For several decades, eggs were commonly portrayed as a major cause of raised cholesterol and cardiovascular disease. That position has been substantially revised: current evidence suggests that dietary cholesterol has a relatively modest effect on blood cholesterol in most people, whereas saturated and trans fats are more important determinants of LDL cholesterol and cardiovascular risk.
The physiology is more nuanced than the older “cholesterol-in, cholesterol-out” model implied. The liver does synthesise cholesterol endogenously, and many people compensate for increased dietary cholesterol by reducing hepatic production, but the degree of compensation varies considerably between individuals. For that reason, eggs are not best understood as “heart-healthy” in all circumstances, but rather as a food whose impact depends on the wider dietary pattern and the individual’s metabolic risk profile.
There is stronger support for improving lipid profiles by changing the quality of dietary fat and increasing fibre intake. Replacing saturated fats with unsaturated fats, particularly polyunsaturated fats, is associated with lower LDL cholesterol and a reduced risk of cardiovascular events, while soluble fibre helps lower LDL cholesterol by interrupting enterohepatic bile acid recycling. In practical terms, this means that foods such as olive oil, nuts, seeds, legumes, oats, vegetables, and oily fish are more consistently supported than a narrow focus on single items such as eggs.
Low-carbohydrate and ketogenic diets are more complex. Many people lose weight on them, which may improve some cardiometabolic markers, but a subset of lean individuals show pronounced rises in LDL cholesterol and related atherogenic markers during carbohydrate restriction. Emerging evidence also indicates that gut microbial changes may contribute to altered lipid metabolism, although this area is still developing and should not be overstated.
Highly restrictive “detox” or “alternative” dietary programs are unsupported by clinical evidence and may be nutritionally unbalanced and thus harmful. They might be claimed to “purify” the body or reset metabolism, but heart health is better served by sustainable patterns that improve LDL cholesterol, support fibre intake, and minimise excess saturated fat.
What does all that mean in practice? Here are a few simple rules that follow from the new insights:
- Do not over-emphasize dietary cholesterol (e.g., eggs) as a primary driver of cardiovascular risk.
- Focus instead on reducing saturated and trans fat intake.
- Replace saturated fats with unsaturated fats, especially polyunsaturated fats (e.g., use olive oil, eat nuts and seeds).
- Increase intake of soluble fibre (e.g., oats, legumes, vegetables) to help lower LDL cholesterol.
- Consider overall dietary patterns rather than judging single foods in isolation.
- Recognize that individual responses to dietary cholesterol vary; tailor intake accordingly if lipid levels are a concern.
- Include foods with consistent cardiovascular benefit, such as oily fish, plant-based foods, and whole grains.
- Be cautious with low-carbohydrate or ketogenic diets, particularly if lean, and monitor lipid profiles if following such diets.
- Prioritize sustainable, balanced eating patterns over restrictive or extreme diets.
- Avoid “detox” or alternative dietary regimens lacking clinical evidence, as they are ineffective or harmful.
Key references
- Carson JAS, Lichtenstein AH, Anderson CAM, et al. Dietary cholesterol and cardiovascular risk: a science advisory from the American Heart Association. Circulation. 2020;141:e39–e53.
- Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368:1279–1290.
- Hooper L, Martin N, Jimoh OF, et al. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. 2020;(5):CD011730.
- British Heart Foundation. Healthy eating – reduce your risk of developing heart disease. 2023. – Search
- NHS. Facts about fat. 2022. – Search
- Ketogenic Diet reduces friendly gut bacteria and raises cholesterol levels
- Gut bacteria can break down cholesterol | Nature Reviews Cardiology
- Healthy eating: applying All Our Health – GOV.UK
3 Responses to Which diet is best for heart health?
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Beyond the “Cholesterol-In, Cholesterol-Out” Model: The Lean Mass Hyper-Responder (LMHR) Phenomenon
Your point that a subset of lean individuals show pronounced rises in LDL cholesterol and related atherogenic markers during carbohydrate restriction highlights one of the most fiercely debated frontiers in modern lipidology. To explore this specific nuance further, we can look at a rapidly growing body of research driven by citizen scientists and metabolic researchers who have formally categorized this exact subgroup.
## Defining the LMHR Phenotype
In recent years, researchers have officially termed this lean subgroup Lean Mass Hyper-Responders (LMHR) (Norwitz et al., 2022). Coined initially by software engineer Dave Feldman and later validated in peer-reviewed literature alongside Dr. Nicholas Norwitz (a Harvard-trained MD/PhD), the LMHR phenotype is a distinct metabolic profile that appears when lean, insulin-sensitive individuals adopt a ketogenic or strict low-carbohydrate diet.
Rather than a generic rise in cholesterol, LMHRs exhibit a highly specific lipid triad (Norwitz et al., 2022):
* LDL Cholesterol: Extremely elevated (200 mg/dL or higher, often climbing past 400 mg/dL)
* HDL Cholesterol: High (80 mg/dL or higher)
* Triglycerides: Exceptionally low (70 mg/dL or lower)
The Lipid Energy Model: Energy Traffic vs. Disease
To explain why this happens preferentially in lean individuals, Feldman, Norwitz, and their colleagues proposed the Lipid Energy Model (LEM).
The model argues that when a lean person with low body fat restricts carbohydrates, their systemic glycogen stores deplete rapidly. To fuel the body, the liver must drastically ramp up the trafficking of fat. It does this by packaging lipids into large numbers of Very Low-Density Lipoproteins (VLDLs) to deliver energy (triglycerides) to tissues like skeletal muscle. As the muscles quickly burn up those triglycerides, the empty remnants are left circulating in the bloodstream—which registers on standard blood panels as an astronomical spike in LDL cholesterol.
To demonstrate that this is a dynamic metabolic traffic pattern rather than genetic damage, Norwitz famously conducted a highly controlled self-experiment:
The Oreo vs. Statin Comparison:
Consuming a strict ketogenic diet, Norwitz had a baseline LDL cholesterol of 545 mg/dL. By deliberately adding a standard serving of Oreo cookies (introducing carbohydrates back into his system) to his daily diet for 16 days, his LDL cholesterol dropped by a staggering 71%. This reduction was far more potent than what is typically achieved by maximum-dose statin medications (Norwitz et al., 2022). When carbohydrates became available, his liver simply stopped needing to broadcast mass amounts of fat-carrying vehicles across his system.
Citizen Science and the KETO Trial:
Because mainstream funding for checking if hyper-high LDL can occasionally be benign is notoriously difficult to secure, Feldman founded the Citizen Science Foundation. Through crowdsourcing and patient-led funding, they partnered with academic institutions—such as the Lundquist Institute at Harbor-UCLA Medical Center—to subject the LMHR phenomenon to rigorous clinical imaging trials.
The landmark results of this effort, known as The KETO Trial, were published in the journal Metabolism (Budoff et al., 2024).
The study evaluated lean individuals who had experienced carbohydrate-restriction-induced LDL cholesterol spikes of 190 mg/dL or higher (with a mean LDL of 272 mg/dL and some as high as 591 mg/dL) for an average of 4.7 years (Budoff et al., 2024). Researchers used advanced Coronary Computed Tomography Angiography (CCTA) to measure their arterial plaque burden and compared them to a matched, healthy control cohort from the Miami Heart study whose average LDL was much lower (123 mg/dL).
The findings challenged traditional cardiovascular assumptions:
* No Significant Difference: There was no significant difference in total coronary plaque burden or coronary artery calcium (CAC) scores between the high-LDL keto group and the low-LDL controls (Budoff et al., 2024).
* No Correlation: Within the carbohydrate-restricted cohort, there was zero correlation between the absolute height of the LDL cholesterol levels and the presence of coronary plaque (Budoff et al., 2024).
Moving the Conversation Forward:
This grassroots scientific movement, the execution of these clinical trials, and the fierce medical debate surrounding them is the central focus of the recent Amazon Prime documentary, The Cholesterol Code.
As you rightly conclude, individual metabolic risk profiles vary considerably, and we must move past judging single items in isolation. The emergence of the LMHR phenotype proves that lipid panels cannot be interpreted in a vacuum; the exact same elevated LDL number may represent a completely different pathology—or a completely different physiology—depending entirely on an individual’s leanness, insulin sensitivity, and wider dietary context.
References
Budoff, M., Manubolu, V. S., Kinninger, A., Norwitz, N. G., Feldman, D., Wood, T. R., Cury, R., Feldman, T., Fialkow, J., & Nasir, K. (2024). Carbohydrate restriction-induced elevations in LDL-cholesterol and atherosclerosis: The KETO Trial. Metabolism, 153, 155854. https://doi.org/10.1016/j.metabol.2024.155854
Norwitz, N. G., Soto-Mota, A., Feldman, D., Parpos, S., & Budoff, M. (2022). Case Report: Hypercholesterolemia Lean Mass Hyper-Responder Phenotype Presents in the Context of a Low Saturated Fat Carbohydrate-Restricted Diet. Frontiers in Endocrinology, 13, 830325. https://doi.org/10.3389/fendo.2022.830325
thanks
Notice:
There’s a documentary film “The Cholesterol Code ” (directed by Jennifer Isenhart and featuring citizen scientist Dave Feldman) available to watch directly on Amazon Prime Video.
The documentary tracks Dave Feldman’s transition from a regular software engineer to an independent researcher following an unexpected lipid result on a low-carbohydrate diet, ultimately mapping out the Lean Mass Hyper-Responder phenomenon and funding the clinical imaging trials discussed above.