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

[Tug Speedman]

Hey everyone. I'm reaching out because I need some guidance.

I was recently looking harder at my numbers — High LDL, Low HDL, the usual fat guy stuff. So I figured Goodlabs would run "everything", mostly because I had a coupon. Well, it came back with a High LPa of 183, and the Goodlabs report isn't exactly comforting since it stamps it out in large bold red text: URGENT.

Background: 51yo Male, currently on Reta. I've dropped 26lbs over the last 8 weeks, going from 265lb down to 239lb so far. My chat bot keeps telling me to focus on losing more weight before making any big assumptions or drawing conclusions, and I tend to agree — I'll retest the lipid panel once I'm nearer my goal weight of 215lbs. Most of my bad blood markers are only slightly out of range. The exceptions are High apoB and LPa, which is still significant information. But there's a fair chance the rest fall in line once I'm skinny boy 4.0 again. 5 years ago I was a jogger, then I got fat again. I'll be jogging again by this winter. When I'm consistent, I average only about 10 miles a week.

Anyway! LPa is a stubborn bastard and doesn't tend to improve much through diet or physical change. So I'm hoping to focus specifically on the INFLAMMATION side of Cardiovascular Events.

My Lair, My Legion, My Gang! Which peps are useful for Inflammation and overall Cardio Protection? I'm not chasing miracles here — I'm already busting my ass doing my part: losing weight, eating mostly clean, no liquid sugars for months, nothing fried for months, no smoking but I do vape nicotine, which is next to go. I'm on Ezetimibe, on 20mg Pravastatin (just started and hate statins), daily Baby Aspirin. And I'm in the middle of the mito protocol LOL. Any input is much appreciated, and I have no secrets — I'll share my lab markers with anyone who's interested. Thank you and Love and Respect to all.

So far, Hexarelin and Humanin seem to have promising traits. Any others?

 

[BBA1969]

Since a GLP-1 is already part of your routine, that box is ticked. For inflammation, Reta and Tirz perform well.

When it comes to inflammation, TB-500, VIP and KPV are the ones that spring to mind next, and among those, the first 2 also offer cardiovascular protection.

 

[Tug Speedman]

BBA1969 said:

Since a GLP-1 is already part of your routine, that box is ticked. For inflammation, Reta and Tirz perform well.

When it comes to inflammation, TB-500, VIP and KPV are the ones that spring to mind next, and among those, the first 2 also offer cardiovascular protection.

I have a kit for TB and another for KPV en route, both from tearing down KLOW. There are notes of mine saying VIP might be theorized for mild COPD, and I’ll investigate that. Thanks for your time

 

[lastresort]

Tug Speedman said:

Hey everyone. I'm reaching out because I need some guidance.

I was recently looking harder at my numbers — High LDL, Low HDL, the usual fat guy stuff. So I figured Goodlabs would run "everything", mostly because I had a coupon. Well, it came back with a High LPa of 183, and the Goodlabs report isn't exactly comforting since it stamps it out in large bold red text: URGENT.

Background: 51yo Male, currently on Reta. I've dropped 26lbs over the last 8 weeks, going from 265lb down to 239lb so far. My chat bot keeps telling me to focus on losing more weight before making any big assumptions or drawing conclusions, and I tend to agree — I'll retest the lipid panel once I'm nearer my goal weight of 215lbs. Most of my bad blood markers are only slightly out of range. The exceptions are High apoB and LPa, which is still significant information. But there's a fair chance the rest fall in line once I'm skinny boy 4.0 again. 5 years ago I was a jogger, then I got fat again. I'll be jogging again by this winter. When I'm consistent, I average only about 10 miles a week.

Anyway! LPa is a stubborn bastard and doesn't tend to improve much through diet or physical change. So I'm hoping to focus specifically on the INFLAMMATION side of Cardiovascular Events.

My Lair, My Legion, My Gang! Which peps are useful for Inflammation and overall Cardio Protection? I'm not chasing miracles here — I'm already busting my ass doing my part: losing weight, eating mostly clean, no liquid sugars for months, nothing fried for months, no smoking but I do vape nicotine, which is next to go. I'm on Ezetimibe, on 20mg Pravastatin (just started and hate statins), daily Baby Aspirin. And I'm in the middle of the mito protocol LOL. Any input is much appreciated, and I have no secrets — I'll share my lab markers with anyone who's interested. Thank you and Love and Respect to all.

So far, Hexarelin and Humanin seem to have promising traits. Any others?

Oat bran

Unripe banana

 

[latviantower]

What does your CRP look like? It’s a major marker of inflammation and a red flag for cardiovascular risk.

For the liver, glutathione is about as good as it gets. You don’t necessarily need to inject it—though I use 150 mg IM every day—but if you go with tablets, choose liposomal; absorption is superior.

Also be sure you’re supplementing CoQ10, since statins have a habit of draining it.

About the statin and dosage your doctor picked, I’d have some questions. At 20 mg, rosuvastatin reduces LDL far more effectively than pravastatin—roughly 50% versus 30%. My cardiac calcium score is extremely high, and I take 40 mg atorvastatin; my LDL has fallen to 40 without side effects. (I also take 300 mg CoQ10.) Not every statin is equivalent!

Best of luck!

 

[catdog]

Worth asking about PCSK9 inhibitors?

 

[Tug Speedman]

latviantower said:

What does your CRP look like? It’s a major marker of inflammation and a red flag for cardiovascular risk.

For the liver, glutathione is about as good as it gets. You don’t necessarily need to inject it—though I use 150 mg IM every day—but if you go with tablets, choose liposomal; absorption is superior.

Also be sure you’re supplementing CoQ10, since statins have a habit of draining it.

About the statin and dosage your doctor picked, I’d have some questions. At 20 mg, rosuvastatin reduces LDL far more effectively than pravastatin—roughly 50% versus 30%. My cardiac calcium score is extremely high, and I take 40 mg atorvastatin; my LDL has fallen to 40 without side effects. (I also take 300 mg CoQ10.) Not every statin is equivalent!

Best of luck!

Latviantower! CRP 1.7, thanks for checking. Glutathione is something I’m fond of; I just emptied a bottle, and not long after, my liver AND kidney labs came back excellent. I stockpile Gluta boxes because I like it so much. I’m also exploring Khavinson peps for the ones that may help cardio.



On statins: a doctor 10 years ago started me on 20 Rosuva. After a year, I dealt with brain fog, tendon pain, and actual muscle wasting—my arms became visibly thinner. I’d hoped to go the trt or shellfish hormone path to build back up, but then my bloodwork came back with this and diverted me from regaining muscle. That doesn’t trouble me much. In my kids’ view, I’m still big and strong

My current doctor wanted me on a statin. I described what happened before, and that’s how I landed on the water based, lower dose Prava 20mg/day. Another draw is scheduled in about 1.5 months, so we’re monitoring it closely.

As for PCSK9! I am eligible for Repatha, and I could even receive it at no cost. My doctor says it’s a biologic and might expose me to respiratory infection, which would disrupt the sleep/study/cpap path I’m just beginning. If the higher-dose statin does poorly, I’ll look into PCSK9—something to decide over the next couple months, I suppose.

There’s also Muvalaplin (oral), plus roughly 4 other RNA therapies in late phase trials that look extremely effective with few side effects. That gives me comfort that my children’s odds rest on even firmer footing. Still, this is why I want to target inflammation / Stress: I think that driver is a meaningful one I can affect. My CAC scan has been ordered.

 

[Habibibi]

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.

 

[Tug Speedman]

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.

"having a low score doesn't mean you don't have unstable plaque".

From what little I grasp, that elevated LPa acts in a way similar to such unstable plaque, and it reacts to inflammation in the artery walls/endothelium, where it can accumulate and create problems.

That explains why, in this thread, my primary focus is on reducing inflammation and keeping the endothelial glycocalyx (EGC) intact.

Even though statin therapy is something I'd rather steer clear of, I'm still here taking part and contributing what I can, since at my age my preferences no longer come first. What I do want is to be around for as many of my children's days as possible. I only hope I haven't waited too long to make a significant difference. Still, I'll keep trying until the bitter end. I appreciate your reply.

 

[JuneBug1956]

You’re truly doing wonderful things for your health. Keep dropping the weight—maybe even a little underweight. Steering clear of diabetes would improve the whole picture enormously. Don’t let up. (Also keep clear of smoking and secondhand smokers…assuming you don’t already.) If you’re on Discord, go over to the Roundtable. Plenty of health practitioners there have the newest educational information.

 

[Tug Speedman]

JuneBug1956 said:

You’re truly doing wonderful things for your health. Keep dropping the weight—maybe even a little underweight. Steering clear of diabetes would improve the whole picture enormously. Don’t let up. (Also keep clear of smoking and secondhand smokers…assuming you don’t already.) If you’re on Discord, go over to the Roundtable. Plenty of health practitioners there have the newest educational information.

Junebug, thanks! The encouragement is genuinely what I need—this stretch has been hard, especially with so many late nights spent digging through research. I was content spending every night looking into Peps, but then this small side quest appears. I'm on Discrd, and it sounds like I really need to join Roundtable. Thanks once more!

 

[SVT810E]

Tug Speedman said:

latviantower said:

What does your CRP look like? It’s a major marker of inflammation and a red flag for cardiovascular risk.

For the liver, glutathione is about as good as it gets. You don’t necessarily need to inject it—though I use 150 mg IM every day—but if you go with tablets, choose liposomal; absorption is superior.

Also be sure you’re supplementing CoQ10, since statins have a habit of draining it.

About the statin and dosage your doctor picked, I’d have some questions. At 20 mg, rosuvastatin reduces LDL far more effectively than pravastatin—roughly 50% versus 30%. My cardiac calcium score is extremely high, and I take 40 mg atorvastatin; my LDL has fallen to 40 without side effects. (I also take 300 mg CoQ10.) Not every statin is equivalent!

Best of luck!

View attachment 151

Latviantower! CRP 1.7, thanks for checking. Glutathione is something I’m fond of; I just emptied a bottle, and not long after, my liver AND kidney labs came back excellent. I stockpile Gluta boxes because I like it so much. I’m also exploring Khavinson peps for the ones that may help cardio.



On statins: a doctor 10 years ago started me on 20 Rosuva. After a year, I dealt with brain fog, tendon pain, and actual muscle wasting—my arms became visibly thinner. I’d hoped to go the trt or shellfish hormone path to build back up, but then my bloodwork came back with this and diverted me from regaining muscle. That doesn’t trouble me much. In my kids’ view, I’m still big and strong

My current doctor wanted me on a statin. I described what happened before, and that’s how I landed on the water based, lower dose Prava 20mg/day. Another draw is scheduled in about 1.5 months, so we’re monitoring it closely.

As for PCSK9! I am eligible for Repatha, and I could even receive it at no cost. My doctor says it’s a biologic and might expose me to respiratory infection, which would disrupt the sleep/study/cpap path I’m just beginning. If the higher-dose statin does poorly, I’ll look into PCSK9—something to decide over the next couple months, I suppose.

There’s also Muvalaplin (oral), plus roughly 4 other RNA therapies in late phase trials that look extremely effective with few side effects. That gives me comfort that my children’s odds rest on even firmer footing. Still, this is why I want to target inflammation / Stress: I think that driver is a meaningful one I can affect. My CAC scan has been ordered.

Oddly enough. Considering TRT could be worthwhile. When it comes to lowering Lp(a), it ranks among the more potent options; smaller studies have reported consistent decreases in high Lp(a), spanning 25-59%.


https://www.atherosclerosis-journal.com/article/0021-9150(95)05756-0/abstract


Steroid cycles at full scale impact Lp(a) even more strongly, though they likely () harm cardiovascular health overall.

 

[Tug Speedman]

SVT810E said:

Tug Speedman said:

latviantower said:

What does your CRP look like? It’s a major marker of inflammation and a red flag for cardiovascular risk.

For the liver, glutathione is about as good as it gets. You don’t necessarily need to inject it—though I use 150 mg IM every day—but if you go with tablets, choose liposomal; absorption is superior.

Also be sure you’re supplementing CoQ10, since statins have a habit of draining it.

About the statin and dosage your doctor picked, I’d have some questions. At 20 mg, rosuvastatin reduces LDL far more effectively than pravastatin—roughly 50% versus 30%. My cardiac calcium score is extremely high, and I take 40 mg atorvastatin; my LDL has fallen to 40 without side effects. (I also take 300 mg CoQ10.) Not every statin is equivalent!

Best of luck!

View attachment 151

Latviantower! CRP 1.7, thanks for checking. Glutathione is something I’m fond of; I just emptied a bottle, and not long after, my liver AND kidney labs came back excellent. I stockpile Gluta boxes because I like it so much. I’m also exploring Khavinson peps for the ones that may help cardio.



On statins: a doctor 10 years ago started me on 20 Rosuva. After a year, I dealt with brain fog, tendon pain, and actual muscle wasting—my arms became visibly thinner. I’d hoped to go the trt or shellfish hormone path to build back up, but then my bloodwork came back with this and diverted me from regaining muscle. That doesn’t trouble me much. In my kids’ view, I’m still big and strong

My current doctor wanted me on a statin. I described what happened before, and that’s how I landed on the water based, lower dose Prava 20mg/day. Another draw is scheduled in about 1.5 months, so we’re monitoring it closely.

As for PCSK9! I am eligible for Repatha, and I could even receive it at no cost. My doctor says it’s a biologic and might expose me to respiratory infection, which would disrupt the sleep/study/cpap path I’m just beginning. If the higher-dose statin does poorly, I’ll look into PCSK9—something to decide over the next couple months, I suppose.

There’s also Muvalaplin (oral), plus roughly 4 other RNA therapies in late phase trials that look extremely effective with few side effects. That gives me comfort that my children’s odds rest on even firmer footing. Still, this is why I want to target inflammation / Stress: I think that driver is a meaningful one I can affect. My CAC scan has been ordered.

Oddly enough. Considering TRT could be worthwhile. When it comes to lowering Lp(a), it ranks among the more potent options; smaller studies have reported consistent decreases in high Lp(a), spanning 25-59%.


https://www.atherosclerosis-journal.com/article/0021-9150(95)05756-0/abstract


Steroid cycles at full scale impact Lp(a) even more strongly, though they likely () harm cardiovascular health overall.

I believe I only caught a hint of that perspective while researching lately. To be honest, my hope is that this is merely a side quest for health reasons and that I can return to optimizing. Still, the pieces line up quite neatly. That’s the reason I’ll forever appreciate the men and women in the gym. They’ve occupied the leading edge for a very long stretch, and the evidence base runs deep. Many thanks, SVT!

 

[sfkid]

Do what the bodybuilding crowd does.

Ezetimibe — it blocks LDL from being taken up by the small intestine.

Rosuvastatin — this isn’t a standard statin. It specifically targets only LDL production in the liver, and the kidneys don’t process it. You won’t get muscle aches or brain fog with it.

When used together at low doses, they’re highly effective and have no side effects...

 

[JuneBug1956]

Tug Speedman said:

JuneBug1956 said:

You’re truly doing wonderful things for your health. Keep dropping the weight—maybe even a little underweight. Steering clear of diabetes would improve the whole picture enormously. Don’t let up. (Also keep clear of smoking and secondhand smokers…assuming you don’t already.) If you’re on Discord, go over to the Roundtable. Plenty of health practitioners there have the newest educational information.

Junebug, thanks! The encouragement is genuinely what I need—this stretch has been hard, especially with so many late nights spent digging through research. I was content spending every night looking into Peps, but then this small side quest appears. I'm on Discrd, and it sounds like I really need to join Roundtable. Thanks once more!

Peppy’s is also a wonderful spot.

 

[lessthanhalf]

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.

 

[Chucky]

Has anyone checked your ejection fraction?

 

[GLiPtest]

Not a complex situation.

Ezetimibe

Statin (Pitavstatin would be my suggestion)

Repatha

That combination pushes lipids down as far as they can go, cuts risk right away, and may even allow some plaque regression; most people using statins plus Repatha achieve that.

When no symptoms are present, imaging or diagnostics won’t reveal anything you can act on. Preventative stents or bypasses are no longer performed. The reason is that “maximal medical therapy,” meaning the combination above, gives outcomes that are equal or superior no matter what blockages exist, assuming you have no chest pain or trouble with exercise.

Repatha lowers LPa by roughly 30%. Before the newer LPa-specific drugs are on the market, your only lever is driving LDL / ApoB as low as possible. Since LPa multiplies risk, reducing your baseline risk as much as possible makes LPa matter less.

You might also get APOE genotype testing. A large share of people with elevated LPa carry APOE4, which raises Alzheimer’s risk considerably; learning this early could let you—and relatives who passed it to you or received it from you—sidestep a possible disaster.

 

[lessthanhalf]

Chucky said:

Has anyone checked your ejection fraction?

Because I had been experiencing strange episodes of breathlessness even while still carrying a lot of excess weight, a stress echo was the first test ordered. Getting it scheduled took an extremely long time, and by the time it actually happened I had already shed a substantial amount of weight. No ischaemia showed up, but the results gave an ejection fraction of 50% along with mild enlargement of the left atrium and left ventricle. That amounts to class b heart failure — no symptoms, yet structural changes plus a mildly reduced ejection fraction, when it should have been 55% or above. From what I have been able to gather, the chance of this progressing into symptomatic heart failure sits at 1-2% per year, provided I stay on beta blockers and ace blockers and do not put back the 80 kilos I lost. On balance that risk is likely greater than the heart attack risk coming from the high CAC, since statins and similar drugs make those easier to bring down. Untreated, the 10 year MACE risk is 20-25%, and roughly half of that with treatment — statin, ezetimibe, clopidogrel — assuming no weight regain. That makes the GLP drugs quite literally necessary for staying alive, because my guess is those risks would explode upward with major weight regain.

Since then I have had an echo every year, or 2 more of them, and nothing significant has changed, which I hope is a good sign. Based on my reading of the science, the CAC and angiogram were likely unnecessary, but I went along with what my GP and cardiologist recommended. The angiogram found 15% stenosis in the right coronary artery and 50% stenosis in the left anterior descending, so there is nothing fixable. It was done mainly to check for critical narrowings that could be corrected to stop heart failure from worsening. As the comment above lays out, I already met the criteria for maximal medical therapy for atherosclerosis, and I was not convinced the science backed having it done, but there is little sense in seeing specialists and then disregarding their advice even when you have read the literature — clinical experience is not something you can get from reading papers.

 

[Blueeyedme]

You're bringing up Lp(a), and I'm in the same boat. Unfortunately, it's inherited and has nothing to do with what you eat, how you train, or how much you weigh—plus no approved therapy exists right now. That said, help could be coming: 3 medications are currently in Phase 3 studies. Their names are Pelacarsen, Olpasiran and Lepodisiran. Make a point of bringing these up with your cardiologist. Until then, I'm confident your doctor will be pushing your lipids down hard. Your ApoB is tied to lifestyle, so it should drop once your weight and lipids are under control. I take 40mg Rosuvastatin plus a Repatha injection every two weeks, and my Total Cholesterol sits at 83 with LDL at 21. I've got what amounts to a nearly full metal jacket of stents, and heart disease runs terribly in my family. Bottom line: this is not a situation to handle on your own with peptides and steroids—you need to be under a cardiologist's care.