Blood Tests on a Ketogenic Diet

What your Cholesterol Results Mean – Dr. Paul Mason

Learn how Dr. Paul Mason uses real patient lab results to explain what your cholesterol numbers actually mean on a ketogenic diet and how to tell if your blood work points to metabolic risk or robust heart health.

This video features sports and exercise physician Dr. Paul Mason breaking down standard cholesterol panels to show why total and LDL cholesterol alone do not reliably predict heart disease risk, especially for people following a ketogenic or low‑carb diet. He explains what lipoproteins really are, how sugar damages LDL particles, why triglycerides and HDL are powerful markers of metabolic health, and how to use simple ratios and patterns to distinguish a benign “type A” cholesterol profile from a high‑risk “type B” pattern. Along the way, he discusses advanced lipid testing, the Feldman protocol’s rapid LDL changes on a high‑fat diet, and the pivotal role of insulin and fasting in driving LDL receptor activity and circulating LDL particle levels.

Summary

Dr. Mason explains that what we casually call “cholesterol” on blood tests are actually different lipoprotein particles (chylomicrons, VLDL, IDL, LDL, HDL) that transport fats, including cholesterol, through the bloodstream.
He distinguishes healthy, buoyant LDL particles from disease‑causing small, dense LDL that have been damaged by sugar‑driven glycation and oxidation, highlighting that carbohydrate‑induced high blood glucose, not saturated fat, is the main culprit in LDL particle injury.
Using gel electrophoresis images, he illustrates “pattern A” LDL (a single healthy peak) versus “pattern B” LDL (multiple abnormal peaks) and shows how damaged LDL penetrates the arterial wall, is taken up by macrophages, and contributes to atherosclerotic plaque.
He shows how standard panels often estimate, rather than directly measure, several lipoproteins, and argues that triglyceride levels, HDL levels, and the triglyceride/HDL ratio are powerful, practical tools to infer whether someone has a protective type A or risky type B cholesterol profile.
Dr. Mason presents data that low triglycerides (for example, under about 0.8 mmol/L) and higher HDL (around 1.5 mmol/L or more) are strongly associated with a favorable type A LDL pattern, which he often sees in patients on long‑term ketogenic diets.
He explains why higher HbA1c and chronic hyperglycemia correlate with more oxidized LDL and higher heart attack risk, clarifying why people with diabetes have substantially higher rates of cardiovascular disease.
The talk reviews the Feldman protocol, where increasing dietary fat for three days can markedly lower measured LDL by upregulating LDL receptors via insulin‑mediated gene expression, and contrasts this with fasting, which can produce transiently higher LDL due to reduced receptor activity.
In closing, he emphasizes that an elevated LDL cholesterol number by itself is not automatically dangerous; what matters is whether the LDL is damaged and whether the overall metabolic picture (triglycerides, HDL, HbA1c, inflammation, and additional tests when needed) points to genuine cardiovascular risk.

Video description

Dr. Paul Mason – “Blood tests on a ketogenic diet – what your cholesterol results mean”

Dr Paul Mason obtained his medical degree with honours from the University of Sydney, and also holds degrees in Physiotherapy and Occupational Health. He is a Specialist Sports Medicine and Exercise Physician.

Dr Mason developed an interest in low carbohydrate diets in 2011. Since then he has spent hundreds of hours reading and analysing the scientific literature.

For the last two years, Dr. Mason has been applying this knowledge in treating metabolic and arthritis patients who have achieved dramatic and sustained weight loss and reductions in joint pain.

This presentation is from the 2018 Low Carb Down Under Sydney conference.

Transcript Summary

What “cholesterol” on your blood test really means

Dr. Paul Mason opens by explaining that the word cholesterol is often used loosely to describe several distinct lipoprotein particles that carry fats through the bloodstream, including cholesterol. He clarifies that these particles—such as chylomicrons, VLDL, IDL, LDL, and HDL—have different sizes and densities, and that calling them all “cholesterol” is like confusing a horse with the cart it pulls. In a fasting blood sample, chylomicrons are largely gone, so standard lipid panels mostly reflect VLDL, IDL, LDL, and HDL, each playing its own role in fat transport.

Lipoprotein classes and why size and density matter

He describes how VLDL particles leave the liver as large, fat‑laden carriers and gradually shrink to IDL and then LDL as they deliver their cargo to tissues, while HDL represents the well‑known “good cholesterol.” The LDL particles we measure are not inherently harmful, and he notes he is happy to have healthy LDL circulating in his own bloodstream. The key issue is not the presence of LDL but whether those LDL particles remain intact or become damaged, which changes their size and density and their impact on cardiovascular risk.

How sugar damages LDL and creates high‑risk “small, dense” particles

Dr. Mason then focuses on how LDL becomes dangerous when exposed to high blood glucose. He explains that glucose can attach to LDL in a process called glycation, which then predisposes the particle to oxidative damage, producing the small, dense LDL that is linked to heart disease. This damaged LDL is not the result of saturated fat intake but of carbohydrate‑driven elevations in blood sugar, which is why he emphasizes that high‑carb diets can be particularly harmful for lipoprotein health.

Visualizing pattern A versus pattern B LDL

To make this concrete, he shows gel electrophoresis data in which LDL particles separate into distinct peaks based on their density. A “pattern A” LDL profile displays a single, smooth peak and reflects a healthy population of LDL particles that have not been significantly glycated or oxidized. By contrast, a “pattern B” profile shows multiple smaller peaks corresponding to damaged LDL subfractions, and this pattern is strongly associated with cardiovascular disease.

Why standard lipid panels estimate some values

Dr. Mason notes that typical cholesterol reports list a total cholesterol value and component values, but these do not always add up because several lipoproteins are not directly measured. Instead of performing time‑consuming and expensive centrifugation, laboratories often estimate VLDL and calculate LDL using assumed relationships, which introduces inaccuracy. HDL is usually directly measured, but he argues that these limitations mean we must interpret standard panels intelligently rather than treating every out‑of‑range value as equally worrisome.

LDL receptors, ApoB, and the life cycle of LDL

He describes the normal life cycle of VLDL and LDL particles, emphasizing the ApoB‑100 protein that sits on each LDL particle like a single “access card.” LDL receptors on liver and peripheral cells recognize ApoB‑100 and use it to clear healthy LDL from circulation, but glycation targets proteins, including ApoB, and can damage this “card” so the receptor no longer recognizes the particle. When LDL cannot be cleared effectively, damaged particles accumulate in the bloodstream, become smaller as they lose cargo, and their particle number rises even if the total cholesterol volume does not appear markedly high.

From oxidized LDL to plaque formation

Dr. Mason explains how oxidized LDL increases the permeability of the endothelial layer lining the arteries, allowing these particles to slip underneath that one‑cell‑thick barrier. Once there, they encounter macrophages equipped with scavenger receptors that preferentially bind damaged LDL, eventually turning into foam cells laden with lipid droplets. Over time, these foam cells and lipid deposits form atherosclerotic plaques that narrow arterial lumens, as illustrated by an example of a severely narrowed left anterior descending coronary artery.

The role of HbA1c and diabetes in heart disease

He connects this biology to clinical markers by pointing out that HbA1c is a powerful blood test for predicting heart disease because it reflects how much glucose has glycated red blood cells. The same high blood glucose that drives HbA1c also damages LDL particles, which explains why people with diabetes experience dramatically higher rates of heart attacks. He highlights that reducing chronic hyperglycemia is central to reducing LDL damage and cardiovascular risk.

Using triglycerides and HDL to infer LDL pattern

The talk then turns to practical interpretation of standard blood tests. Dr. Mason shares research showing that low triglycerides are strongly associated with a protective pattern A LDL profile, while high triglycerides correlate with high‑risk pattern B. He notes that triglyceride levels below about 0.5 mmol/L almost always indicate pattern A, whereas levels above about 2 mmol/L are strongly indicative of pattern B, with intermediate values being less definitive.

HDL levels and the triglyceride/HDL ratio

He offers similar guidance for HDL, observing that low HDL (around 0.4–0.5 mmol/L or less) is linked with pattern B, while HDL above about 1.5 mmol/L points to pattern A. He presents a patient with high total cholesterol but very high HDL—levels typical of ketogenic dieters—and explains why this supports reassurance rather than alarm. Combining triglycerides and HDL into the triglyceride/HDL ratio provides another robust marker; for example, a ratio below about 0.8 mmol/L is generally reassuring, whereas values above about 1.8 are concerning for pattern B.

How this applies to patients on a ketogenic diet

Dr. Mason points out that nearly all of his patients who have been on a ketogenic diet for an extended period have at least one, and often several, excellent markers—very low triglycerides, high HDL, or a favorable triglyceride/HDL ratio. In such cases, he usually does not worry about an elevated LDL cholesterol number by itself because the overall pattern strongly suggests type A LDL and low cardiovascular risk. Only when these key markers fall into grey zones does he move to more advanced testing and nuanced clinical decisions.

When to order additional tests

For patients whose standard lipid profiles are ambiguous, he considers further investigations like HbA1c, coronary artery calcium scoring, detailed lipid subfraction analysis, and inflammatory markers. These additional tests help paint a fuller picture of cardiovascular risk and guide individualized decisions that patients should discuss with their own physicians. He stresses that this stepwise approach avoids unnecessary anxiety and treatment for people whose apparently high LDL is actually part of a benign pattern.

The Feldman protocol and rapid LDL changes

He then describes the Feldman protocol, in which people with very high LDL on a ketogenic diet adopt a very high‑fat diet for three days and then repeat their blood test, often seeing LDL “crash” to much lower levels. This phenomenon, he explains, relates to LDL receptor regulation: higher calorie intake increases insulin, which in turn increases genetic expression of LDL receptors and improves their affinity for LDL particles. As receptor numbers and activity rise over several days, healthy LDL is pulled more rapidly from circulation, lowering measured LDL cholesterol.

Insulin, fasting, and LDL receptor dynamics

Dr. Mason contrasts this with fasting, which lowers insulin and downregulates LDL receptor expression, allowing LDL to build up transiently in the bloodstream. This explains why many people see higher LDL if they fast longer than the usual 8–10 hours before a blood draw. He notes that statin medications work partly by increasing LDL receptor activity, thereby reducing circulating LDL particle count, though their overall role must still be weighed carefully case by case.

Key takeaways about LDL on a ketogenic diet

In his closing remarks, Dr. Mason reiterates that high LDL is not automatically harmful, and that the real danger lies in damaged, oxidized LDL driven by high blood sugar and poor metabolic health. He emphasizes the value of focusing on triglycerides, HDL, the triglyceride/HDL ratio, HbA1c, and, when indicated, advanced tests to determine whether someone has a low‑risk type A or high‑risk type B profile. He concludes that for his highly muscular, lean keto patient with low triglycerides and high HDL, he would confidently approve life insurance coverage because the data show a metabolically healthy, low‑risk cardiovascular picture despite elevated total cholesterol.