Plenty of carnivore dieters report feeling better than they have in years.
Then comes a lab report with an LDL of 250 or even 300.
Doctors often reach for the prescription pad right away.
In a recent YouTube interview with Dr. Ken Berry, Harvard-trained MD and Oxford PhD Nick Norwitz dissected two brand-new papers that might change that conversation.
Do they change what happens next? The answer is more nuanced than either camp admits, and it ends with six questions worth taking to your next appointment.
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The Cardiology Paper Showing apoB Risk “Vanishing”
The first paper, led by prominent lipidologist Alan Sniderman, appeared in the European Journal of Preventive Cardiology. Norwitz called one line “a very powerful quote coming from a cardiology journal.”
When HDL cholesterol is high … the effect of changing apoB vanishes.
The analysis covered roughly 293,000 people. Norwitz stressed that these were not lean mass hyper-responders or carnivore dieters, just a general population sorted by one marker.
The authors even used a striking word for the pattern.
This might explain the apparent immunity of some individuals to the clinical consequences of very high LDL and apoB.
How to Read the Graph
- Vertical axis: hazard ratio, where 1.0 means neutral risk, above 1.0 means higher risk, and below 1.0 means lower risk.
- Horizontal axis: apoB measured in standard deviations from average, with +2 landing near the 98th percentile.
- Separate lines: each represents a different HDL level, from very low (poor metabolic health) to very high.
Two patterns jumped out. Higher HDL meant lower risk, and the slope relating apoB to risk flattened from steep to almost flat as HDL climbed.
Norwitz placed the lowest line, at two standard deviations, around 84 mg/dL of HDL in this cohort. That is close to the lean mass hyper-responder threshold.
Why “Causal” Does Not Mean “Most Important”
Norwitz called causality perhaps the most abused word in cardiology. LDL and apoB dominate the conversation because they are part of a causal cascade and are easy to lower.
Understand that causality is not importance.
His analogies were vivid. Oxygen is causal to fire, yet removing all of it suffocates you, and wheels are causal to car accidents, yet a wheel-free car goes nowhere.
HDL cholesterol, he explained, works more like a litmus test of metabolic health than a lever to pull. Context matters too, since high HDL from lean, healthy metabolism differs from high HDL driven by binge drinking.
Not a Free Pass: The Fine Print
Norwitz was careful here. For most people, the graph shows a clear positive slope, meaning higher apoB tracks with higher cardiovascular risk, especially at low HDL.
Nor did he suggest crossing 84 mg/dL makes anyone immune. Population data describe groups, not individuals.
It doesn’t mean you should be on pharmacotherapy. That’s obviously not my claim to make either way.
He also noted that statins do more than lower LDL. They can improve nitric oxide levels and calm arterial inflammation, so in someone with inflamed arteries and poor metabolic health, those effects may matter.
His practical advice: stay thoughtful, avoid extrapolating blindly from population data, and ask whether the evidence behind a recommendation applies to your profile. He framed the burden of proof this way:
Find me the study that shows that I would benefit from taking a statin.
Paper Two: A “Guardian of the Artery” Gene
The second paper, published in Cell, centered on an immunoregulatory gene called GIMAP6. Norwitz nicknamed the protein “guardian of the artery,” his own label rather than the official name.
In animals missing the gene, the aorta became packed with inflammatory immune cells and the vessel wall turned leaky. Cholesterol stayed normal.
Humans carrying these mutations also have normal cholesterol, yet develop cardiovascular disease and die early. Norwitz highlighted a dot plot spanning three human datasets, including the UK Biobank, where odds of atherosclerosis reached about eight-fold.
Compared with classic familial hypercholesterolemia (LDL receptor mutations), the risk looked equal or even greater. The scale is logarithmic, so visual differences understate the gap.
Norwitz drew a bigger lesson. Leakiness and inflammation appeared to precede plaque, which challenges the simple picture of LDL particles drifting into a passive wall.
An inflamed environment may make the artery wall stickier, so particles get trapped more easily. The takeaway he offered: keep inflammation in your body and arteries low.
Berry added that he wished the paper had addressed the glycocalyx, the fuzzy lining inside vessels. Norwitz agreed it is likely damaged in these patients but asked how clinicians would measure and target it.
Check the Sky Instead of the Forecast
Norwitz compared biomarkers to a weather app predicting a 60% chance of rain. If sunshine fills the sky outside, trust your eyes.
You can look in your arteries if you have access to tools.
Cardiac imaging can reveal whether plaque exists, which Norwitz said beats any single biomarker. Berry agreed that an LDL number is only a prediction.
Six Questions to Ask Your Cardiologist
Norwitz does not recommend rejecting medicine outright. Instead, he suggested walking in with questions:
- How does my metabolic health influence your assessment of my heart health risk?
- What evidence supports treatment in someone with my metabolic profile?
- What is my expected absolute risk reduction from the treatment you recommend?
- What testing would change your decision?
- What are the potential harms of treatment?
- What are the alternatives?
Pay attention to how answers arrive. Norwitz said you do not need a medical degree to tell whether someone is working with you or patronizing you.
Markers Beyond LDL Worth Tracking
- Blood pressure: described as very important.
- HDL and triglycerides: read together with LDL, since the whole pattern tells the story.
- Waist-to-hip ratio: a tape-measure proxy for visceral fat, aiming below 0.8 for women and below 0.95 for men.
- A1C and fasting insulin: both normal, with Berry noting that published research flags fasting insulin above 13 as hyperinsulinemia and personally preferring a number closer to 5.
- hs-CRP: ideally below 1, as an inflammation marker.
- Cardiac imaging: if accessible.
When the Doctor Bristles
Berry asked what it means if a cardiologist grows defensive at these questions. Norwitz’s answer was blunt.
Find a new doctor.
He softened it with empathy. A doctor may genuinely believe they are protecting a patient, and handing over decisions is a legitimate choice for someone who prefers that.
Patients who want a partnership, though, should seek a clinician who treats them as one. Norwitz also described himself as an n=1 with extremely high LDL and apoB, a reminder that individual cases illustrate questions rather than settle them.
