all. Even LCL-C is pretty much off the hook as there's no increase in crime where they are, except there's still one suspect, a guy with small particle size who goes by the name "beady-eyes", seems to be around more when there's crime, but the guy who goes by the name "fluffy" comes out clean. The cops report this to the DA, but they don't want to hear it. They've got their theory of the crime and they're going after the whole LDL-C clan. Meanwhile, the cops have hired a new detective and they're getting more interested in analyzing the crime at a higher level, beyond just CVD, they realize that a bunch of less obvious but earlier crimes occur in the area of inflammation. They're less convinced that these inflammation crimes are caused by the LDL-C clan and want to work on finding suspects. The problem is that the DA's office doesn't support this effort, nor does the chief of police. So the new detective is standing there with collected evidence, but the higher-ups are rolling with the old case against LDL-C.


Stay tuned for the next episode: A new DA gets elected and the old case get's thrown out.
 
Ya know - I wish there were more qualified technically trained medical doctors commenting on this topic, here.
 
I find this conversation very interesting, and would like to ask a simple question: For primary prevention, how much will taking a statin reduce my chance of having a CVD event?

In the linked video, Dr. David Diamond analyzes some of the most influential statin papers and explains that the absolute risk reduction is about 1%. The rates of reduction touted by drug companies and others of 36% or more are usually referring to relative risk, which in my opinion is very deceptive.

https://youtu.be/psnkNqLA4Os

Yes, Dr. Diamond is absolutely correct about the absolute risk reduction being about 1%. And, to even achieve a "possible" risk reduction of 1%, you need to take a drug (statin) that has all sorts of potential negative side effects (muscle pain, diabetes, cancer). I guess everyone can make up their own mind about whether it's worth it or not - for me, it's absolutely not worth it.

I've stated this before, but I think it's important to remember that at least half of all people that have a major coronary event, have a total serum cholesterol level that would be considered "normal" (not high).

You see media articles (and press releases from the drug companies) all the time citing risk reductions of 20,30, 40 percent from taking a certain drug........and in almost every case, they are talking about relative risk reduction (but they don't make that clear). I always do some digging to find out what the absolute risk reduction is, and in many cases, it's similar to statins, or even less than 1%.
 
Just for fun.
AFIK neither HDL nor LDL are cholesterol.
Thus can not possibly be bad or good chloesterols. They both are transporters of cholesterol molecules. And cholesterol molecules are required by every cell of the body.
 
Have you had a CAC (Coronary Calcium) test? It's what convinced me to lower my cholesterol. I had 3 tests spaced out over several years and the score was increasing. After lowering my cholesterol the progression stopped. Your mileage may of course vary.


The discussion here as well as the attached Youtube video (done by an engineer...I like that type of "thinking") convinced me to get a CAC scan. I get it next week and costs a whopping $50. I am anxious to see that it tells me and how it compares to the Framingham screen.

The overarching question that I have is WHY heart disease is still the #1 killer in the US (1 in 4 deaths) when statins have been around for such a long time?


RAE, the study you quote below is from 2010. It is simply outdated information.





Here is a link to the USPSTF 2016 Recommendation:

https://www.uspreventiveservicestas...l/statin-use-in-adults-preventive-medication1

The AHA/ACC Guidelines are even more current, last updated March 2019, also found benefit for statins for primary prevention of cardiovascular disease in some adults.

And yet even this recommendation has a caveat:

To determine whether a patient is a candidate for statin therapy, clinicians must first determine the patient’s risk of having a future CVD event. However, clinicians’ ability to accurately identify a patient’s true risk is imperfect, because the best currently available risk estimation tool, which uses the Pooled Cohort Equations from the 2013 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on the assessment of cardiovascular risk,1 has been shown to overestimate actual risk in multiple external validation cohorts.2-4 The reasons for this possible overestimation are still unclear. The Pooled Cohort Equations were derived from prospective cohorts of volunteers from studies conducted in the 1990s and may not be generalizable to a more contemporary and diverse patient population seen in current clinical practice. Furthermore, no statin clinical trials enrolled patients based on a specific risk threshold calculated using a CVD risk prediction tool; rather, patients had 1 or more CVD risk factors other than age and sex as a requirement for trial enrollment.
 
70 yo diabetic and have been on a statin for 20 years, originally due to high cholesterol and blood pressure and a family history of heart disease. Just had a CAC last week and it was 0, same as my last one that was about 6 years ago. My LDL is 46. A1C is low prediabetic, but at least my blood lipids are not raising a concern with my PCP. Anyway, even with a perfect CAC, I understand an individual could still have a blockage.
 
Anyway, even with a perfect CAC, I understand an individual could still have a blockage.

How would this be possible? If there is blockage, it would think it would be visible on the CT. I am not trying to be snide, I am really curious.
 
I'm curious too. I believe that you can have calcified plaque and plaque that hasn't yet calcified and that only the calcified is what shows up on that test. I had the calcium score and the CIMT (carotid-artery intima–media thickness) tests. My doc said that the CIMT would show signs first, and only later, after calcification would calcium score go up.
 
ExFlyBoy5;2292473 The overarching question that I have is WHY heart disease is still the #1 killer in the US (1 in 4 deaths) when statins have been around for such a long time?[/QUOTE said:
Maybe because LDL-C is not causative for coronary disease, but just a marker for some other issue that statins don't/can't address??
 
You can have a low score on the CAC test and still be at risk for heart disease, because not all diseased arteries have calcium deposits. Conversely, you could have a fairly high score on the CAC test even if your arteries do not have signs of heart disease.

This is from the Univ. of Michigan Health website:

Key points to rememberA coronary calcium scan checks for calcium buildup in the coronary arteries. Calcium in these arteries may be a sign of heart disease. A high score on a calcium scan can mean that you have a higher chance of having a heart attack than someone with a low score.
  • The results of a coronary calcium scan may prompt you to make some lifestyle changes, such as exercising, eating better, losing weight, and quitting smoking. You might also decide to take medicine such as cholesterol or blood pressure medicine.
  • People who are at medium risk for heart disease will get the most benefit from this test. Your doctor can help you find out your risk. Knowing your risk for a heart attack is a key part of your decision to get a scan.
  • A calcium scan is not helpful to patients who have a low or high risk of heart disease.
  • A calcium scan can give your doctor more information about your risk for heart disease. If you have a high score, you and your doctor may decide to start or change treatment to lower your risk.
  • You could get a high score from the test even if your arteries do not have signs of heart disease. This could lead to other tests or treatments that you don't need.
  • Not all arteries that have early signs of heart disease have calcium. So you could get a low calcium score and still be at risk.
 
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