Thank you to Dr Malhotra for drawing attention to a controversial subject.
It was thoroughly gratifying to read the following key points in Dr Malhotra’s article:
1) Dietary carbohydrates increase levels of highly atherogenic small, dense LDL cholesterol (sdLDL-C).
2) Dietary saturated fat increases levels of both HDL cholesterol (which is inversely correlated with cardiovascular disease) and large buoyant LDL cholesterol (which is not known to be atherogenic).
A couple of points that weren’t mentioned in the article: the type of monosaccharide consumed also matters – many recent studies show that fructose seems to alter the LDL subclass profile more adversely than glucose does.
And when looking at a cholesterol profile, we need to start scrutinising the Triglyceride:HDL ratio, or even the triglyceride level alone, and stop focussing on the total LDL level.
(Because besides direct measurement of sdLDL, which is not currently available in most labs, the best predictor of sdLDL is the Triglyceride:HDL ratio or the triglyceride level alone).
For many years we have been unwittingly giving incorrect advice to our patients – for example from the 70’s onwards we have been telling them to cut down on eggs and other cholesterol rich foods (it has now been known for many years that dietary cholesterol does in fact reduce levels of sdLDL-C ); and that they should eat margarine instead of butter (at that time unbeknownst to us margarine used to be full of trans fats, and now they are full of pro-inflammatory omega-6 PUFAs).
It will take many years to convince the general public that dietary cholesterol and saturated fat are not the villains that they were once purported to be, and that it is in fact sugar, bread, rice, pasta, and sweet drinks (including juices and smoothies) that we should be avoiding instead of fat. We need to urgently start undoing the harm that we have done with the dietary advice that has been meted out over the last few decades; it is going to take a good few years, if not an entire generation, to counteract the current engrained thinking that a low-fat diet is the best diet. For example, despite headlines in the popular press proclaiming that it is now ok to eat eggs, it is still a widely held belief in the general population that egg yolks are a no-no.
I have an interest in nutrition and after having conducted much online research (mostly on pubmed) I have been trying for a few years to convince my medical friends of the following points, to no avail. (For some reason it has been much easier to convince non-medical friends):
• Food is not just a simple fuel for our bodies – we should remember that food is also a type of environmental exposure.
• Proper nutrition offers one of the cheapest and most effective ways of decreasing the risk of cardiovascular disease and many other Western diseases, including obesity.
• Small, dense LDL particles are particularly atherogenic.
• Levels of small, dense LDL particles are closely correlated with carbohydrate intake.
• Fructose increases levels of small, dense LDL particles more than glucose does.
• Saturated fat increases levels of HDL cholesterol.
• Saturated fat increases levels of large buoyant LDL cholesterol.
• A calorie to me isn’t the same as a calorie to you, because we both metabolise them differently.
• Chronic low-grade inflammation is a key step in most Western diseases (including obesity) and the ratio of omega 6 fatty acids to omega 3 fatty acids is crucial to the development inflammation.
• In general omega-6 PUFA are pro-inflammatory and omega-3 PUFA are anti-inflammatory.
• Just replacing carbohydrates with any old type of fat won’t do: we need to try and increase the ratio of omega-3 PUFA to omega-6 PUFA, (ideally it [the omega 6 to omega 3 ratio] should be around 3:1 or lower – hard to achieve when the average vegetable oil has a ratio of 15:1).
• The current obesity epidemic in Western countries might not be only about ‘too much food and too little exercise’; it is probably also due to a complex interaction between genetics, epigenetics, and the microbiota, (the usual suspects of food and exercise both cause epigenetic and gut microbiota changes).
• Cereal grains promote an inflammatory microbiota (and also cause leptin resistance). iv
• A diet of grain-free whole foods with carbohydrate and fibre from fruits and vegetables may produce a gastrointestinal microbiota consistent with our evolutionary condition, potentially explaining the exceptional macronutrient-independent metabolic health of populations consuming a Palaeolithic type diet.
(For those interested, part of the explanation for the atherogenicity of sdLDL-C is due to their reduced systemic clearance by the LDL receptor; their increased vulnerability to oxidation; they are retained preferentially by artery walls; and they carry lipoprotein-associated phopholipase, which has an important role in atherosclerosis).
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Insulin Resistance, Small LDL Particles, and Risk for Atherosclerotic Disease.
Competing interests: None declared