My blood (LDL or total) cholesterol has gone up on the diet. Does this mean that I am at increased risk of developing a heart attack and so need to take a cholesterol-lowering statin drug?

The evidence is that the average response of the blood (LDL or total) cholesterol concentration to an increased fat intake (in the absence of a high carbohydrate diet) on the Banting diet, measured in thousands of patients, is NO CHANGE. Yet we know that values do go up in some subjects. So in an equal number the value must go down, which most cardiologists would consider to be good. How can an “unhealthy” diet produce changes that are either very unhealthy or very healthy? It does not make immediate sense so we need to dig a bit deeper.

There are 2 models for how heart disease develops – the cholesterol theory and the insulin theory. The cholesterol theory holds that cholesterol in the blood rises when one eats a high fat diet and this clogs the arteries causing heart attack. The treatment is therefore simple – avoid all fat from the diet. Also, if your cholesterol is elevated then logically it is also important to reduce it with the use of a cholesterol-lowering “statin” drug. Simple.

The insulin theory holds the opposite – that it is carbohydrate in the diet that causes heart disease, most especially in those with the condition of insulin resistance (IR). When those with IR eat a high carbohydrate diet, they will likely develop Non-Alcoholic Fatty Liver Disease (NAFLD) and the Metabolic Syndrome (MS) described below. It is these conditions which then predict the probability that heart disease will develop.

What we know is that the cholesterol theory of heart disease has never been proven. The best evidence that the science behind this theory is “junk” can be found in Nina Teicholz’s book, The Big Fat Surprise. It seems that we have been seriously misled by science, industry and politics to accept a theory for which there is no good evidence. Then there is an entire $40 million dollar a year industry – the cholesterol lowering (statin) drug industry – that seeks to insure that we continue to accept this unproven theory without question. (But fortunately resistance to this untruth is growing daily.)

According to the cholesterol theory, the only factors in your blood which you need to worry about are either your total or your LDL-cholesterol concentrations – anything that makes either go up is bad, anything that causes either to go down is good. Statin drugs reduce both and so are good as is a low fat diet. The only trouble is that even the most religiously followed low fat diet will drop the total cholesterol by a homeopathic amount (about 0.2mmol/L), which would be too little to make any difference even if cholesterol was the true cause of arterial “clogging”. Worse, no study has yet shown that changing to a low fat diet prevents heart disease, even if it lowers blood cholesterol concentrations.

According to the insulin theory, it is consistently elevated blood insulin concentrations that cause the constellation of conditions we recognise as NAFLD and the Metabolic Syndrome (MS) and it is these conditions that really put one at risk of heart attack because it is the direct cause of these conditions – most especially continually elevated blood insulin concentrations (hyperinsulinaemia) that lead to heart attack. Note that NAFLD and MS develop in those with IR who eat high carbohydrate diets for more than a few decades. Eating fat is NOT the cause except if it is too little fat (and consequently too much carbohydrate).

The key features of NAFLD and MS are abdominal obesity, type 2 diabetes, hypertension, gout and atherogenic dyslipidaemia, which includes elevated blood triglyceride concentrations, increased triglyceride remnant lipoproteins, increased apolipoprotein B (apoB) concentrations, increased numbers of small dense LDL-
cholesterol particles and lower blood HDL-cholesterol concentrations. Other blood markers of heart attack risk in those with MS include elevated blood glucose, insulin and glycated haemoglobin (HbA1c) concentrations.

All these abnormalities reverse on a high fat diet, but are worsened on a high carbohydrate diet. In addition, those with NAFLD and MS will lose weight and their blood pressures fall when they restrict their carbohydrate intakes. The end result is that persons with NAFLD and MS improve their health dramatically when they begin to eat a low carbohydrate diet EVEN IF THEIR TOTAL CHOLESTEROL RISES somewhat. That is because it is NOT cholesterol that puts us at risk of heart disease. Rather it is that constellation of abnormalities that occur in those with NAFLD and MS (as listed above) and which usually improve dramatically when a diet with low carbohydrate  intake is ingested.

In addition we now understand that there are at least 2 components of the so-called “bad” LDL-cholesterol. The two components are (i) small dense LDL particles, which contribute significantly to arterial damage and heart disease. These might be called the Bad Bad Cholesterol! And (ii) the large fluffy LDL-cholesterol particles, which do not contribute at all to heart attack risk. We might call these Good Bad Cholesterol!

Also, it is clear that it is the total number of LDL particles in the bloodstream that increase heart attack risk. So if the blood LDL cholesterol concentration rises, this can be because of an increase in the number of Bad Bad Cholesterol particles, which would be BAD, or it can be because of an increase in the number of Good Bad Cholesterol particles, which would not be so bad. In fact the blood LDL cholesterol value might INCREASE despite a REDUCTION in the number of cholesterol particles if the increase is due to an increase in the Good Bad Cholesterol particles.

So you see, it is impossible to interpret the meaning of a change in the blood cholesterol concentration without knowing what happened to the cholesterol particle numbers and also all the other variables known to modify heart attack risk.

So my answer is the following: If you adopt a low carbohydrate diet you must monitor all the variables discussed above to know if the diet is helping you. If the vast majority of these variables improve, then logically it does not matter what happens to your total LDL cholesterol, since it is entirely possible that this change was brought about by an increase in large fluffy Good Bad Cholesterol particles with a reduction in the small dense Bad Bad Cholesterol particles, producing an overall reduction in cholesterol particle numbers.

So here is the Table you need to understand:

I think it is fairly obvious which diet those with IR and the MS should be eating if they want to reduce their risk of heart attack and optimise their health.

So that is it.

Both your health and your risk of heart disease is about many factors other than simply your blood cholesterol concentration.

Please distribute this email to anyone you think might benefit from reading it.

Written by Prof Timothy Noakes OMS

MBChB, MD, DSc, PhD(hc), FACSM, (hon) FFSEM (UK), (hon) FFSEM (Ire)