
A lady walked into my clinic last week and said in a rather disheartened voice, “I know my high cholesterol runs in my family. I’ve been trying for so long to bring it down and I think it is still high. I don’t know what else I can do!”
She had seen one of our nurses six months before who gave her the standard advice for cholesterol lowering - reducing the amount of fat in her diet by cutting down on red meat, choosing lean meats instead, switching to a low-fat dairy, eating less cheese, ditching butter for a plant-spread alternative.
My patient’s cholesterol markers had changed since, but only by a couple of decimal points and still stayed raised. When I looked at her Hba test it was at 40, which is really close to the level of prediabetes (diagnosed at Hba of 42 mmol/mol (or 6.0%). The picture of what was happening to her cholesterol markers and metabolic health became clear.
We have been told to be mindful of our cholesterol levels since the late 60s, many people I see in my clinic know their cholesterol numbers by heart. It is one test that everyone knows a fair bit about. But do we really? Do we presently have a good understanding of the implications cholesterol test has on our risk of heart disease, or are we on a slightly wrong track here? Let’s look at the evidence from science.
The lipids test, or your cholesterol test in plain language, has been offered by general practitioners and cardiologists since the early 60s, when the diet-heart hypothesis was born. I wrote about how this hypothesis was proposed by the American physiologist Ancel Keys and how he supported his theory for the role of saturated fat in the development of atherosclerotic disease with his findings from the Seven Countries study, see my post about it here.
Why do we measure cholesterol routinely?
The main reason is due to mortality from heart disease. Since the 50s deaths from heart disease, including myocardial infarctions, coronary artery disease and other heart-related conditions have been number one cause of death worldwide. Although, it is estimated that knowledge in the medical field has been doubling every 3 years since 2010 [Adam Grant “Think Again”], with the advances in medical interventions we have not been able to improve on the main cause of death worldwide - cardiovascular disease remains the top cause of mortality in 2025.
Back in the 50s physicians and cardiologists based their rationale for measuring cholesterol in the blood on a few lines of evidence:
- Several diet experiments which reported that saturated fat increased total cholesterol (TC)
- Presence of cholesterol esters in human atherosclerosis plaques
- The belief that saturated fat increased the level of cholesterol in the blood, predisposing to cholesterol deposition in arteries and ultimately CVD
- Experiments on animals (by a Russian doctor Anitschkov) who fed rabbits a high cholesterol diet (but are rabbits carnivores?), as a result, their arteries thickened and filled up with cholesterol (but are the thickenings in the arteries of rabbits the same as the thickenings of the arteries in humans?)
The fact unknown to many people, including many physicians, is that this theory based on the effects of fat in the diet and development of atherosclerotic disease remained a theory, was never proven or agreed upon by scientists and researchers, but since the 60s was promoted as the dietary recommendation for the population en masse.
A report to the American Heart Association (AHA) in 1957 stated, “The aim of this discussion is to summarize and evaluate evidence for and against the concept that the fat content of the average present-day North American or north European diet is a significant factor in the genesis of cerebral, myocardial, renal, or peripheral atherosclerosis. To date there is no incontrovertible evidence for such a relationship…”. The authors also wrote, “…Atherosclerosis in all probability has no single cause. It results most likely from a combination of factors, or is, as Page suggests, a multifaceted disease”…In the opinion of the authors of this review, there is not enough evidence available to permit a rigid stand on what the relationship is between nutrition, particularly the fat content of the diet, and atherosclerosis and coronary heart disease”.
Most astonishingly, in their conclusion the authors stated, “Thus, the evidence at present does not convey any specific implications for drastic dietary changes, specifically in the quantity or type of fat in the diet of the general population, on the premise that such changes will definitely lessen the incidence of coronary or cerebral artery disease”.
Despite this report, a few years later the AHA, without any additional research evidence, issued a recommendation for reduced intake of saturated and total fat and an increased intake of polyunsaturated fat. In its 1961 report the AHA reported these changes “…as a possible means of preventing atherosclerosis and decreasing the risk of heart attacks and strokes”
To-date more than 20 review papers have been published to conclude there is no link between saturated fat and heart disease and cardiovascular mortality. But the dietary recommendations based on the assumptions from more than 50 years ago prevail, mostly due to the fact that there’s a strong influence of dogma in the medical community. How many physicians routinely check the findings of scientific reports, especially in such a fickle, ever-changing field as nutrition?

A study published just 10 days ago in the Journal of the American College of Cardiology: Advances, examined the role of high cholesterol levels in people on ketogenic diets and their risk of atherosclerotic disease. Following the dietary patterns of participants for one year, the researchers found no correlation between atherosclerosis and extremely high cholesterol levels. The participants had followed a ketogenic diet for an average of 5 years. The authors concluded that the lipid hypothesis, which postulates that elevations in apolipoprotein B (ApoB) and low-density lipoprotein cholesterol (LDL-C) are significant risk factors for atherosclerosis and should be primary treatment targets, could be wrong, as the study participants, known as Lean Mass Hyper-Responders (LMHRs), were found to have high LDL-C and ApoB levels without evidence of baseline coronary artery disease or disease progression over time.
The authors concluded that while assessing people cardiovascular risk and potential treatment, a more personalised approach is warranted.
Since the 60s our tests for cholesterol markers have advanced a lot. Back then it was only total cholesterol that was measured. Total cholesterol is still being measured, but most physicians know that it is not a great indicator for one’s risk of heart disease. A cholesterol ratio is a better one, a non-HDL cholesterol is also somewhat telling and so are the triglycerides.
But first things first: in your cholesterol test, you will find a total cholesterol (in the UK the NHS sets the healthy levels to be below 5 mmol/L), high-density lipoprotein cholesterol (HDL-C) - the desired range is between 1.2 and 1.6 mmol/L; low-density lipoprotein cholesterol (LDL-C) - preferably within the 2-3 mmol/L range and non-HDL cholesterol, up to 2.6 mmol/L.
But first things first: in your cholesterol test, you will find a total cholesterol (in the UK the NHS sets the healthy levels to be below 5 mmol/L), high-density lipoprotein cholesterol (HDL-C) - the desired range is between 1.2 and 1.6 mmol/L; low-density lipoprotein cholesterol (LDL-C) - preferably within the 2-3 mmol/L range and non-HDL cholesterol, up to 2.6 mmol/L.
It is important to know that the cholesterol markers we test in the blood is a proxy measurement, as it indirectly reflects the liver's production and your body's ability to regulate cholesterol levels. Cholesterol is produced in the liver, regulated by the liver and is also ‘decided’ by the liver how much of it to use, how much to excrete. Thus, blood cholesterol is a test which gives us information about the overall cholesterol status in the blood, as influenced by the liver's activity.
Cholesterol levels in your blood test are not reflective of your diet of yesterday, this week or even the past month. These are cumulative effects of your diet, levels of exercise, your smoking status, intake of alcohol, your genetic profile and your age. When people embark on the journey to proactively lower cholesterol, with diet along, the cholesterol markers take a long time to shift, and when they do these shifts are minor. The biggest changes to cholesterol levels are observed when one stops smoking or cuts down or entirely removes alcohol from their diet.
So what about my patient who still had raised cholesterol markers after she followed the advice for dietary changes to bring her cholesterol down? While doing her diet assessment, I learned that to compensate for the lower energy available from her new diet, she began eating more rice, pasta, more bread. She was not told that sugary foods could impact her cholesterol levels, and thus her daily mid-morning snack included a cup of coffee and a few biscuits. It was time for me to bring out the main heart disease culprit - SUGAR.
This is where we need to come back to examine triglycerides, as I mentioned them before. Triglycerides are an important measure of your heart health. As you consume foods that are rich in added sugars or sources of refined carbohydrates, they are turned into blood sugar (glucose) by the body, the liver further metabolises them into fats. High triglycerides levels indicate you have insulin resistance, a sign of metabolic syndrome cluster of diseases.
It is estimated that high triglycerides may contribute to hardening of the arteries or thickening of the artery walls, arteriosclerosis. Extremely high triglycerides can also cause acute inflammation of the pancreas (pancreatitis).
The liver is the master organ of our metabolism. It is the liver that metabolises fats, protein and also carbohydrates, including all types of sugar. As our hunter-gatherer ancestors relied on sources of carbohydrates in their environment from fibrous foods - such as plants, roots of plants, vegetables and sometimes even barks from trees, their liver was not flooded with sources of excess sugar - fruit were scarce, berries and honey were a very rare occurrence in their diet. Being ubiquitous now, sugar can dominate one’s diet as part of their sweet foods intake, but also as an integral part of many savoury foods, which lo and behold, if we had intense levels of physical activity, those comparable to our ancestors - like building huts, moving through vast territories or hunting for a wild bore for hours on end, these would be a capable enough job for the liver to handle. But as we over-consume refined carbohydrates and high-sugar foods, the liver reacts by producing too much fat, the fat that is not only stored in subcutaneous tissue (under the skin), but also in the liver itself. It is these metabolic processes that become the sequence of events leading to one’s high cholesterol levels.
So if it is not the cholesterol test, what is the best predictor for a risk of heart disease?

Your HbA1c, or Hba test for short. This is glycated haemoglobin - a test that shows how your body has been able to handle blood sugar levels (glucose) for the last 2-3 months. Raised blood sugar causes insulin resistance, a condition of dysregulated insulin and glucose levels, precedes diabetes type 2 diagnosis by about 10-15 years. This is the leading cause of cardiovascular disease.
When there’s proliferation of sugar in the blood stream, the arteries and veins become rigid, stiff, and the blood finds it difficult to pass through, as a result the heart pumps faster and blood pressure is raised. Over longterm inflammation caused by sugar further damages blood vessels, making them susceptible to micro injuries and rupture. Fatty deposits may start forming in the blood vessels, as results of high levels of sugar in the blood.
So the evidence is here: if you want to support your heart to stay healthy, keep low the intake of sugars, both natural and artificial, as well as the amount of refined carbohydrates you eat. Check your HbA1c levels regularly. By controlling your blood sugar, you are keeping your inflammation at bay protecting not only your heart, but health of the whole body.
Check out my Reverse Insulin Resistance Diet Plan to get the full list of foods to cut down on or remove to keep your blood sugar balanced, and the foods to enrich your diet with instead. The plan includes menus for breakfasts, lunches and dinners teaching you how to cook delicious meals to support your long-term health.
Have you had questions about your cholesterol levels that were answered by your doctor? Or maybe it is your family history of cholesterol that concerns you?
Share in comments.
Stay healthy, be joyful!
Love,
Katya
Share in comments.
Stay healthy, be joyful!
Love,
Katya