Cardiovascular Health

#2052

I honestly don’t know about 0mg/dl. But I’m quite well convinced that there’s no such thing as “too low”.

However, I would think that your method of reaching very low levels is important. For me to get sub-40, I’d likely need to go high intensity statin, maybe up the Ezetimibe, increase the frequency of Repatha. And while I strongly believe in the drugs, none are without side effects, and higher doses pretty much always mean more off-target drug effects.

I think the best evidence we have is the PESA study:

Sorry to hear about your acquaintance. But yes, this is unfortunately super common, and the evidence shows again and again and again that “normal” levels of circulating LDL-C can build plaque and kill you. If you’re interested in living to 100 you need to choose good parents (i.e. be genetically lucky never having high LDL-C, or being very resistant to plaque formation/rupture), or you need to control your lipids.

I know a neighbour who died in his sleep from a massive heart attack at 45. Fit, healthy and active guy on the outside. I used to see him always loading up the van to take his kids camping, hiking etc. Fit and healthy on the outside, but building plaque on the inside. Now he’s dead and they hit adolescence without a dad. You simply don’t know how the genetic lottery was drawn until you test and treat.

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#2053

What is the taste and texture like compared to whey?

#2054

That’s why everyone should take Ezetemibe and a low dose statin. Or at least Ezetemibe. Arteriosclerosis affects everyone to some degree and will kill 1 out of 3 people on this planet.

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#2055

It’s fine, though likely whey tastes better (to me - last time I’ve had whey protein was about 25 years ago). However, I find the issue of taste irrelevant in the case of protein powders, because the way I consume it - in a soup/slurry with tons of other ingredients, the taste is completely overwhelmed by the other ingredients.

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#2056

I have mine in a bowl of cereal in the morning with other powders. And I have it with yogurt, or oatmeal.

I do a pretty good oatmeal dish with cinnamon and blueberries.

what about bempedoic acid instead of statin?

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#2057

Bempedoic Acid is preferable to a statin. However most doctors won’t prescribe it and it’s too expensive for most ordinary folk.

The only way Bempedoic Acid works is if you order it from India, and that’s a bridge too far for 98% of the worlds population.

We’re the lucky 2%.

I take Bempedoic Acid and Ezetemibe (daily) along with 5 mg Atorvastatin (4 days a week due to muscle fatigue).

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#2058

I appreciate the time you took with your detailed answer.

I agree there is no reason for me to ever do another CAC. In fact, I’ve had 3!

I had one when I was aprox 40 that put me in the aprox 95th% and was then convinced to do another one years later with the thinking that, well, not many people have much plaque at 40, so now that you are older, perhaps your relative percentile will have decreased now that everyone else has caught up… as expected, that did not happen, nope, not even close! And then at almost 50, my current doc met me during an executive physical and didn’t believe my results, so he convinced me to do another one (the ol’, you look fit and healthy, so those numbers couldn’t be accurate)

My blood pressure happens to be great, and I savor it as it’s one of the only positive health things I have going on!!! I’m normally around 110/70. Interestingly, after they put a bp cuff on both arms and got similar numbers (which no one had ever done), the doc did another thing I had not previously seen. He put on a different type of cuff with a hand held device that resembled a compass which is apparently more accurate. That result was aprox 117/74.

I don’t take statins because they make me feel glued to the sofa, but if I thought they could be life saving for me, in addition to what I’m already doing, I would be open to giving them another try. I haven’t tried them in over a decade. And on that note, good to see you also respect the opinions of Braunwald, who @AnUser shared with me.

I agree that, for me, I don’t need a CLEERLY CCTA to learn I have hidden heart disease in order to create a treatment plan and convince me to eat well, etc. It would be nice to see that I have very little soft plaque for a sigh of relief, but I would imagine those odds are extremely low for someone with my CAC score, so having radiation for that hope doesn’t seem like a good gamble.

My ONLY incentive to have one is due to @DeStrider ’s tragic example. My goal would 100% be to only detect if there was something imminent that was going to happen in order to prevent dropping dead with no warnings. And I guess, yeah, if things looked bad, I’d happily decide to suffer and take statins even if I didn’t feel as well… death is a huge motivator!!!

My mother’s father dropped dead of a heart attack in his 40’s with no warning. My father had one in his 40s with no warning (was fine afterwards). My ex brother in law had an ekg for an unrelated reason, and they said he had a major heart attack the week prior and 1/3 of his heart muscle died (I don’t know how they knew the timing).

The only thing he knew was that after a soccer game, he was unusually tired. He’s probably only alive now due to the dumb luck of this other procedure he was going to have, which then facilitated him getting on medications to prevent another incident.

@AustraliaLongevity It seems that we are genetically wired to be able to tolerate sat fat or not (maybe never THAT many eggs in one sitting, but I don’t really know). I had heard many reports that sat fat in fermented foods doesn’t impact your lipids, so in the fall, I had one coconut kefir drink on many days for a month and then ran labs… my lipids went up…. back to my no coconut sad life *heavy sigh. PS I don’t notice anything from taking ezetimibe. Also, I use two different protein powders. I use Kachava which is just because it’s yummy to me and makes choking down protein more enjoyable. But, I also buy NorCal Organic Pea Protein powder… it’s not yummy but it’s perfectly fine to me. I’ve tried various other brands of vegan protein and I like it more than everything other than Kachava. I do hear whey tastes better but I don’t know ?

@DeStrider I might have missed the explanation, but why is bempedoic acid preferable to a statin? I’m now taking Brillo EZ but I just don’t notice anything dramatic since adding ba to my ezetimibe, which is why I ask. Just curious.

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#2059

As in side effects?

Yea I think it’s time I get on some of these medications. I want to wait until my next comprehensive blood test before doing that though just to see how my current protocol is affecting my lipids and other markers.

BTW does anyone know some good markers to throw in my blood test? I was thinking Lp(a).

#2060

Oh sorry, that was unclear… yes, I meant side effects. It had a positive effect on my labs, but I don’t feel any side effects from it.

I agree you should add Lp(a)
Apob, as I assume you’ll do
I’m sure there are a million other good items to add, but I’m not a good source for those.

#2061

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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#2062

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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#2063

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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#2064

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 !!! :slight_smile:

Did I mention I have awesome blood pressure? :wink:

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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#2065

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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#2066

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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#2067

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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#2068

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! :stuck_out_tongue:

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#2069

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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#2070

So plaque volume can be regressed but not reversed? What’s the distinction there?

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#2071

The distinction is that we don’t have decade-spanning clinical trials showing complete plaque reversal over time.

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