#21

In their study, first published July 19, 2021, in the European Heart Journal, the researchers suggest that for people with relatively low levels of LDL cholesterol, a measured RC level greater than 24 micrograms per deciliter (24 millionths of a gram in a little more than a quart) of blood have a 40–50% higher risk for major heart disease or stroke.

Calculate yours:

https://erase.ualberta.ca/remnant-calculator/

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#22

Thanks Gregg that was nice of you to do that for me - I don’t understand how just doing that can tell remnant cholesterol but I’ll take an excellent number among all the other bad ones. :slight_smile: I got through 2 hours of Peter and Tom today but am burnt out for now. Thanks for posting Admin.

#23

You should try some lab test that determines specific production markers and absorption markers, the tests have been cited by Tom Dayspring and are available in specialized labs, like this one.

https://bostonheartdiagnostics.com/test/boston-heart-cholesterol-balance-test/

I think you may also be both, Destrider addressed this eventuality by adopting a brute force strategy, taking 3 drugs.

#24

I hate to be a party pooper, but based on that chart I could not rule out the possibility of atherosclerosis.
First, the first subgroup is very limited in number: n=2, so the probability of atherosclerosis being zero is a very unreliable conclusion. I would rather take the first 3 subgroups with n=52, according to such extended subgroup you would have a 15-20% probability (estimated by myself) to have atherosclerosis. This conclusion is far more realistic.
But it is not all. In the graph the temporal horizon is not specified. According to Allan Schneider and the school of modern lipidologists, the timespan for atherosclerosis to develop would be about 30 years. So, if their hypothesis is true, a very important parameter is missing, perhaps it’s cited in the text of the article, perhaps not, if the timespan evaluated by the study is sufficiently long, close to 30 years, then the conclusions would be reliable, otherwise less and less reliable the shorter the timespan.

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#25

We do have other studies showing plaque regression starting at <80mg/dL LDL-C.

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#26

Yes, the n=2 bothered me. However I am also excited by the fact that my father and I have an ApoB below 50 of which there are no members of this study. There’s also some evidence that very low levels of LDL and ApoB can cause arteriosclerosis to regress. We have my father’s CAC score of 352 as a baseline (from his 77 years of LDL 130 before he took this seriously). We are interested to see if we can lower this score with low LDL and ApoB.

According to his echocardiogram though, the doctor sees nothing to be worried about or require any action such as a stent.

I also tend to err on the optimistic side as I hope the placebo effect will kick in and my body will perform better. Mind over matter as they say.

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#27

Very astute strategy that stacks a 4th factor, of a mental nature, on top of the 3 pharmaceutical factors already used. I admire this brute-force approach.

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#28

That’s very interesting that the drugs may knock down the score. I was strictly plant based a couple of years and followed Dr. Caldwell Esselstyn and he showed an x-ray of an artery becoming unblocked after his patient went plant based but his program for those with serious heart disease is very very strict.

#29

Thanks - I don’t think I want to go as far as sending blood off but will tell my doc about this and the option of 3 drugs. One thing I noticed looking through their tests though is that Interleukin 6 is an indicator of heart disease or inflammation. I went to Stanford for my chronic fatigue and they tested a bunch of those interleukins and 6 was in normal range. I looked back at the results during COVID because it was mentioned a lot in regards to that. Course, I was 60 then, not 71.

#30

Do any of you statin aficionados know if there is a real difference between the glycemic impact of long-term use of one statin vs another holding LDL-C lowering impact constant? E.g. any difference between 10mg of simvastatin and 20mg of pravastatin?

#31

It’s not from lowering LDL-c.

Atorvastatin > Rosuvastatin when it comes to diabetes risk.

Pitavastatin > Atorvastatin for increases in blood glucose.

#32

FWIW: I have been on statins of some kind since 1990 and never had any issues (that I know of…). I am almost 66 and take 10mg ezetimibe and 10mg rosuvastatin both in the evening. I also take fenofibrate 48mg in the morning. crestor IS a statin. ezetimibe is not a statin. I’m thinking of stopping the fenofibrate as my numbers are pretty good w/o taking it and it can cause issues in older people.

#33

(Post Deleted By Author)

#34

Just so it’s clear…

Atorvastatin is superior to rosuvastatin when it comes to diabetes risk and cataracts:

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#35

I say holding LDL-C lowering constant deliberately.

To the extent the glycemic impact is through HMG-CoA reductase inhibition it will be a class effect. I don’t need anybody to explain that rosuvastatin has a greater LDL-C reduction than other statins at the same dose, but that’s not the point.

I am interested in understanding if there are differences between the statins holding LDL-C impact (not dose) constant.

#36

Yes, like I told you, unless you believe the 0.1 mmol/L difference in HMGCR Inhibition is the cause.

#37

This is what ChatGPT said. It’s consistent with your two directional claims.

Statin Dose for ~25% LDL-C Reduction Impact on A1c Risk of New-Onset Diabetes
Pravastatin 20 mg Minimal to neutral impact Low risk, possibly neutral effect
Simvastatin 10 mg Slight increase in A1c (~0.1%) Moderate risk
Atorvastatin 10 mg Slight increase in A1c (~0.1%) Moderate to high risk
Rosuvastatin 5 mg Slight increase in A1c (~0.1-0.2%) Moderate to high risk
Fluvastatin 40 mg Minimal impact, possibly slight increase Low risk
Lovastatin 20 mg Minimal impact, possibly slight increase Low to moderate risk
Pitavastatin 1 mg Minimal to neutral impact Low risk
#38

The incidence of diabetes was 39% higher with rosuvastatin compared to atorvastatin at around the same level of HMGCR inhibition.

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#39

I am going to ask my doctor about pravastatin. I want to reduce my CVD risk for the long term, but I don’t need to nuke my apoB.

#40

Just to be clear I wrote about pitavastatin, not pravastatin.

I don’t worry that much about different statins except which one I tolerate the best, but based on the data lipitor seems safer than crestor.

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