Ezetemibe is an add on. It is best used with a statin and/or Bempedoic Acid. My family and I have had excellent results with Ezetemibe and RCTs have also shown the same.
I’m sorry your results didn’t turn out as well as the RCTs, but we all have different reactions to different medications.
Right. I was hoping ezetimibe as add on to the pitavastatin would be a win, but it completely wrecked my lipid profile. Since 08/09/25 I’ve been on Brillo EZ, 180mg/day bempedoic acid and 10mg/day ezetimibe in addition to the pitavastatin 4mg/day. October 28, I will have my next test, so curious to see what happens. I’m not optimistic. My options are shrinking. I may have to start thinking about a PCSK9i, while waiting for some drug to crush my also sky high Lp(a). What a mess.
And all of this on a diet optimized to eliminate as far as possible saturated fat, EPIC amounts of fiber, including multiple kinds of soluble fiber, psyllium etc., pescetarian etc. good exercise, low stress etc.
Yes, we all have our individual biological makeups, and mine is trying to kill me by atherosclerosis (fortunately, CAC score zero at 65yo).
I can only envy people’s good lipid profiles and responsiveness to meds. Luck of the draw, I pulled a joker from the lipid panel deck. 
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A_User
#2377
I don’t see any other option than testing a PCSK9 inhibitor if you want to decrease that apoB further. I would do one 150 mg Praluent pen x1 month (Q4W) to start with and see how apoB is at the end of the month after dosing and some time after.
I couldn’t find it anywhere though.
“The surge in demand has led to limited availability in China, and some other countries,” Sanofi said in a statement, adding that “at the moment Praluent’s supply in China has already stopped.”
Or if PCSK9 inhibitors aren’t available there’s less evidence but a 6-month siRNA PCSK9i like inclisiran.
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Yes, I’ll look into a PCSK9i, early next year, still some tweaking in the meanwhile.
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A_User
#2379
Technically you could go on a high intensity statin like all of the Ivy League doctors love to put people on (compared to humble NJ doctor Dayspring with his low dose statin + ezetimibe combo). Then add on top of that ezetimibe and maybe bempedoic acid afterwards.
Combine with oat beta glucans supplement and maybe portfolio diet, check OGTT test (insulin resistance), Boston cholesterol balance test if you’re overabsorber or oversynthesizer, probably the latter.
Lots of unsolicited advice but it’s a discussion forum after all.
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Hey, advice always welcome! I already do beta glucan, for possble IR I’ll be trialling low dose pioglitazone early next year, so still some tweaking to do.
HIS, pitavastatin is only dosed at moderate intensity (4mg), so it would mean switching to something like rosuvastatin at the highest dose, maybe atorvastatin 80mg. I’m not anxious to switch, as I like the pitavastatin profile, not raising Lp(a), which is already sky high for me, no blood sugar raisng (I’m prediabetic A1c 5.7), and in general you don’t gain proportionally as much going up in dosage from statins. It’s an option in a pinch, I guess. I might think about going off label with 8mg pitavastatin, there were some studies in Asia at that dosage, good tolerance, but that’s starting to push my risk tolerance.
I guess PCSK9i is the most likely. We’ll see.
A_User
#2381
I think it was like 4-5 pp reduction in LDL-C/apoB for every doubling of the dose, so it could be a 10% reduction. If that pushed up your absorption it would be synergistic with ezetimibe, maybe that’ll be the case with your fourth test with adding in bempedoic acid.
I’d avoid 8 mg pitavastatin as well and yeah prediabetes seem difficult. Obicetrapib, you’re our only hope (effects + cost + availability + oral).
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Negligible changes indeed. For me, Ezetimibe alone, nor Rosuvastatin alone, didn’t have much effect. But when combined (10mg of each per day) they halved my LDL-C.
Are you extremely sensitive to statins? We might have discussed this previously and I’ve forgotten (sorry), but obviously 4mg of the weakest statin isn’t going to be super effective.
No idea how to explain the A-1 result. Lab error, I assume?
And I wouldn’t say you’re too cursed if you have a CAC of 0 at 60 years old. My 41 year old colleague just learned he has a CAC of 330.
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A_User
#2383
Pitavastatin not pravastatin.
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Pitavastatin is not the weakest statin (certainly not per mg!), and 4mg is the equivalent of about 20mg atorvastatin, which is considered moderate. And previously I was on 10mg atorvastatin. So this is an escalation. I have not had any side effects from these two statins. Why such abysmal results from adding 10mg ezetimibe, I don’t know. More importantly, the lipid profile deteriorated catastrophically. I have never had such a huge number of small LDL particles ever, not even when I was just on 10mg atorvastatin (measured October 2023), or on pitavastatin 4mg alone (measured April 2025), or pita + BA (measured June 2025). And not just the particle number, but average size of the LDL (and HDL!) collapsed. No matter where one looks it’s a sharp deterioration, HDL, deterioration, VLDL likewise.
It’s a disaster. To say I’m unimpressed with ezetimibe is an understatement of the century. Now we’ll see what a few months of pita + BA + EZ gets me. I’ll throw in telmisartan and pioglitazone (marginal effect of possibly tiny improvements in lipid profile), and then I’m tapped out (other than switching to a HIS). I guess a PCSK9i is next, until obi comes online.
And yes, CAC of zero measured at 65yo (December 2023) is the only flickering light at the end of this deep dark lipid tunnel. I will need to do a CT angio to see if I’m not stuffed to the gills with soft plaque nonetheless. I amaze myself that with these lipids I’m not dead yet. FWIW, a recent EKG was just fine. And no CVD symptoms, or exercise limitations. Hopefully means I won’t keel over before obicetrapib drops.
Now I’ll reveal something that I myself cannot believe, despite seeing it with my own eyes. It defies biology. Makes me question my own sanity. Namely, I used to have a mild (not very prominent) Frank’s sign. At least until late last year, when it was the last time that I took a close look. OK, so a week ago, I suddenly noticed that the Frank’s sign was completely gone, no matter how closely I looked at it. What?? How is this biologically possible? The only thing I can think of is perhaps a rapamycin effect? The longer I live, the less I understand, really I thought the opposite should be happening. Instead of older and wiser we become odder and wider.
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Bicep
#2385
I’ve been busy and missed some of this, but what rate of Rapa have you used throughout this test? Rapa screws up my lipids and glucose. I know this from testing. Taking it weekly is too often for me. Just throwing that out there. Ymmv
I suppose rapa negatively affecting lipids is a possibility, but that is not clear from these tests. I’ve always had high LDL, before statins as well as on statins. These last three tests were all different from each other in results, but the first test, with pita alone, I was on 6mg/1-week Eris/Biocon rapa for like 11 weeks. Second test (pita + BA) was after a 7 week rapa break followed by three weeks of 6mg/1-week Zydus brand (so test was after 3 weeks of rapa). Third test (pita + EZ) was after 8 weeks of Eris/Biocon 6mg/1-week. I don’t see a clear rapa pattern impact here. And as for glucose, definitely no impact from rapa that I can see - A1c 5.7 - 5.8 same as it’s been for 10+ years (5.7 - 5.9). Empagliflozin 25mg/day may have cut down my FBG to just below 100mg/dL, as for the past few years it’s been above 100 consistently in the morning (103-110).
I don’t pretend to understand the what and why of my lipids, but regarding rapa, I keep one thing in mind - something Matt Kaeberlein said about mice. He said that mice on rapa would often have glucose and lipid derangements, but after about 20 weeks on rapa, those values would come down to better levels than before rapa. So I’m hoping for perhaps a similar effect. If rapa is messing with the lipids, perhaps that’s temporary, and in time things will stabilize - perhaps, hopefully.
For now, while the lipid situation is depressing, I’m not despondent - there are still a couple of levers left to get my lipids into civilized territory.
Davin8r
#2387
I hope a PCSK9i is a viable option for you and that insurance will cover it. It certainly should be, given that you’ve tried/failed just about everything else.
Yes, PCKS9i is definitely on the table, but out of pocket. Insurance wil not cover, according to my doctor.
Davin8r
#2389
Are you sure your doctor isn’t just being lazy because he or she doesn’t want to do the prior authorization? I’d call your insurance company and ask directly. Repatha or Praluent. Also would be good idea to inquire about Leqvio (inclisiran).
Beth
#2390
Fyi, my insurance doesn’t cover it either and my cardiologist did everything they could, and have a history of not being able to tolerate statins. Having said that, I have the coupon from repatha and I get several months a year for only $15… so I still pay a fortune but only about 6 months of a fortune.
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Sadly even my cardiologist couldn’t get the insurance to cover. I’ll just have to pay out of pocket. At this point I’m curious to see if a PCSK9i added on top of what I already take would get my LDL to budge anywhere near 70. Insane. You’d think my untreated LDL would be like 600 or something, but it’s more like 160-170. It’s just extremely stubborn. But who knows, maybe pita + BA + EZ will result in some miracle. I’m glad I did these experiments by trying the various combos, so I can see how the individual drugs work.
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Old paper, but Sniderman is lead author. He did a great interview on Peter Attia’s podcast some time ago. So, nostalgic posting.
Age and Cardiovascular Risk Attributable to Apolipoprotein B, Low‐Density Lipoprotein Cholesterol or Non‐High‐Density Lipoprotein Cholesterol
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A_User
#2393
It could be the rapamycin and SGLT2 inhibitor keeping your apoB higher.
Maybe. I guess I could take an empagliflozin and rapamycin holiday to find out, but there’s not much point, as even if that is so, I don’t want to quit either, so there’s little practical consequence of that data.