LPa at 183, Worried About Heart Disease — Which Peptides Best Target Inflammation?

[lessthanhalf]

I'll add my voice to the suggestion to get a cardiologist involved. Even if someone has dropped a lot of weight, a past weight of more than 500 lbs can still leave them in a very high-risk group, regardless of whether other lab values look fine. In my own case, it wasn't until after the weight came off that I learned my heart had already taken some damage. That knowledge affects how hard you should push treatment, so hearing from a specialist is worthwhile. Cardiology happens to be one of the most research-driven fields in medicine, which helps.

 

[Chucky]

lessthanhalf said:


The first thing done was a stress echo, as I had some odd symptoms of weird breathlessness while still very overweight, and it took forever to get it organised and I had already lost a lot of weight by the time it got done. No ischaemia was seen, but it showed an ejection fraction of 50% and mild left atrial and ventricular enlargement, so class b heart failure ( without symptoms but structural changes and mildly reduced ejection fraction, should have been 55%+ ) As best I can find out this has a risk of turning into symptomatic heart failure of 1-2% a year, assuming I take blockers and ace blockers and do not regain the 80 kilos I lost, overall this is probably a bigger risk than the risk of heart attacks from the high CAC, as reducing those risks with statins etc is easier. 10 year risk untreated 20-25% MACE , about half that with treatment , statin, ezetimibe, clopidogrel, assuming I do not regain weight, making the GLP drugs literally required to stay alive, as I would guess those risks would skyrocket with massive weight regain.

I have had an echo done every year since or 2 more with no significant changes which is hopefully a good sign. My reading of the science said the CAC and angiogram were probably not needed, but I deferred to my GP and cardiologist's advice. Angiogram showed 15% right coronary artery stenosis and 50% left anterior descending stenosis, so no fixable problems. ( mainly done to see if critical narrowings that could be fixed to prevent worsening heart failure, as the above comment explains I already qualified for maximal medical therapy for atherosclerosis, I was not sure the science supported getting it done, but not much point seeing specialists then ignoring their advice even if you have read the literature, clinical experience cannot be obtained by reading papers)

Click to expand...

You should definitely keep monitoring that. Last year it almost put me in a pine box. I happened to be at the gym when it hit, which was lucky, since a couple of ER doctors and nurses happened to be working out there as well. At the hospital, my ejection fraction was 39%, so I dodged one. After a triple bypass and a total overhaul of how I train, I’m hovering near 55% now.

 

[lessthanhalf]

Good to hear you came through it; outcomes aren’t always favorable. In my case, the harm accumulated quietly and gradually—decades of obesity, ulcerative colitis, ongoing inflammation, and very likely leaky gut problems. Beyond treating my body with more care and using medications, there isn’t much left except trying to make the progression as slow as I can. With GLP drugs, maintaining weight loss over the long haul becomes far more achievable, and that makes a big difference; it simply wasn’t an option in the past.

 

[Sector]

Pairing 5mg rosuvastatin with 10mg ezetimibe should clean up your cholesterol panel quite well—ldl, apob, hdl, and triglycerides ought to all move in the right direction. A low dose of rosuvastatin may additionally aid hs-CRP (inflammation) readings.

Since most of the upside comes from a low dose, I’d suggest adding ezetimibe to that low dose too; the two work very synergistically and stack, and for the majority ezetimibe is basically free of side effects and tolerated very well.

A lot of people give statins a bad name because they typically visit their doctor once a problem has built up over time, the doctor then prescribes a high-dose statin, and at a higher dose you’re more likely to experience far more side effects, while only gaining a marginal (insignificant) reduction. The dose is what makes it poisonous.

What’s the answer? Low-dose statin + ezetimibe (good for lowering, minimizes sides, and also improves bloodwork)

For anyone wanting to go really deep down the rabbit hole, this is a great read on cardiovascular health



Cardiovascular disease is a solved problem – Total Health Optimization

totalhealthoptimization.com

 

[Habibibi]

lessthanhalf said:

Habibibi said:

At this point, limiting the harm from elevated lpa mostly depends on driving ldl/apob down as far as possible (into the low 40s, and lower is always preferable). In practice, that tends to require statins plus pcsk9 inhibitors. GLP1s bring hscrp down, so that is beneficial.

The CAC score is nearly always of little value: a low number does not rule out unstable plaque, and unstable plaque is more dangerous regardless. A high number is not very telling either—when you take a statin, your CAC score will rise, since statins stabilize plaques, which appear calcified in the CAC.

That isn’t right.

For forecasting future cardiovascular events, CAC is highly accurate—maybe even better than angiography. Angiography does have great value when the goal is locating critical stenoses that could require stenting or surgery. What CAC reveals, though, is total plaque burden, and that ties very strongly to long-term risk. The majority of infarcts happen where there is no major narrowing. Instead, they arise where inflamed plaque ruptures, triggers clotting, and leads to a heart attack. The larger the plaque area, the greater the chance of that sequence.

Following changes with CAC isn’t generally useful or standard, apart from repeating it after 5 or more years in someone whose CAC is low. One key effect of statins is plaque stabilization. CAC usually comes into play when normal risk assessment puts someone at an intermediate level and a decision is needed about lipid-lowering therapy. If risk is already high, treatment is warranted regardless, and CAC adds little actionable information. With a zero CAC score, long-term absolute cardiovascular risk is very low; that is why zero scores have been examined using real-world long-term outcomes—a much stronger measure than the idea that non-calcified plaque might be a risk factor.

A few years back I got a CAC score. Mine was high, 645, and I was told that at age 57 this placed me in the 97th percentile for risk. I read a great deal, including the latest guidance from the US and Australia on how coronary artery disease is managed.

Right, that’s what I meant: it isn’t much use for prevention. It also doesn’t help when deciding if lipid-lowering therapy should be used, since apob serves as the gold standard, and lower apob is preferable.

 

[Tug Speedman]

Appreciate every response, everyone. Just 2 days back I got put on Pravastatin at 20mg/day, and Ezetimibe has already been part of my routine for roughly 8 months. Tomorrow is my CAC scan. Around 7 weeks ago I began dropping weight (using Reta). I was 265lbs at the start and now sit at 240lbs. My target is "skinny enough to make a difference for my health". For about 4 months nothing fried has passed my lips, I avoid liquid sugars, and carbs stay low (though I do take in a small amount daily). Exercise happens only about once weekly right now, but as I get lighter on my feet that is improving. Truthfully I am eager to get back to jogging. And yes, I might even accept the risk of muscle wasting once more and return to Rosuvastatin, reasoning "lets control what we can, for now". Possibly I end up in a clinical trial, or on Repatha + Statin + ezetimibe + etc. Or perhaps this Prava + Zetia I am taking, combined with shedding a total of 40-60lbs, produces the results I want. Time will tell.

To those who brought up seeing a cardiologist, Thank you! But I had already committed to that before it was mentioned. Mine is scheduled for tomorrow.

That said, it wasn't what I asked. Why? Because nearly any cardiologist focused on keeping Insurance claims moving will repeat the same line, "you cannot change high LPa, so the best thing to do is manage what we can". That statement is true, we know it. Yet we also know peptides are capable of remarkable things. Consider GLP1, the very reason we are ALL here. Has it rescued many lives from CV death? , Probably. But a cardiologist would never say so unless a full study over a long period of time is completed, approved for release and published in a medical journal somewhere. Right? So while I get to know the best that modern (FDA approved) medicine can offer, I will remain curious about what I can do on my own behalf to improve MY odds. Nothing wrong with that right?

I've come across claims that NAD+ Injections are a big No because oversaturation may accelerate possible clogging through something called "4Py", And similar warnings I've seen about Subq L-carnitine too (there goes the Lipo blends). That is partly why I wanted to ask in the first place. If certain Peptides and even supplements are a big NO. Then are any of them a Maybe, or even a Yes. For example, I was able to confirm NAC (the glutathione precursor) is a Yes!. Also my question concerned Inflammation reducing support, especially for the cardiovascular system. Thanks again everyone, ALL input is very much apprecited!

PS, did anyone else know that too much NAD+ and L-Carnitine can accelerate atherosclerosis? Has any ones cardiologist told them so? See, were learning in here!

 

[lessthanhalf]

Am I right that you're already taking a GLP? Evidence supports their ability—though perhaps not for reta at this point—to lower LDL triglycerides, HB1AC, plus heart attacks, strokes, and some forms of heart failure. They're a treatment worth using to cut cardiovascular risk, particularly when someone is obese or even just overweight.

Have your kidney and liver functions been checked? What about urine protein? (In severe obesity, abnormal results here are quite common, and that can point toward needing stronger lipid-lowering therapy or antiplatelet drugs even when all other findings are fine.) Metabolic syndrome may also affect the kidneys and liver, not only the heart.

 

[Tug Speedman]

lessthanhalf said:

Am I right that you're already taking a GLP? Evidence supports their ability—though perhaps not for reta at this point—to lower LDL triglycerides, HB1AC, plus heart attacks, strokes, and some forms of heart failure. They're a treatment worth using to cut cardiovascular risk, particularly when someone is obese or even just overweight.

Have your kidney and liver functions been checked? What about urine protein? (In severe obesity, abnormal results here are quite common, and that can point toward needing stronger lipid-lowering therapy or antiplatelet drugs even when all other findings are fine.) Metabolic syndrome may also affect the kidneys and liver, not only the heart.

Thanks for spending your time on this, lessthanhalf!

Every one of the 7 liver markers came back in the ideal band. Kidney markers were the same, with one exception: Anion Gap sat at 13.0, slightly elevated, which seems tied to ketones that weren’t measured. EGFR @ 85 was within range, though only barely—it landed in the Yellow. I eat low-carb rather than zero-carb, and the same goes for sugars. Urine looked clear and yellow, with no protein, blood, or nitrite.

Separately, one marker from another panel suggested insulin resistance. Let me find it. Got it: HOMA2-IR @ 1.6 landed Out of Range. Ferritin @ 247 was Out of Range too, though I’d eaten a fat liver steak a week before, so I’ll check that again next time.

In some way, I want to attribute the good liver and kidney numbers to the Glutathione round I finished a few weeks before the draw. I’ve kept my eating fairly clean over the past 5-8 months, and Reta definitely makes choosing clean foods effortless.

The charts label me Morbidly Obese; my scale puts my BMI at 31 (in the Red). Still, at 6'2" and 240lbs, I look a lot better than I did at 265 almost 2 months back. When I drop into the 215-220 range, people are going to start asking whether I’m sick. Yet the charts claim I’m meant to be 190lbs. I might go down close to that, but we’ll see—I still have to toss 100lb buckets of chemical around all day at work, so I can’t just shrink away.

 

[Sector]

Tug Speedman said:

View attachment 155

View attachment 156

Appreciate every response, everyone. Just 2 days back I got put on Pravastatin at 20mg/day, and Ezetimibe has already been part of my routine for roughly 8 months. Tomorrow is my CAC scan. Around 7 weeks ago I began dropping weight (using Reta). I was 265lbs at the start and now sit at 240lbs. My target is "skinny enough to make a difference for my health". For about 4 months nothing fried has passed my lips, I avoid liquid sugars, and carbs stay low (though I do take in a small amount daily). Exercise happens only about once weekly right now, but as I get lighter on my feet that is improving. Truthfully I am eager to get back to jogging. And yes, I might even accept the risk of muscle wasting once more and return to Rosuvastatin, reasoning "lets control what we can, for now". Possibly I end up in a clinical trial, or on Repatha + Statin + ezetimibe + etc. Or perhaps this Prava + Zetia I am taking, combined with shedding a total of 40-60lbs, produces the results I want. Time will tell.

To those who brought up seeing a cardiologist, Thank you! But I had already committed to that before it was mentioned. Mine is scheduled for tomorrow.

That said, it wasn't what I asked. Why? Because nearly any cardiologist focused on keeping Insurance claims moving will repeat the same line, "you cannot change high LPa, so the best thing to do is manage what we can". That statement is true, we know it. Yet we also know peptides are capable of remarkable things. Consider GLP1, the very reason we are ALL here. Has it rescued many lives from CV death? , Probably. But a cardiologist would never say so unless a full study over a long period of time is completed, approved for release and published in a medical journal somewhere. Right? So while I get to know the best that modern (FDA approved) medicine can offer, I will remain curious about what I can do on my own behalf to improve MY odds. Nothing wrong with that right?

I've come across claims that NAD+ Injections are a big No because oversaturation may accelerate possible clogging through something called "4Py", And similar warnings I've seen about Subq L-carnitine too (there goes the Lipo blends). That is partly why I wanted to ask in the first place. If certain Peptides and even supplements are a big NO. Then are any of them a Maybe, or even a Yes. For example, I was able to confirm NAC (the glutathione precursor) is a Yes!. Also my question concerned Inflammation reducing support, especially for the cardiovascular system. Thanks again everyone, ALL input is very much apprecited!

PS, did anyone else know that too much NAD+ and L-Carnitine can accelerate atherosclerosis? Has any ones cardiologist told them so? See, were learning in here!

That claim is wildly misleading—bordering on outright untrue. Did your cardiologist actually tell you that? If yes, I’d be seriously worried and would look for another cardiologist, perhaps one specializing in sports cardiology.

Now, regarding L-carnitine:

Some gut microbes turn L-carnitine into TMA, and the liver then turns that into TMAO. In certain studies, higher TMAO has been linked to a greater likelihood of cardiovascular disease. But a link is not proof of cause, and TMAO production differs widely between individuals because of their gut microbiome. As of now, there is no definitive proof that ordinary L-carnitine supplementation directly speeds up atherosclerosis in people.

^^ The crucial point is that your gut microbiome influences TMAO levels.

Nad + has an even stronger safety background:

Here the evidence is far less robust. The bulk of research has actually considered NAD+ potentially helpful for mitochondrial function and metabolic health. At present, no convincing human data show that NAD+ supplementation accelerates atherosclerosis.

 

[Tug Speedman]

Sector said:

Tug Speedman said:

View attachment 155

View attachment 156

Appreciate every response, everyone. Just 2 days back I got put on Pravastatin at 20mg/day, and Ezetimibe has already been part of my routine for roughly 8 months. Tomorrow is my CAC scan. Around 7 weeks ago I began dropping weight (using Reta). I was 265lbs at the start and now sit at 240lbs. My target is "skinny enough to make a difference for my health". For about 4 months nothing fried has passed my lips, I avoid liquid sugars, and carbs stay low (though I do take in a small amount daily). Exercise happens only about once weekly right now, but as I get lighter on my feet that is improving. Truthfully I am eager to get back to jogging. And yes, I might even accept the risk of muscle wasting once more and return to Rosuvastatin, reasoning "lets control what we can, for now". Possibly I end up in a clinical trial, or on Repatha + Statin + ezetimibe + etc. Or perhaps this Prava + Zetia I am taking, combined with shedding a total of 40-60lbs, produces the results I want. Time will tell.

To those who brought up seeing a cardiologist, Thank you! But I had already committed to that before it was mentioned. Mine is scheduled for tomorrow.

That said, it wasn't what I asked. Why? Because nearly any cardiologist focused on keeping Insurance claims moving will repeat the same line, "you cannot change high LPa, so the best thing to do is manage what we can". That statement is true, we know it. Yet we also know peptides are capable of remarkable things. Consider GLP1, the very reason we are ALL here. Has it rescued many lives from CV death? , Probably. But a cardiologist would never say so unless a full study over a long period of time is completed, approved for release and published in a medical journal somewhere. Right? So while I get to know the best that modern (FDA approved) medicine can offer, I will remain curious about what I can do on my own behalf to improve MY odds. Nothing wrong with that right?

I've come across claims that NAD+ Injections are a big No because oversaturation may accelerate possible clogging through something called "4Py", And similar warnings I've seen about Subq L-carnitine too (there goes the Lipo blends). That is partly why I wanted to ask in the first place. If certain Peptides and even supplements are a big NO. Then are any of them a Maybe, or even a Yes. For example, I was able to confirm NAC (the glutathione precursor) is a Yes!. Also my question concerned Inflammation reducing support, especially for the cardiovascular system. Thanks again everyone, ALL input is very much apprecited!

PS, did anyone else know that too much NAD+ and L-Carnitine can accelerate atherosclerosis? Has any ones cardiologist told them so? See, were learning in here!

That claim is wildly misleading—bordering on outright untrue. Did your cardiologist actually tell you that? If yes, I’d be seriously worried and would look for another cardiologist, perhaps one specializing in sports cardiology.

Now, regarding L-carnitine:

Some gut microbes turn L-carnitine into TMA, and the liver then turns that into TMAO. In certain studies, higher TMAO has been linked to a greater likelihood of cardiovascular disease. But a link is not proof of cause, and TMAO production differs widely between individuals because of their gut microbiome. As of now, there is no definitive proof that ordinary L-carnitine supplementation directly speeds up atherosclerosis in people.

^^ The crucial point is that your gut microbiome influences TMAO levels.

Nad + has an even stronger safety background:

Here the evidence is far less robust. The bulk of research has actually considered NAD+ potentially helpful for mitochondrial function and metabolic health. At present, no convincing human data show that NAD+ supplementation accelerates atherosclerosis.

It wasn't my cardiologist who told me that; it was Google . Truth is, I still haven't gotten a real conversation with my cardiologist. So until that happens, this forum and Google are what I've got while I wait . My CAC scan happened 3 days ago; I was told 2 days until results. But now they won't hand them over until an appointment is open. Even though I was the one who requested the CAC, and I paid on site out of my own pocket. On top of that, at least 2 or 3, maybe, online Cardiologist/Influencer people are waiting on my results.

Then I typed this into Google: "L carnitine supplementation and CVD" ""The answer came back mixed: L-carnitine has complicated, mixed effects on cardiovascular disease (CVD). It can support cardiac energy metabolism, but high doses may be converted by gut bacteria into TMAO, a compound tied to atherosclerosis and heart attacks.

I know you said association isn't proof of causation. Yet TMAO tends to be elevated when someone's gut microbiome is poor. Google even gave me a prevalence figure for that. 50%-66% of people in the US. That's over half the US population. For the UK, an article I came across puts gut disbyosis at 7 of 10 adults. That's ALOT of TMAO wandering around York. https://wecovr.com/guides/uk-2026-shock-new-data-reveals-over-7-in-10-britons-battle-a-gut/

My next search was "NAD+ supplementation and CVD" The response: preclinical data points to NAD+ and its precursors (NR, NMN) as possibly supportive for heart health. A major caveat came from research in 2024, though: too-large doses accumulate a metabolite (4PY) that directly sets off vascular inflammation and is linked to greater risk of heart attacks and strokes.

Once both search results are in front of you, would high-dose injections of either feel okay, simply because "Association doesn't prove causation"??? I don't think it would for me. Moving on to different choices seems easier, right?

So with all that, theoretically a person could use both without issue. For L-carnitine, though, I'd want to look at inflammation markers, do a proper round of good probiotics, and improve diet before rolling the dice on a heart attack by taking L-carnitine. NAD+ is the same story: a test can show how saturated you are. Who gets that test midway through their Nad cycle? Anyone.???.......Anyone.???........