Earthling

Earthling Verified account @_earthling74 · 3d

You're welcome Eric, and I suppose own your labs is cheaper if you are running single biomarkers/panels. Most people aren't doing that though. Here's a typical initial panel I might want to see on a new patient for example. It's not even close honestly. Then factor in that Goodlabs also offers a completely free panel with even more biomarkers than this if you just donate blood (good for more people anyway), and then it's an absolute no brainer who is offering a more cost saving service.

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Eric Rodgers Verified account @DrEricRodgers · 4d

Save money on your lab work!
ownyourlabs.com

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Grok Verified account @grok · Nov 1

The premise mixes two things. Keys' 1953 graph used 6 countries with the most comparable national stats then available. The 22-country plot came from a 1957 critique by others, not his data. The actual Seven Countries Study began in 1958 with its own fieldwork on 16 cohorts chosen for dietary contrast and practical collaboration, not selected from those national figures. Modern guidelines draw on decades of additional trials, cohorts, and meta-analyses beyond any single 1950s study, though the saturated-fat debate continues.

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Nick Norwitz MD PhD Verified account @nicknorwitz · Oct 31

I'm happy to see these results from the FLOWPROMOTE RCT, showing that lipid-modifying pharmacotherapy led to plaque regression in the majority of patients over the course of 18 months.

And I think this provides an excellent moment to interject nuance, where there's generally a tendency to become more polarized.

First, because I know it's of interest, and often misrepresented, bear in mind that at no point have I ever said lipid-lowering medications are universally bad, nor have I provided individualized prescriptive recommendations.

Because, as with almost everything in health, it's all about individualized risk-benefit analysis.

And the data suggest larger absolute benefits in those who are at HIGH cardiovascular risk, including those with confirmed cardiovascular disease, or features of metabolic syndrome.

The patients here were in said category
👉 Half with hypertension
👉 ~60% being former smokers
👉 Overweight on average
👉 Diagnosed coronary artery disease (e.g., coronary stenosis greater than 50% 👉 per inclusion criteria).

🚨They also had high baseline plaque (Baseline mean/median: 375 / 316 mm3)

nb: Keto-CTA comparison: (mean/median: 51/25 mm3)

(Though I won't get on a soap box about the 'noise floor' here.)

Bottom line, these were high risk people and the perfect subjects for this trial.

Conclusion?

The data show benefits with respect to cardiovascular health in this population.

That’s not a surprise, although the regression (assuming the reads are reliable...topic for another time), are impressive.

All I would caution against is extrapolating from this high-risk population to the much broader and unsubstantiated conclusion that aggressive lipid-lowering therapy is necessary for everyone as a preventive measure.

That’s not dogmatic. It’s logic and reason.

As a recent complementary perspective case in point, the European Journal of Preventive Cardiology paper (PMID: 42533703), looking at interactions between HDL and ApoB, found for those with high HDL (just one marker of good metabolic health), there was no observed relationship between ApoB and 10-year cardiovascular disease risk. And that is just one marker.

In every circumstance we see here, the context matters, whether you're prescribing pharmacotherapy or trying a diet.

Bottom line: These are very positive results.

And beyond anything, I'm very happy for the patients whose outcomes and cardiovascular risk are improving.

I think that's something we should all celebrate. Fair enough?

📖 Primary reference: JAMA Cardio. Oct 30, 2026. doi: 10.1001/jamacardio.2026.4788

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Dr Terry Simpson Verified account @drterrysimpson · Oct 29

There is a remarkable difference between finding evidence that challenges your assumptions and finding evidence that conveniently reassures you that you are the exception.

This is an interesting paper by Sniderman and colleagues, examining nearly 294,000 UK Biobank participants and finding that higher HDL cholesterol modifies the association between ApoB and cardiovascular events. The interaction is real, statistically significant, and worthy of further investigation. But the leap from an observational association to suggesting that an individual with an LDL of 574 mg/dL and ApoB above 350 might be immune to atherosclerosis is quite another matter.

In fact, the authors specifically caution that the observed interaction should not be taken as firm clinical evidence that ApoB ceases to be atherogenic or doesn't require treatment when HDL is high. That's a rather important sentence to leave out when you're discussing immunity.

A statistical model showing attenuation of risk at high HDL is not a clinical trial. Nor does it establish that raising HDL is protective, or that someone with extraordinarily elevated ApoB can safely ignore decades of exposure. We've spent years discovering that increasing HDL cholesterol pharmacologically doesn't reliably reduce cardiovascular events. HDL is an interesting biomarker, but biomarkers and causal mechanisms aren't interchangeable.

And then there is the problem of extrapolation. The ordinary distribution of ApoB in UK Biobank is not populated by large numbers of otherwise healthy individuals walking around with an LDL approaching 600. A modeled relationship at the extremes of HDL doesn't validate a personal experiment at the extremes of ApoB.

Which brings me to my friend Simon Hill, @theproof, who recently published something I found considerably more rigorous and intellectually open.

Simon had coronary CT angiograms suggesting a remarkable 48% reduction in plaque volume over 16.5 months. He could have celebrated, announced that his diet had reversed atherosclerosis, and made an excellent marketing campaign out of it. Instead, he examined the scans using three different analysis platforms. One suggested substantial regression, another progression, and the third essentially no change.

Rather than promoting the most flattering result, he openly discussed the uncertainty. That's what scientific curiosity looks like when the evidence doesn't cooperate with your expectations.

Simon also has something that makes this discussion more than academic. His father had a myocardial infarction at 41 and his grandfather at 49. Simon is now 40. He has lived with the consequences of cardiovascular disease in his family, and it's understandable that he wants to reduce his risk as much as reasonably possible. He has even started a PCSK9 inhibitor despite having an ApoB around 70–80 without medication.

We can debate whether targeting an ApoB below 40 with Repatha offers sufficient additional clinical benefit in someone with his particular risk profile. That's a legitimate discussion. But I applaud his desire to live longer and his willingness to question his own most favorable findings.

I understand the emotional component of this better than most. My own coronary calcium score is 90. I take rosuvastatin and ezetimibe, achieved an LDL around 60, and have seen it fall further since starting tirzepatide. I have no particular desire to measure every cubic millimeter of plaque in my coronary arteries. I know there is atherosclerosis, I know what the evidence supports, and I am treating the risk factors I can change.

Simon wants more information and more aggressive prevention. I am comfortable treating what I already know. Neither approach requires pretending that uncertainty has disappeared.

We physicians spend our lives talking about hazard ratios, plaque volumes, confidence intervals, and relative risk reductions. Yet one disrupted coronary plaque with a superimposed thrombus can turn all those abstractions into a very final event. That's why I care more about preventing myocardial infarctions than winning a competition over whose scan looks better.

The remarkable thing about the comparison is that both Simon and Norwitz have favorable personal findings. Simon asks whether his are reliable. Norwitz highlights an observational study that might explain why his own findings are reassuring.

There is a lesson there about confirmation bias, and it applies to all of us, physicians included.

The Sniderman paper deserves attention. It may teach us something important about HDL biology and cardiovascular risk. But it does not establish immunity from ApoB, and it certainly doesn't overturn the causal evidence supporting LDL lowering.

Science progresses when we investigate the observations that don't fit our models, not when we promote the observations that make us feel invulnerable.

After all, the goal isn't to prove that your arteries are special. It's to live long enough that they never become the reason you aren't.

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