Thank you, this is all very helpful information. @AgentSmith

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@jnorm ezetimibe will bump your liver enzymes. An AST of 42 isn’t too bad but if you are concerned you can take 1/2 or even a 1/3 of that 10 mg dose and get pretty much the same effect on your lipids. That will likely allow your AST to return to normal. I’d do that before I added TUDCA.

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What dosage are you taking to get total T of ~2400, if you don’t mind me asking?

400/week of the cypionate ester. IM’ing EoD.
That was my trough iirc.

I’ve always wondered how it scales. Does T go up linearly with dose, or is there a curve? Probably individual.

One more piece of evidence: Cardiovascular Health - #1725 by RapAdmin

Pooled analysis revealed that combination LLT significantly more effectively reduced the LDL-C level from baseline (mean difference, −12.96 mg/dL; 95% CI, −17.27 to −8.65; P<.001) and significantly reduced all-cause mortality (OR, 0.81; 95% CI, 0.67 to 0.97; P=.02), major adverse cardiovascular events (OR, 0.82; 95% CI, 0.69 to 0.97; P=.02), and stroke incidence (OR, 0.83; 95% CI, 0.75 to 0.91; P<.001), with an insignificant effect on cardiovascular mortality (OR, 0.86; 95% CI, 0.65 to 1.12; P=.26) when compared with statin monotherapy. The risk of adverse events and the therapy discontinuation rate were comparable between groups.

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Comparative Cardiovascular Outcomes of Triple Lipid-Lowering Therapy versus Double Therapy in Patients with Atherosclerotic Cardiovascular Disease

After propensity score matching, baseline characteristics including hypertension (85.4% vs 85.3%), diabetes (46.3% vs 46.3%), and prior myocardial infarction (29.8% vs 29.6%) were well-balanced between groups. The statin plus ezetimibe group showed significantly lower risk across multiple outcomes compared to statin monotherapy: all-cause mortality (HR 1.445, 95% CI 1.412-1.480), dementia (HR 1.498, 95% CI 1.447-1.550), cardiac arrest (HR 1.332, 95% CI 1.263-1.404), and stroke (HR 1.253, 95% CI 1.202-1.306). More modest risk reductions were observed for atrial fibrillation (HR 1.132, 95% CI 1.110-1.154) and heart failure (HR 1.075, 95% CI 1.059-1.091), while ventricular tachycardia showed no significant difference between groups (HR 1.035, 95% CI 0.999-1.072).

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Apologies if I missed this. Does anyone have any empirical data on the merit of the generalization that low or normal triglycerides (well below 100) with elevated LDL suggests being a hyper adsorber whereas an elevated lipid profile with high trigs is more suggestive of being a hyperproducer? If one is a hyperproducer is 10 mg/day ezetimibe the ceiling or can it safely be taken at higher doses and to what effect?

Ezetimibe primarily blocks the (NPC1L1) cholesterol transporter in the intestine. The 10mg dose is enough to nearly saturate that effect (blocking 50-60% of cholesterol ingestion) that’s why it’s not dose dependent.

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I think you would certainly need to follow Liver function tests if taking more than 10 of ezetimibe. Even at 10 I see my LFT’s bump (with statin on board as well). As @cl-user says you don’t get a lot of benefit above 5 so you are already pretty much maxed out at 10 mg. I try hard not to put pressure on my liver even if the enzyme bumps are clinically minor, they indicate stress on the liver.

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There isn’t any need to take more than 10 mg of Ezetimibe. It isn’t worth the risk to your liver for any minuscule additive gain.

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Might as well share my numbers, since I meet those criteria. These are averages from at lest 3 readings, taken over at least 3 month intervals (i.e. each results is a Jan, April, Sept or similar):

Untreated:
LDL-C: 180 mg/dl
HDL-C: 53 mg/dl
Trigs: 70.4 mg/dl
HBA1C: 5.0%
ALT: 42

I have familial hypercholesterolemia, and likely the “hyper absorption” type. As you can see, my trigs were low, HDL-C was good, metabolic health great, but I had some fatty liver and sky high LDL-C.

After treatment with Rosuvastatin 10mg:
LDL-C: 177 mg/dl
HDL-C: 60 mg/dl
Trigs: 67 mg/dl
HBA1C: 5.2%
ALT: 25.0

So for me, the statin alone did very little for LDL-C, but did seem to help with the liver.

Rosuvastatin 5mg, and Ezetimide 5 mg: (half doses of each. Only 1 time for this result):
LDL-C: 93 mg/dl
HDL-C 58 mg/dl
Trigs 59 mg/dl
HBA1C: 5.0%
ALT: didn’t measure

Rosuvastatin 10 mg, and Ezetimibe 10 mg: (using the proper doses)
LDL-C: 71 mg/dl
HDL-C: 45 mg/dl
Trigs: 56 mg/dl
HBA1C: 5.2%
ALT: 31.4

So addition of Ezetimibe was incredibly effective at LDL-C lowering. The 5mg is definitely very effective, but 10 mg is still better. The statin at 10 mg does seem to add 0.2% onto my HBA1C. You can see when I reduced the statin to 5 mg, my A1C went back down again. None of the medications has any measurable negative effects on the liver either. In fact, all the results are better than pre-treatment, and ultrasound showed that a small amount of fatty liver totally resolved once I started treatment.

And for reference, I now use 10 mg Rosu, 10 mg Ezet, and Repatha (injectable PCSK9i):
LDL-C: 43 mg/dl
HDL-C: 58 mg/dl
Trigs: 62 mg/dl
HBA1C: 5.2%
ALT: 28.3

Pretty happy with this. And I totally agree with the others that 5 mg Ezetimibe is very powerful in combination with a statin, and 10 mg gets you some incremental additional benefit. I can’t see any value in going higher. If you want to lower LDL-C more, just add a different drug.

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What did cabergoline do for you here?

Instead of taking it regularly can ezetimibe be taken with particularly fatty meals in the same way acarbose is taken with starchy meals?

Half life of 22 hours

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I suppose I could use it like this if I don’t consume fatty meals often. I was thinking for the occasional fatty bit of meat or meal high in butter or saturated fat.

Does this mean you could take less than 10 with good effect?

Why? It’s dirty cheap and you won’t get your LDL too low. Just take it every day.

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No reason to not add ezetimibe as an adjunct to any lipid-lowering protocol. It’s cheap, generic, and very safe. It’s basically a “free lunch”.

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Sure but why would you do that? The threshold varies from person to person and the dose was set to 10mg so that it works for most individuals.
You can try to find your personal minimum effective dose but it’s a cheap medication.

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