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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Dr. Greger is not a fan of eggs. Cites studies. Short video, approx. 3 minutes.
Is One Egg a Day Too Much? (Dr. Greger)
I posit I look healthier and fitter than the doc. I have been eating at least 6 eggs a week for many decades. My mother ate eggs almost daily for her whole life, and tons of bacon. She came from a farming background, and eating such foods was typical for people in that community. She was never overweight and lived to age 93.
There are plenty of YouTube docs, etc., that will refute what he is saying.
Your lipid levels are key. As I have previously posted, my lipid levels are very low. And yes, I take atorvastatin and bempedoic acid.
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C’mon Desertshores, you must know by now that anecdotal “evidence” is essentially worthless. “My uncle smoked 6 packs a day for 60 years and died at the age of 106 from a tractor accident.”
This is why scientific studies are done.
Greger directly addresses this in the video.
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I don’t want to watch the video but is he refering to dietary cholesterol being an issue? If so, ezetimibe comes to the rescue.
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I personally don’t listen to extreme doctors, Dr Gregrer isn’t objective as a pro vegan. It the same problem with keto doctors, carnivore doctors, or whatever doctor. Eggs are the perfect source of complete and ultra digest protein, it is high in minerals such as iodine and selenium wich people tend to be deficient in, and the best dietary source of choline and b vitamin in general. It also contain zeaxanthin for eyes health. To me we should eat way more eggs.
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No, time and again anecdotal evidence has led the way to discovery and studies.
Of course anecdotal evidence is not as good as randomized trials. But it differs mainly from observational trials only in the number of reports.
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I’m not necessarily endorsing Dr. Greger’s stance, just presenting his case. Dietary cholesterol is part, but only part of the case. He does cite studies fwiw. I personally do eat eggs regularly, though it’s usually around 2-3 a week, rarely 4. I think, that as so often, there are individual differences, for some, eggs may be pretty negative, while for others not at all. As usual, it’s the totality of the diet that matters. To give an extreme example, imagine that you are quite deficient in protein and vit. B12 - do you think eating some eggs would be a health negative in this scenario? It’s absurd. Everyone has their own “best diet” for them. Broad population level trends may not apply to you specifically.
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Greger is Good, Actually
Although I wouldn’t link Greger to a meat eater or carnivore, he’s pretty good on average. I can only speak from experience whenever I have a suspected health issue I look up what Greger have said, take that as you will.
He partly red-pilled me on LDL-C and saturated fats 10 years ago, He has discussed longevity for a long time, he seems to care (not in it for $ only). Similarly I think David Sinclair Is Good, Actually.
If I would link something to a meat eater I would link Peter Attia instead or Nutrition Made Simple.
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Does eating eggs contribute to atherosclerosis? Likely for some people, but it may not be the added cholesterol. Those at risk are producers of TMAO. Whether or not you generate TMAO after eating eggs depends on your gut microbiota. I, unfortunately do generate TMAO in significant quantities after eating eggs, and likely other animal protein. You can determine your TMAO production proclivity by having a blood test for TMAO. On a close to vegan diet my TMAO levels are very low. After eating eggs my TMAO levels are sky high. Sadly, as a result I eat very few eggs.
Here’s an explanation from “openevidence.com” for the question “Are TMAO levels linked to risk of heart disease ?”
Elevated levels of trimethylamine N-oxide (TMAO) are associated with an increased risk of cardiovascular disease (CVD) and coronary heart disease in multiple large cohort and prospective studies, though the strength and independence of this association may be influenced by renal function and dietary patterns . Egg consumption is a significant dietary contributor to circulating TMAO, with the association being more pronounced in certain populations, such as Americans and US Hispanics/Latinos.[1][5-6]
Mechanistic and experimental evidence suggests TMAO may promote atherosclerosis and CVD through effects on cholesterol metabolism, inflammation, and platelet activation, but causality in humans remains debated and may be confounded by kidney function and other risk factors.[3][7-10] Some studies and reviews note that TMAO is more strongly linked to plaque instability and adverse cardiometabolic biomarkers than to the extent of atherosclerosis itself, and that modest elevations in TMAO from diet may not be directly pathogenic in healthy individuals.[5][8][10]
Further research is needed to clarify the causal role of TMAO in CVD, especially regarding the impact of egg-induced TMAO elevation in diverse populations.[7][11]
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Leading Journal
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Since joining this forum, I have read numerous studies, and one of the main limitations I have found is the lack of consideration for confounding factors.
This uncertainty raises questions about whether the variable being examined is actually the one causing the effect.
One of the main things I want to see when examining aspects like diet is a BMI table or graph versus the variable being examined. It would be a relatively easy and reasonable thing to do in any study involving diet, exercise.
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I agree. It’s a bit of a curse of that type of science really. I’m not an epidemiological expert at all, but I get the impression that it’s almost impossible to really consider all confounding factors while still having a meaningful conclusion. Like the question “is exercise good for you?” is handled by normalising for income and geographical location, but also BMI, body fat %, bone density etc. In other words, during the process, you end up actually removing a lot of the benefits which were derived from the exercise.