Got my updated lipid panel back and I'm legitimately shocked. I've been on tirzepatide 10mg for 7 months. No changes to diet other than eating less (because appetite is demolished). Here are my full numbers:

I was previously told I'd need a fibrate or high-dose statin to get my triglycerides under control. My PCP was borderline speechless. He said the non-HDL and TC/HDL ratio improvements are especially meaningful for risk assessment.

Has anyone else seen this kind of triglyceride response? Is this typical or am I an outlier?

You're not an outlier. This is very consistent with what we see in clinical practice and in the SURPASS trial data for tirzepatide. The dual GIP/GLP-1 mechanism appears to have particularly potent effects on triglyceride-rich lipoproteins.

In the SURPASS-4 trial, tirzepatide 15 mg reduced triglycerides by 24.8% from baseline vs. insulin glargine.^[1] Your baseline of 358 mg/dL would put you in a higher-response category, since patients with elevated baseline TGs tend to see the largest absolute reductions.

The mechanism involves multiple pathways:

• Reduced hepatic VLDL production (your VLDL dropped from 72 to 30)
• Enhanced lipoprotein lipase activity (GIP-mediated)
• Improved hepatic insulin sensitivity reducing de novo lipogenesis
• Reduced postprandial lipemia from delayed gastric emptying and reduced food intake

Your HDL increase (+14 mg/dL) is the reciprocal of TG reduction — as TGs fall, HDL particle clearance slows, and HDL levels rise. This is a very favorable metabolic signature.

^[1] Del Prato S, Kahn SE, Pavo I, et al. Tirzepatide versus insulin glargine in type 2 diabetes and increased cardiovascular risk (SURPASS-4). Lancet. 2021;398(10313):1811-1824.

I'd strongly recommend getting an ApoB level at your next draw. With your triglycerides having been that high (358), your calculated LDL-C of 108 is almost certainly underestimating your true atherogenic burden. The Friedewald equation becomes unreliable when TGs exceed 200 mg/dL.

ApoB directly counts atherogenic particles (each VLDL, IDL, LDL, and Lp(a) particle carries exactly one ApoB molecule). In someone with your lipid profile, ApoB might tell a different story than LDL-C.

I'd target ApoB <90 mg/dL for primary prevention, or <80 mg/dL if you have additional risk factors.

Here's a comparison of lipid effects across GLP-1 and dual-agonist trials to contextualize these results:

The OP's triglyceride response is above the trial mean, but this is expected given the high baseline. Percentage reductions are always larger with higher starting values. The absolute result (TG 152) is what matters clinically, and getting below 150 mg/dL should be the next target.

Thanks for all this context. I just checked — my ApoB was 158 mg/dL at baseline but hasn't been rechecked. I'll make sure it's on the next panel. The Friedewald issue is a great point I wouldn't have known about.

One follow-up: my doctor mentioned that with TGs that high at baseline, I was at risk for pancreatitis. Now that they're at 152, is that risk essentially gone? And should I still consider adding a statin for the LDL?