*Not* taking statins

This is a long post. Cholesterol metabolism is extremely complicated. Lipidology is a subspecialty. My knowledge, even as a general physician, is a bit limited. I'm going to create an analogy to help clarify my concerns.

Plant sterols, such as Cholestoff, do lower cholesterol levels. But they are likely not the answer. There may be harm. We don't know.

Lowering cholesterol is not the goal. The goal is to prevent and/or delay atherosclerosis, which leads to cardiovascular disease, as well as Alzheimer's disease and other forms of dementia. High LDL cholesterol, in particular found in small LDL particles, is associated with an increased risk of cardiovascular disease. Low HDL cholesterol is actually more strongly associated with increased risk of cardiovascular disease. Cholesterol is an essential component of every cell membrane in our bodies. We need cholesterol to live. We make the vast majority of our own cholesterol; relatively little comes from our diet.

There is little known about the effect of plant sterols on cardiovascular disease and Alzheimer's disease. Studies are ongoing, but are largely done with mouse models. Human studies are big and expensive, and are not controlled trials. Some mouse studies suggest that elevated plant sterols may be associated with an increased risk of atherogenesis. Additionally, in one mouse study, accumulation of plant sterols in the brain is strongly associated with neurodegeneration.

My analogy: Our LDL and HDL particles are different types of transport "busses" for cholesterol, the "passengers".

The HDL apolipoprotein is called apoA (think of it like the HDL bus driver). The HDL bus picks up excess cholesterol from the tissues and moves it out, by carrying the cholesterol to the liver, where it is used to make bile salts, which are dumped into the intestine by way of the gall bladder. HDL particles also take cholesterol to the sex organs and adrenal glands to be used to make various hormones. So the HDL bus is a waste management system, with a small amount of recycling to a couple of organs for good measure.

The LDL bus is more like a city bus, moving cholesterol around the body to the rest of the cells, except the brain, which makes all of its own cholesterol. Amongst the cholesterol the "passengers" on the bus) are a very small number of plant sterol molecules, we'll call them "aliens". The vast majority of ingested plant sterol molecules are not allowed into the body, and do not board the bus at all.

The LDL bus driver is a protein called apoB. If we have many busses, not filled with passengers, these are small LDL particles, and are much more closely associated with cardiovascular disease than the larger LDL particles. More apoB, more LDL particles, more buses with few passengers. LDL particle number is one of the most important things to measure, and most physicians don't measure it. They just measure the total LDL-C, or the number of passengers on all of the LDL buses.

The analogy would be a traffic jam of many mostly-empty buses (small LDL particles) vs a smaller number of full buses taking passengers where they need to go. The many emptier buses do much more harm to the environment than a few full buses.

What about the "alien" plant sterols? A large supplement of plant sterols will overwhelm the body's efforts to prevent them from entering the body and getting on the bus. The "alien" plant sterols will displace cholesterol "passengers" on your LDL buses, along with interfering with absorption of dietary cholesterol. Since more aliens have displaced the passengers, the LDL cholesterol number will be lower. You still don’t know the important particle count, the number of LDL buses, because you aren’t measuring it.

Plant sterols lower measurable LDL cholesterol. So what? That isn’t the desirable endpoint. Reducing cardiovascular and Alzheimer’s disease risks are what we want. We don't know if plant sterols have any effect on these endpoints. We don’t know if the aliens on the LDL buses are good or bad. We know that our bodies try to keep them out and get rid of them promptly. This suggests that our bodies treat plant sterols as undesirable aliens. Why is that?

Statins, on the other hand, reduce cholesterol synthesis in the liver. They also increase clearance of LDL particles. Since the vast majority of our cholesterol is synthesized in the liver, a statin can have a dramatic effect on LDL cholesterol. The reduction of cardiovascular risk is also statistically significant with use of a statin.

Proceed with caution if you choose plant sterol supplementation over a statin to lower cholesterol. Remember why you are doing it.
 
Another tidbit of info on causes of neuropathy, statins are a major cause...On another group, we have a huge group with neuropathy...and I ended up with it from hip replacement mess, not statins.

And there is a huge group that believe cholesterol is a huge myth, and which came first cholesterol or the drugs. The word cholesterol was NEVER known in my parent's lives and they lived into 90's....ummmm
 
I had fun writing the post. The bus analogy finally clarified for me LDL and HDL cholesterol particles. There's also VLDLs and IDLs and chylomicrons, but I didn't get into that. Thanks for the feedback. What has been said is the more you study this stuff, the less you think you know. It's true!
 
This is a long post. Cholesterol metabolism is extremely complicated. Lipidology is a subspecialty. My knowledge, even as a general physician, is a bit limited. I'm going to create an analogy to help clarify my concerns.

Plant sterols, such as Cholestoff, do lower cholesterol levels. But they are likely not the answer. There may be harm. We don't know.

Lowering cholesterol is not the goal. The goal is to prevent and/or delay atherosclerosis, which leads to cardiovascular disease, as well as Alzheimer's disease and other forms of dementia. High LDL cholesterol, in particular found in small LDL particles, is associated with an increased risk of cardiovascular disease. Low HDL cholesterol is actually more strongly associated with increased risk of cardiovascular disease. Cholesterol is an essential component of every cell membrane in our bodies. We need cholesterol to live. We make the vast majority of our own cholesterol; relatively little comes from our diet.

There is little known about the effect of plant sterols on cardiovascular disease and Alzheimer's disease. Studies are ongoing, but are largely done with mouse models. Human studies are big and expensive, and are not controlled trials. Some mouse studies suggest that elevated plant sterols may be associated with an increased risk of atherogenesis. Additionally, in one mouse study, accumulation of plant sterols in the brain is strongly associated with neurodegeneration.

My analogy: Our LDL and HDL particles are different types of transport "busses" for cholesterol, the "passengers".

The HDL apolipoprotein is called apoA (think of it like the HDL bus driver). The HDL bus picks up excess cholesterol from the tissues and moves it out, by carrying the cholesterol to the liver, where it is used to make bile salts, which are dumped into the intestine by way of the gall bladder. HDL particles also take cholesterol to the sex organs and adrenal glands to be used to make various hormones. So the HDL bus is a waste management system, with a small amount of recycling to a couple of organs for good measure.

The LDL bus is more like a city bus, moving cholesterol around the body to the rest of the cells, except the brain, which makes all of its own cholesterol. Amongst the cholesterol the "passengers" on the bus) are a very small number of plant sterol molecules, we'll call them "aliens". The vast majority of ingested plant sterol molecules are not allowed into the body, and do not board the bus at all.

The LDL bus driver is a protein called apoB. If we have many busses, not filled with passengers, these are small LDL particles, and are much more closely associated with cardiovascular disease than the larger LDL particles. More apoB, more LDL particles, more buses with few passengers. LDL particle number is one of the most important things to measure, and most physicians don't measure it. They just measure the total LDL-C, or the number of passengers on all of the LDL buses.

The analogy would be a traffic jam of many mostly-empty buses (small LDL particles) vs a smaller number of full buses taking passengers where they need to go. The many emptier buses do much more harm to the environment than a few full buses.

What about the "alien" plant sterols? A large supplement of plant sterols will overwhelm the body's efforts to prevent them from entering the body and getting on the bus. The "alien" plant sterols will displace cholesterol "passengers" on your LDL buses, along with interfering with absorption of dietary cholesterol. Since more aliens have displaced the passengers, the LDL cholesterol number will be lower. You still don’t know the important particle count, the number of LDL buses, because you aren’t measuring it.

Plant sterols lower measurable LDL cholesterol. So what? That isn’t the desirable endpoint. Reducing cardiovascular and Alzheimer’s disease risks are what we want. We don't know if plant sterols have any effect on these endpoints. We don’t know if the aliens on the LDL buses are good or bad. We know that our bodies try to keep them out and get rid of them promptly. This suggests that our bodies treat plant sterols as undesirable aliens. Why is that?

Statins, on the other hand, reduce cholesterol synthesis in the liver. They also increase clearance of LDL particles. Since the vast majority of our cholesterol is synthesized in the liver, a statin can have a dramatic effect on LDL cholesterol. The reduction of cardiovascular risk is also statistically significant with use of a statin.

Proceed with caution if you choose plant sterol supplementation over a statin to lower cholesterol. Remember why you are doing it.
This is a great explanation. I usually use dump trucks (the VLDL/LDL series) and street sweepers (HDL) but the buses work too. I like the 'drivers' and I'm going to use that! (If I may) Thanks.

The whole thing goes back 50+ years and to 'when all you have is a hammer, everything looks like a nail'. Cholesterol is definitely not the problem.
 
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I had fun writing the post. The bus analogy finally clarified for me LDL and HDL cholesterol particles. There's also VLDLs and IDLs and chylomicrons, but I didn't get into that. Thanks for the feedback. What has been said is the more you study this stuff, the less you think you know. It's true!

I loved your bus analogy. Thanks for providing that. I had heard buses and passengers mentioned before, but your version helped get it into my noggin.

I think I'm going to need an Apo B test.
 
Just because you would lie about this doesn't mean we all would
[emoji1]

I've been a pescatarian since 1986 so my diet is pretty pretty. I WILL lie about the doctor telling me to lose a few pounds though! :LOL:

Actually, about a month ago, I started with a nutritionist who can provide me with an interesting vegetarian meal plan. I needed some motivation and accountability to start cooking good, healthy meals again. I have been eating too many Trader Joe's frozen vegetarian meals since the pandemic started. I've lost 7 pounds over the last month by eating more food every day! My 4 COVID pounds are gone plus a few more.
 
I've not read every post. Got started late. Just wondering if there are opinions from the group regarding those already diagnosed with CAD? My cardiologist did not recommend statins even though my cholesterol was above the "guideline." My PCP agreed so I didn't take them for several years.

(A quick aside here to explain my "philosophy" on following doctor's recommendations on use of meds. I pay these experts/scientists/artists a LOT of money - well, me and MC and supplement, heh, heh - SO, I think I should take their advice or find someone else to give me advice, but I digress - again.)

When I had CAD symptoms and ended up with stents, BOTH my docs recommended the highest level statins. They have worked incredibly well on the numbers. No (easy) way to know if they have decreased the rate of plaque formation. BOTH docs claim that "outcomes" for those with CAD are much better on statins. Curious if anyone would disagree with this and if so, why. Not pulling the pin on a grenade, here. Just actually wondering about the strong opinions about NOT using "routine" statin for "high" cholesterol vs use as CAD treatment. Thanks.
 
I loved your bus analogy. Thanks for providing that. I had heard buses and passengers mentioned before, but your version helped get it into my noggin.



I think I'm going to need an Apo B test.



I wasn’t able to get an apoB test but an LDL-C particle count is a decent substitute. LabCorp will do it without a doctor’s order but you need to pay for it. It’s called an NMR lipoprofile, and it reports all the usual numbers, with the LDL particle number named LDL-P. I have recently switched to a concierge doc who uses LabCorp and charges a discounted rate. I feel very fortunate to have easy access to such tests. DH tried to get the test but his doc wouldn’t order it because it wasn’t in the computer system. He switched to my doc and will get the test the next time.

This is what it looks like:

https://www.labcorp.com/tests/related-documents/L15035
 
I wasn’t able to get an apoB test but an LDL-C particle count is a decent substitute. LabCorp will do it without a doctor’s order but you need to pay for it. It’s called an NMR lipoprofile, and it reports all the usual numbers, with the LDL particle number named LDL-P. I have recently switched to a concierge doc who uses LabCorp and charges a discounted rate. I feel very fortunate to have easy access to such tests. DH tried to get the test but his doc wouldn’t order it because it wasn’t in the computer system. He switched to my doc and will get the test the next time.

This is what it looks like:

https://www.labcorp.com/tests/related-documents/L15035

I’ve read about the NMR particle tests but some doctors have said it has too many problems and recommend Apo B instead. One doc of mine said he doesn’t use the particle test because “they aren’t good yet”.

I found walk-in-labs offers Apo B, so if my PCP doesn’t know what to do, I’ll do it myself.
 
Statins in people who have cardiac disease have shown benefits. The NNT review.

https://www.thennt.com/nnt/statins-for-heart-disease-prevention-with-known-heart-disease/

I hate to say it but these numbers are hardly encouraging
Oh but it gets so much better... here is the real problem.

"Caveats: Virtually all of the major statin studies were paid for and conducted by their respective pharmaceutical company. A long history of misrepresentation of data and occasionally fraudulent reporting of data suggests that these results are often much more optimistic than subsequent data produced by researchers and parties that do not have a financial stake in the results. These additional studies may however take years. Also, harm from these drugs is difficult to predict, partly because harms are often difficult to anticipate and are often poorly tracked. Such findings often come up years after new drugs have been on the market."

This is one of the reasons sites like NNT and Cochrane are so valuable and why governments need to get back to being serious about funding trials.
 
Oh but it gets so much better... here is the real problem.

"Caveats: Virtually all of the major statin studies were paid for and conducted by their respective pharmaceutical company. A long history of misrepresentation of data and occasionally fraudulent reporting of data suggests that these results are often much more optimistic than subsequent data produced by researchers and parties that do not have a financial stake in the results. These additional studies may however take years. Also, harm from these drugs is difficult to predict, partly because harms are often difficult to anticipate and are often poorly tracked. Such findings often come up years after new drugs have been on the market."

This is one of the reasons sites like NNT and Cochrane are so valuable and why governments need to get back to being serious about funding trials.


That's eye opening, the ratios of those harmed are lower than the ratios of those helped. These were people that already had heart disease, any study with people having high cholesterol and no disease?


Part of the reason I'm on statins is because my dad had a heart attack at 43 yrs old and a couple more after that. Lived to 73 and died of a bleed in the brain. He was on a blood thinner.



I'm 65 now and starting to wonder if statins (rosuvaststin/Crestor) are doing me any good. Will they prevent anything if I take them for the next 20 years?
 
That's eye opening, the ratios of those harmed are lower than the ratios of those helped. These were people that already had heart disease, any study with people having high cholesterol and no disease?


Part of the reason I'm on statins is because my dad had a heart attack at 43 yrs old and a couple more after that. Lived to 73 and died of a bleed in the brain. He was on a blood thinner.



I'm 65 now and starting to wonder if statins (rosuvaststin/Crestor) are doing me any good. Will they prevent anything if I take them for the next 20 years?

Reminds me of the old joke:

Farmer 1 "You gotta grow radishes with your buckwheat."

Farmer 2 "Why radishes with your buckwheat?"

Farmer 1 "To keep the wolverines off your land, of course!"

Farmer 2 "There's not a wolverine within a 1000 miles of here."

Farmer 1 "See. It's working."

Sorry for the the little bit of humor. (Yes, very little.) Guess I'm having a Hudson and Landry flashback. Now returning you to our regularly scheduled symposium on statin use since YMMV. :cool:
 
Purely anecdotal but once again I've learned my lesson. I got my cholesterol number down to the acceptable range after dropping my atorvastatin down from 20 to 10 mg. During the covid lockdown my Dr would not renew my Rx without a visit ($$$ I'm sure). I elected to forego the Rx and ended up with a right side bundle blockage. Now I'm back with 10 mg and normal lipid levels. Like I always say you have to figure it out for yourself.
 
I've been a pescatarian since 1986 so my diet is pretty pretty. I WILL lie about the doctor telling me to lose a few pounds though! :LOL:

Actually, about a month ago, I started with a nutritionist who can provide me with an interesting vegetarian meal plan. I needed some motivation and accountability to start cooking good, healthy meals again. I have been eating too many Trader Joe's frozen vegetarian meals since the pandemic started. I've lost 7 pounds over the last month by eating more food every day! My 4 COVID pounds are gone plus a few more.

How did you find them?
 
No one has ever (without cherry picking the data) shown that cholesterol has anything to do with heart disease. The original seminal study was seriously flawed and eliminated any data that didn't validate their hypothesis. That is very bad science yet still quoted as the reason for assuming cholesterol has anything at all to do with heart disease. It is an associative finding and not proven to be causative. So curing something that is a symptom doesn't stop the actual disease. I believe the real culprit is poor food, high sugar diets, pesticide use, etc. Returning to our old diets pre-WWII is probably enough to stop all of this. Of course, there are proven means to reverse all of this by switching to a ketogenic diet and eating low carbohydrate foods from clean sources. But, the western diet uses so much sugar it is actually insane and extremely addictive so tough to change. I am now nearing 1 year on the keto diet and am in the best shape of my life. I can't reverse everything but I am the same weight I was when I graduated high school (50 years ago) and physically as good as ever with super endurance. I have no disease at all now. Even my gastric reflux is gone. My hair went from white back to semi-blonde. So, there is definitely something good to be said to the keto diet just from my own results. The labs are all perfect now as well. I even had high Vitamin D levels without supplements.

Finding clean foods is a challenge though. This was a major part of our decision to move to Hungary where GMO foods are illegal and all foods are free range, and only use pesticides with a 72 hour half-life. There are no factory foods here at all, no preservatives, no nothing. You look at labels and all that is in there is actual food. It is mandatory to show where foods come from and I avoid anything not produced in Hungary. It is not difficult to do.
 
I had fun writing the post. The bus analogy finally clarified for me LDL and HDL cholesterol particles. There's also VLDLs and IDLs and chylomicrons, but I didn't get into that. Thanks for the feedback. What has been said is the more you study this stuff, the less you think you know. It's true!

Thank you so much for writing the post the way you did. It is helpful.

I am anticipating a slightly energetic discussion with my somewhat young new doctor in 5 months. Last vist he told me to lose weight so I went on a keto diet which is helping. But my LDL went from accepted range to out of range. (151 - typically it runs closer to 100 calculated.). He wants to put me on statins and I don't really want that.

We will see what the LDL is before my next appointment. Maybe I can get him to measure small and large LDL. My cardiac score - just done - was perfect. No detectable deposits. 63 years old.
 
ImThinkin - The heart score is a hit or miss. I supervised a large scale clinical trial using EBCT in younger men (under age 65) and it proved worthless. It is good for older men (above age 70) and has value. It is useful as it establishes calcium deposits in plaque which are what causes platelets to aggregate and start the inflammatory/coagulation cascade resulting in an ischemic event. Earlier attempts were made to measure plaque in carotid arteries and again proved worthless. I myself fell victim to this problem while in the military back in 1999. They determined I had major plaque deposits and started me on 100 mg/day lipitor (10 times the normal dose). The result was I had cataracts in 3 months due to the high dose lipitor. Later, the use of ultrasound for plaque measurement was debunked and found to not only be worthless but led to inappropriate treatments (like myself). I haven't had a statin since and had the cataracts removed in both eyes.

I wouldn't worry about any lipid levels at all. I believe (and many others as well) that our lipid levels go up as we age and it is perfectly normal. HDL was not found to actually be protective following a study where they engineered a particular type of HDL found in a genetically related group of people in Italy with zero heart disease but high lipid levels. It was hypothesized that they had n altered HDL molecule which protected them. Injecting this into others (in animal models) actually did nothing at all. The basic problem is we must have cholesterol and it must be readily available. All out hormones are made from it. Altering the lipid metabolism in the liver (which is what statins do) alters a lot of different things. Some are bad such as significantly higher risk of gallstones. In my case lipid deposits in the eyes causing cataracts. Personally, I don't believe in medication as a solution when diet and exercise perform better. Overall deaths due to ischemic events hasn't significantly altered despite massive use of statins which ought to be a major clue. It has gone down a bit but usually people going onto statins also modify their diets, at least for a short time so separating out the cause/effect is difficult without doing a long term (not 3 months) double blinded major study.
 
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