I stopped taking any powders for that reason. Being mostly a vegetarian, I’m trying to supplement protein, and decided in favor of whey as byproduct of kefir when heated to make home cheese. My blood albumin is normal so I figured it works. And it’s always fresh.
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Bempedoic Acid is superior to a statin because it has far fewer potential side effects and roughly the same effectiveness of a statin. It’s just harder for most people to afford/purchase.
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Hey Beth, thanks for the detailed reply also! That’s an “impressive” family history, wow!
For the part I quoted, I don’t think any more scans can predict or tell you that something is imminently going to happen - at least, none that I am aware of. And you’re already being super proactive. And actually, I disagree with you. I think with all your interventions, IMO it’s unlikely you’d have significant soft plaque nowadays anyway. Low inflammation, low BP, low lipids. What would be building it?
If you never tested it before, yes Lp(a) is definitely worth doing. It’s very genetically determined, so if yours comes back low, then that’s awesome news and you basically don’t have to worry about it. If it comes back high, it means you have some extra CVD risk and you’d want to be more aggressive than usual at tackling LDL-C/ApoB. Supposedly some drugs for Lp(a) are doing well in trials and should be with us in 1-3 years.
Homocysteine might also be a potentially useful thing to measure. It’s a marker that correlates quite well with vascular inflammation, oxidative stress and thrombogenicity - obviously all important for cardiovascular disease. (Though it’s not totally clear that homocysteine participates in the disease process, or that trying to lower it is beneficial.) But perhaps knowing whether yours is optimal, normal or high could help direct other decisions.
hsCRP is also pretty valuable IMO as a general marker. Again, it’s a really good “where am I at?” kind of marker. If it comes back low, you’re all good. If it comes back higher than expected, there’s something to address.
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Ha, if you wanted to be really impressed, I could share that my mom’s mom had ALS, mom had Parkinson’s and my grandmother’s only other child, my aunt, has something ‘like’ Parkinson’s (I always forget the name). One could say I’ve won the genetic lottery !!! 
Did I mention I have awesome blood pressure? 
Ok, so I might be learning something important here for the first time…
So, I have assumed that I was building a lot plaque my entire life until I started repatha a few years ago (I don’t remember when but I was a fairly early adopter… so what is that, maybe 7 or 8 years ago ish?), and then building much less or no plaque more recently when starting ezetimibe a year ago.
So what happened to all the soft plaque I was building until repatha — and then the small amounts I was building until I got my apob down to the low 40s only this year?
I assume some of it turned into hard plaque. And then, I assume some of it remained soft (I don’t know why I assume this? I never thought to ask!). And I also assume nothing gets rid of soft plaque… that it either hardens or hangs around as soft?
So, if I’ve been building plaque steadily as time went on until my later years when I became aggressive (I’m 59), wouldn’t it follow that a bunch of it is still there hanging around as soft?
Are you by chance saying that the stuff that was soft prior to me becoming aggressive MIGHT have all hardened by now?
Or are you saying that if I have a lot of soft, I’ve had it for a while now, and nothing has happened yet so no reason to think that will change now?
I realize hard plaque could break off at any moment and this might be my last post … but I also would have to think something could change with my soft plaque or something, otherwise why would the cardiologist want me to come back in 6 months for a stress test?
Your comment opened up a lot of new questions that I never knew to have, so thank you for that! The more I learn the more I realize I don’t know!
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FWIW, one way in which statins stabilize plaque is by calcifying it. That’s why you might get a higher CAC score after being on a statin for some time (obviously it doesn’t happen overnight). Calcified plaque may contribute a bit to stenosis, but the main danger is ruptured soft plaque blockage in MACE situations, and calcified plaque is less prone to that. If you want to try a statin again, you might give pitavastatin a go, as it’s less prone to muscoskeletal and glucose issues. And yes, you want to keep systemic inflammation low. If you are measuring hsCRP, it’s even more useful to measure IL-6, because the CRP can refect short term transient inflammatory episodes, while IL-6 gives you better insight into your inflammatory status. IL-6 is also better correlated with CVD outcomes than hsCRP, especially in the context of Lp(a), I posted a bunch of papers showing that. Of course, as always, the question is, ok, you have that info about IL-6, but what can you do about it.
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You might want to review this post I made here, showing that events lower further to 30 mg/dl LDL-C and regression of plaque linearly increases to 20 mg/dl (and lack of data of lower than that presumably).
It’s Linear All The Way Down, it seems. We already know it’s the case for higher LDL-C levels.
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There is also the option to play around with 1mg pitavastatin, 1.25mg rosuvastatin or 20mg pravastatin along with 2.5-10mg ezetimibe which is realistically as good as it gets in terms of statin tolerability and LDL-C reduction.
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Soft plaque can stabilise (and calcify, thus increasing CAC), but it also absolutely can also be regressed and reduced in volume. That’s shown in many studies. Some of the volume reduction is removal of lipids (if circulating concentrations are lower in the blood than in the vessel wall, you can get diffusion in the opposite direction), some of it might be removed by HDL particles, and some of the volume reduction it is the resolution of inflammation, immune cell apoptosis etc, all of which shrink the plaque.
I don’t want to be too misleadingly over-optimistic about it because what I know of the literature shows that regression in volume can happen, but probably not a true “reversal”. I think yes, probably you were building more soft plaque while your lipids etc were bad. But you’re now doing all of the key parts like lowering ApoB, lowering inflammation (you mentioned colchicine) and preventing further damage. So IMO there’s no reason to believe yours wouldn’t have partially regressed and you probably shouldn’t be laying down any more soft plaque. And whatever was there should calcify and stabilise (which can take ~5 years in untreated people but might speed up to 2-5 years in people doing aggressive therapy like you)
(Obviously you can’t know without a scan, but that goes to our earlier conversation that there probably isn’t much value since you’re already aggressively treating it).
Anyway, it seems you’re doing everything right, and obviously you’ve got a nice cardiologist! As for why they want to stress test you - you’d have to ask them! 
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Once you have plaque there’s no going back. All you can do is reduce your risk of an event and not make it become worse than it already is, and the later you take action, the higher the residual risk will be. It’s not possible to reverse ASCAD. It’s also the reason why pharma companies can’t claim reversal.
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So plaque volume can be regressed but not reversed? What’s the distinction there?
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The distinction is that we don’t have decade-spanning clinical trials showing complete plaque reversal over time.
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And perhaps the distinction should be between soft plaque (possible to reverse) and calcified plaque (not currently possible to reverse)
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It looks like you won’t increase total plaque volume and even regress and to a clinical relevant degree over 3 yrs, that’s how long trials seems to have been at most, using gold standard IVUS.
There are many who keep their LDL-C suboptimal and continue to increase their total plaque volume.
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Some trials have shown a reduction in plaque “volume”. Bear in mind the total volume is made up from a lot of stuff - lipids, immune cells, immune cells which ate too much lipid (foam cells), smooth muscle cell infiltration and proliferation, plus general fluid accumulation and inflammation.
If you can put yourself into a very anti-atherogenic state - with low circulation lipoproteins, low inflammation etc, that volume can be reduced due to some removal of lipids, and resolution of the lipids. That’s what we would call “regression”, and you might see a change in the total volume on a scan, probably correlating with overall stabilisation of the plaque. This is a part of how secondary prevention works to prevent future events.
Calcified plaque can’t be reversed, and I can’t plausibly think how it could be done aside from surgical procedures. Even then, I’m not totally sure you’d want to disturb stabilised plaque. If blood flow is not obstructed, maybe it’s better to leave it (but I’m not a cardiologist or cardiac surgeon, so I don’t know).
“Reversal” implies that you can go back to normal, which I don’t think is possible. Once you have lipid accumulation, I am not aware of anything that can remove it all and restore a totally fresh artery wall.
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Thanks to all of you for the master class on all things plaque! Truly incredible!!!
I truly appreciate the time you have all put into educating me!
@CronosTempi, my crp from 1/25 was .75. I don’t know what ‘excellent’ would be, but I assume that is pretty good? Also, I will go through my past labs, but I don’t believe I’ve ever tested for IL-6, so thanks for that tip.
Thanks to all of you for the master class on all things plaque! Truly incredible!!!
I truly appreciate the time you have all put into educating me!
My crp from 1/25 was .75, @ronso
. I don’t know what ‘great’ would be, but I assume that is pretty good… just a guess!
I will go through all my labs, but I don’t believe I’ve ever tested for rllllll , so thanks for that tip.
Also, I will start toying with the idea of trying a statin again… maybe crumbs a couple times per week, hmmm?
This would be to try to receive more benefits by reducing my apob from 43 and my ldl c from 38, as a result of the information you’ve shared with me @anuser. . The other alternative is to discuss the possibility of increasing the dose of my other rx’s.
@relaxed, your efforts paid off because you painted a really clear picture for me, which is not easy to do
If I’m understanding your comment correctly, once you stop laying down new plaque, your soft plaque calcifies within 5 years -ish ? If this is true, that is definitely incentive for me to try a a statin again or increase my other meds because, thus far, I have had no luck getting my apob in the 30’s .
Also, I will start toying with the idea of trying a statin again… maybe crumbs a couple times per week, hmmm?
This would be as a result of the information you have shared @AnUser and how reducing my apob from 43 and my ldl c from 38 might still provide significant benefit. The other alternative is to discuss the possibility of increasing the dose of my other rx’s. I still need to see what ideas Braunwald shares as soon as I can dig in.
@relaxed, your efforts paid off because you painted a really clear picture for me, which is not easy to do
If I’m understanding your comment correctly, once you stop laying down new plaque, your soft plaque calcifies within 5 years -ish ? If this is true, that is definitely incentive for me to try a a statin again or increase my other meds because, thus far, I have had no luck getting my apob in the 30’s .
Again and again, thank you all so very much……
Approximately, yes, assuming you’ve resolved whatever was causing the new soft plaque formation! (But of course usual caveat that these are best guesses, since obviously we don’t have multiple opportunities to sample peoples arteries and put them under the microscope etc).
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Our discussions on reduction targets for lipids and inflammation to stop or slow down atherosclerosis are based on the risk data from many studies. This data is helpful but has (at least) two problems. First, as far as I can tell, none of these studies include data on LP(a), so that we have no idea how minimal or excessive numbers of study participants with high LP(a) numbers have influenced the lipid reduction targets that we are using to try to figure out what to do for ourselves. Second, exactly none of these studies include any data on participants taking intermittent low dose (ie - 6mg/wk) of Rapamycin. The following (2019) article, which is not an easy read, suggests that those of us using low dose, intermittent Rapa may be getting significant benefit in terms of its reduction of the atherosclerotic process. If that’s the case, then the lipid targets we are trying to achieve using statins etc may be more than needed with our intermittent low dose Rapa use.
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The studies’ vibes are telling me that an LDL-C <70mg/dL is enough for the average overweight person with low lp(A) and pre-diabetes at most. If you have high lp(A) or diabetes, aim for <55mg/dL. If you have high both, aim for <40mg/dL.
Luckily I have both low lp(A) and HbA1c.
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Good points. I think we need to take a 1 + 1 + 1 approach.
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We pretty well understand LDL-C/ApoB.
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And we are now pretty well understanding the risks from Lp(a) and its independence and interdependence with ApoB:
https://www.ahajournals.org/doi/10.1161/ATV.0000000000000147
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.124.069556
- And then we have Rapamycin, which is the biggest unknown. Maybe it helps by reducing atherosclerosis, but maybe it hurts by making lipids/glucose worse (at least on blood tests, they look worse.)
However, I would point out that it’s probably not super helpful to try and be too accurate or pedantic about biology. After all, all of these things are probabilities and there’s a ton of variability between individuals. There are people who have had lifelong > 200mg/dl LDL-C and have no atherosclerosis when they die of something else, and some people are unlucky with lifelong <100mg/dl who die of early MI. So even if we had good evidence, it’s no guarantee. All you can do is try and stack the odds in your favour.
To my mind, I think most people should simply want ApoB and Lp(a) to be as low as they can reasonably achieve, using the methods they’re happy to use and tolerate. And I would say that’s a good idea, regardless of whether taking Rapamycin or not.
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I believe that to be the case. After starting rapamycin at ~82 years old, I am essentially pain-free except for some lower back problems when walking.
I have been taking 5 or 6 mg with grapefruit juice. For those wondering about grapefruit juice and possible negative effects, I have never noticed any, and I have been using it with rapamycin for years.
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