Seven Years of 700 Cholesterol Without Coronary Atherosclerosis: A Lean Mass Hyper-Responder Case Report

Abstract

Background: While reducing LDL cholesterol (LDL-C) remains central focuses of conventional preventive cardiology, substantial heterogeneity exists in the cardiovascular risk associated with even extreme LDL-C elevations, likely depending heavily on the broader metabolic context. Specifically, the lean mass hyper-responder (LMHR) phenotype—characterized by markedly elevated LDL-C with elevated high-density lipoprotein cholesterol (HDL-C) and low triglycerides in the setting of a ketogenic diet—has recently been described, though its long-term risk profile remains poorly defined. Case Presentation: We describe a male in his 30s without any congenital dyslipidemia who adopted a ketogenic diet for the management of ulcerative colitis and who subsequently exhibited a sixfold increase in LDL-C from a baseline of 95 mg/dL to 574 mg/dL, with total cholesterol of up to 705 mg/dL, HDL-C at 124 mg/dL, and triglycerides at 34 mg/dL. Despite maintaining these extreme lipid levels for nearly seven years, he demonstrated no coronary plaque or stenosis on coronary computed tomography angiography (CCTA; CAD-RADS = 0). Additionally, quantification of coronary plaque as assessed by AI-guided quantified analysis by Heartflow® identified 0 mm3 plaque in any vessels, placing him in the lowest percentile for atherosclerotic plaque. Conclusions: This case represents an extreme and extensively characterized example of the LMHR phenotype and highlights the limitations of extrapolating cardiovascular risk from LDL-C levels alone without consideration of broader patient context and the etiology of hypercholesterolemia. While a single case cannot redefine clinical practice, this well-characterized case is consistent with emergent literature on LMHR, and careful study of such individuals may provide valuable insights into lipid metabolism, atherosclerosis biology, and precision cardiovascular risk assessment.

Entire paper at;

https://www.mdpi.com/2079-9721/14/5/168

3 Likes

Seven Years at 700: The Marathon Runner Whose Sky-High Cholesterol Left His Arteries Spotless

A lean, athletic man in his 30s adopted a ketogenic diet to control ulcerative colitis and watched his LDL cholesterol climb sixfold, from 95 to 574 mg/dL, with total cholesterol peaking above 700 mg/dL. He held those levels for close to seven years while taking essentially no lipid-lowering drugs. Two separate CT angiograms, plus AI-guided plaque quantification, found zero coronary plaque and no stenosis, placing him in the lowest percentile for atherosclerosis. The authors present him as an extreme, exhaustively documented example of the lean mass hyper-responder phenotype and argue that LDL number alone, stripped of metabolic context, is a poor predictor of arterial disease in this specific group. The paper does not claim high LDL is safe for everyone.

The textbook says the arithmetic is simple. Push LDL cholesterol high enough, for long enough, and plaque accumulates in the coronary arteries. The man at the center of this case report has spent nearly seven years testing that arithmetic on his own body, and the plaque has not arrived.

He is described as a lean, competitive endurance athlete with body fat under 12 percent and a resting heart rate in the 40s. In his early 20s he adopted a strict ketogenic diet, roughly 80 percent fat and 2 percent carbohydrate, to manage ulcerative colitis that ordinary drugs had failed to control. The diet worked for his gut. It also rewired his lipid panel in dramatic fashion. His LDL cholesterol rose from a pre-diet 95 mg/dL to a measured peak of 574, his total cholesterol reached 705, and his apolipoprotein B, the count of atherogenic particles, more than quadrupled to 335 mg/dL.

Under conventional risk models these are alarming figures. Yet the rest of his profile broke the usual pattern. His HDL cholesterol rose to 124, his triglycerides fell to 34, his fasting insulin stayed rock bottom, and his inflammatory marker dropped. This triad of very high LDL, very high HDL, and low triglycerides in a lean, insulin-sensitive person defines what researchers now call the lean mass hyper-responder.

The decisive data came from imaging. On CT angiography in 2021 and again in 2026, and on AI-guided quantification by a clinically validated platform, his coronary arteries showed a calcium score of zero, no stenosis, and a total plaque volume of 0 cubic millimeters. He sits in the lowest percentile for plaque despite carrying possibly the highest sustained LDL burden ever documented on serial cardiac imaging.

The authors are careful. One patient cannot overturn decades of cardiology, and this individual also carries elevated lipoprotein(a), a genetic risk factor. But the case dovetails with a larger cohort of 100 similar individuals in which baseline plaque, not LDL or apoB, predicted future plaque. The uncomfortable implication is that the same cholesterol number may carry very different meaning depending on who is carrying it.

Actionable Insights

The honest headline first: this is one person, and nothing here means high LDL is harmless for you. What the case offers is a set of levers, and it lets us size them.

The clearest practical lesson is about metabolic context. The traits that travel with this man’s apparent resistance to plaque are low body fat, high physical activity, low triglycerides, and low fasting insulin. Those are the same markers that predict good cardiovascular outcomes across the general population, and they are largely within your control.

The second lesson is how strongly diet moves LDL in lean, low-carb responders. When this patient added about 100 grams of carbohydrate a day for just 16 days, his LDL fell 71 percent. To put that magnitude in plain terms, that single dietary change lowered his cholesterol more than high-dose statin therapy did. For comparison, his statin cut LDL 31 percent, bempedoic acid 28 percent, and ezetimibe 56 percent. So the effect size of a food change here rivaled or beat prescription drugs.

The takeaway is not to eat Oreos. It is that if you follow a low-carb diet and see LDL spike, that spike is often reversible through diet, and the size of the reversal can be large. Track particle count (apoB), image plaque directly if warranted, and treat the whole metabolic picture rather than a single number. [Confidence: Medium]

1 Like

To allow your cholesterol to run that high, for that long, is absolute insanity. While this individual may have gotten away with this (and I truly doubt that he has), if 1000 people did the same thing, the overwhelming majority of them would not experience zero plaque accumulation.

I can admit the case is fascinating and am surprised to see that there was zero plaque accumulation (and I’m happy they published this case report). BUT damn near every cardiologist is going to caution anyone from doing something so risky.

I find it hard to believe that this individual isn’t at increased risks for a lot of very serious health problems… I hope he has a big life insurance policy and that he’s prepared for the very real risk of an early death.

1 Like

Just to let you know, the person is an MD, PhD

Knew what he was doing in detail.

2 Likes

I think it’s Nick Norwitz. Bold self-experimenter, but sloppy interpreter of medical studies. I hope it works out for him.

1 Like

He should continue this experiment for as long as possible.

1 Like

I don’t think this is a case of saturated fat raising lipids, although I can be wrong, but its the carbohydrate restriction. It might be similar to Viva Longevity! where his lipids were higher than normal, but that was a case of unsaturated fat restriction.

There is no serial lipid data showing the levels over the 6 yrs 8 months, what was the level like? Also 6 yrs and 8 months is not long for CVD.

The claims about apoB and the 100 person cohort is controversial, I’ve seen reports they have a much higher prevalence of fast progressors than other similar cohorts. ApoB being high to very high in everyone doesn’t allow an analysis comparing low and high levels.

1 Like

Correct if you look at the published paper, you see his name and contact:;

His MD is from Harvard and his PhD is from Oxford

Nicholas G. Norwitz

His email address is;

nicholas_norwitz@hms.harvard.edu

To all the people with the wise comments.

How many of you have a MD, PhD?

Above is his email contact, you could have a conversation/debate with him.

“People who say it cannot be done should not interrupt those who are doing it.”

2 Likes

Well, that may not be long, but it is definitely long enough to kill you if you do the wrong things LOL. Plus, why is it so hard for people to understand (accept) that heart health and preventing CVD is way more complicated than just watching your lipids and cholesterol levels. There’s so many n=1 of people with high LDL-C numbers all their lives and they lived to very old age. I have one such case, where one of my cousins had high LDL-C all his life (lowest 120’s) and \never did any meds yet he lived to 101. Would I do same as him? Absolutely not. I’ll make sure my LDL-c stays relatively tame in the 60-80 range and would NEVER feel comfortable to let it go over 100.

Clearly, not everyone gets affected the same way. However, it is common knowledge (for general population) that keeping LDL-c level low is better than having it high. Obviously, many other things need to happen simultaneously (such as exercise, low inflammation, and low insulin/FG etc.) also.

Bottom line, no need to overdo it as @Beth was doing with 5 powerful lipid lowering meds and then she could barely walk. So, for me it is very clear keep LDL-C in normal range (I would NEVER go under 60, even if you put a gun to my head) and do many other things to keep insulin, FG, and HsCRP normal or optimal, and that should be fine as far as CVD is concerned.
To each their own but if you are still thinking that you need to have your LDL-C ZERO or even 20 to me it means you have no clue what you are doing and that is fine by me.

3 Likes

Point well taken, but it was not nearly that bad… incredibly sore and limited during my workouts, but generally fine other than strength training. Just don’t want anyone feeling sorry for me :slight_smile:

2 Likes

Understood, but I should be allowed to exaggerate a bit to make my point LOL.

2 Likes

Wait wait wait I missed this. What were you doing and what happened?! :grimacing:

2 Likes

I won’t bury the lead… I think I’m intolerant to statins… but here ya go!

1 Like

Hmm any possible connection to Bempedoid Acid too? It is bad for tendons from what I understand and if so could that possibly manifest as tendon related soreness after a workout?

It takes people with FH (genetic high cholesterol) ~22 years to start having events, but these are otherwise average people.

Because people with the opposite phenotype (genetic low LDL for life) have no heart disease even though they’re like everyone else: smokers, etc.

Yeah, that’s survivorship bias.

70 mg/dl is totally fine, around the 5th percentile, so 95% of people have higher LDL-c, and nothing that requires action in the short term for healthy people.

There will be more studies that elucidates the efficacy and safety of lower levels within the next couple of years. Some people don’t want to wait like if they are high risk, or try and regress or prevent plaque in N=1 biohacking fashion.

5 Likes

I agree with that, just that’s what it was called, and why it makes sense to not use centenarian anecdotes.

Nothing much is going to happen either way. LDL-c doesn’t really have a useful purpose, it goes to the liver, cells produce their own cholesterol, and there’s still cholesterol in HDL-c. People who reach <70 LDL-C in trials doesn’t drop dead like flies, at best they have less heart disease events. It’s been studied to some extent but it’s a rare level to have, so we’ll see as new studies comes out.

1 Like

That’s it. Norwitz et al are forcing their levels to the stratosphere, all they gain is plaque, in the heart, around the brain.

He hypothesized that using statins lower his energy because LDL lowering impacting his hypothetical energy transport model.

He’s on two LLT (bempedoic acid and ezetimibe) now because of “brain health unrelated to lipids”, and there’s no mention of this despite it dramatically impacting his LDL-c levels. It should be celebrated, but he should stop with the self-dishonesty IMO, and join the LDL-c lowering camp. It’s not so bad. We could use more MD PhD’s here.

Or he’s going to continue being captured by his audience and not say what’s unpopular among the public, but true.

7 Likes