Why do I care? Well I follow a low carb diet – why because it really works for me. I find it easier to lose and maintain weight (important for my sport) and also I am trying to prove (by experimenting on myself) that you don’t need large amounts of carbs and sugar for optimum athletic performance. But still people say, well all this is fine, but if you keep eating all that fat you’re gonna die of a heart attack!
So I though I would spend a bit of time this afternoon to explain why I think cholesterol intake has nothing to do with heart attacks.
The conventional wisdom of course is that high cholesterol intake in the form of saturated fat causes cardio vascular disease (CVD). But why? This belief is so wide-spread that most people will think you are simply bonkers if you disagree. But 99.9999% of people have never questioned this hypothesis and have no idea why or how high cholesterol might be causing CVD. They just assume that the scientists and doctors know. But they don’t No one has ever shown the mechanism by which this supposed link might work. The most that has ever been shown is a correlation and I’ll talk about that further on in the article.
How did this come about?
Rates of heart disease really began to increase significantly about fifty years ago and tests in the fifties and sixties showed an association between heart disease and fat deposits along artery walls. And as cholesterol was found to be present in those deposits and as doctors had previously associated familial hypercholesterolaemia (hereditary high blood cholesterol) with heart disease, they concluded that cholesterol must be to blame.
Now familial hypercholesterolemia is a genuine metabolic disorder. Its hereditary and it effects around 1 in 500 people. You can read about it here. But just because people with a metabolic condition that causes the body to produce too much cholesterol get CVD, doesn’t mean that a normal level of cholesterol in the rest of us might be the cause.
The trouble was there was absolutely no evidence that the cholesterol was causing the strange deposits on the artery walls, it was simply contained within and around them. It might be worth at this stage spending a few minutes looking at what cholesterol is and what it does in the body.
What is cholesterol and why do we need it?
This entry in Wikipedia pretty much sums up what cholesterol does for us.
Cholesterol is required to build and maintain membranes; it regulates membrane fluidity over the range of physiological temperatures. The hydroxyl group on cholesterol interacts with the polar head groups of the membrane phospholipids and sphingolipids, while the bulky steroid and the hydrocarbon chain are embedded in the membrane, alongside the nonpolar fatty acid chain of the other lipids. In this structural role, cholesterol reduces the permeability of the plasma membrane to protons (positive hydrogen ions) and sodium ions.
Within the cell membrane, cholesterol also functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of invaginated caveolae and clathrin-coated pits, including caveola-dependent and clathrin-dependent endocytosis. The role of cholesterol in such endocytosis can be investigated by using methyl beta cyclodextrin (MβCD) to remove cholesterol from the plasma membrane. Recently, cholesterol has also been implicated in cell signaling processes, assisting in the formation of lipid rafts in the plasma membrane. In many neurons, a myelin sheath, rich in cholesterol, since it is derived from compacted layers of Schwann cell membrane, provides insulation for more efficient conduction of impulses.
Within cells, cholesterol is the precursor molecule in several biochemical pathways. In the liver, cholesterol is converted to bile, which is then stored in the gallbladder. Bile contains bile salts, which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins, Vitamin A, Vitamin D, Vitamin E, and Vitamin K. Cholesterol is an important precursor molecule for the synthesis of Vitamin D and the steroid hormones, including the adrenal gland hormones cortisol and aldosterone as well as the sex hormones progesterone, estrogens, and testosterone, and their derivatives.
Some research indicates that cholesterol may act as an antioxidant.
In other words Cholesterol is a perfectly normal substance for us to have in our body, it’s needed for everything from controlling hormone levels to building and repairing cells. In fact an adult man typically produces about 1,000 mg of cholesterol a day (regardless of diet) and in the west the typical diet supplies around only 200 – 300 mg of cholesterol a day. In fact what happens when you eat more cholesterol is your body reacts by producing less its self, thereby regulating the amount in circulation in your body at any one time.
This means the amount of cholesterol you produce is very largely fixed by your genetics, not your diet and it’s perfectly normal to find a person on a low fat diet with higher levels of cholesterol than someone else on a high fat diet. In other words the amount of cholesterol in your body has very little to do with what you eat.
So why the confusion?
So what was the cholesterol found in the strange deposits on the artery walls doing? The short answer is helping the body to protect against the bad effects of having strange deposits attached to your artery walls. It works like this. The plaque builds up on the arteries, your body reacts by sending cholesterol to coat the plaque and try to protect you against it’s adverse effects, so more plaque equals more cholesterol. And because more plaque means more CVD, there is a correlation between high levels of cholesterol and high levels of CVD. But, AND THIS IS REALY IMPORTANT, the logic is broken. It’s a bit like saying. People who have a broken bones often have plaster-casts, so lets look at the incidences of broken bones in people with plater-casts, discovering that there is a strong coloration and then concluding that plaster-casts cause broken bones!
The truth is there has never been any science that has got even close to showing how cholesterol (this perfectly natural substance that is in virtually every cell in our body) could cause CVD and believe me there has been no shortage of people trying.
But still the myth persists. You read it everywhere.
Triglycerides, cholesterol and CVD
These three things get confused all the time. Look at this that I found on the BBC website today.
Cardio Vascular Disease – What is it?
CVD kills one in three people in the UK. While some contributing factors can’t be altered, we can change our lifestyle. CVD is caused by a build-up of fatty streaks and cholesterol in the blood vessels.”
Yes OK with you so far. But then they go on.
Natural wear and tear to blood vessels makes it easier for fatty cholesterol to leak in and get stuck to the artery walls. This build-up causes the arteries to narrow, reducing the heart’s ability to pump blood through them to the body. If they become completely blocked, it will cause a heart attack or a stroke if the blockage occurs in the brain’s blood vessels. …
Importantly this is presented as a fact – not a theory – and no actual science is quoted to support it. And it’s written my a doctor! What I think is going on here is that the author has confused arterial plaque (atherosclerosis) with cholesterol as if they were the same thing!
The next big confusion is that triglycerides (fat in your blood) and cholesterol get mixed up. There does indeed seem to be a good correlation between your level of triglycerides and the amount of arterial plaque (atherosclerosis) and your likelihood of suffering from CVD. But then people make the following connection which again has no basis in fact. Triglycerides are a form of fat and cholesterol is contained in fat so the triglycerides must be causing the cholesterol to build up. But it’s not. And there is no evidence that it is.
What is happening is that the same thing that is causing the high levels of triglycerides is also causing the plaque. And it turns out the thing that is doing this is chronic inflammation caused by insulin resistance! Study after study in recent years is showing the link between carbohydrate intake, insulin resistance, type 2 diabetes, metabolic syndrome and CVD.
Insulin is the hormone that controls fat storage. If you eat carbs, your body produces insulin and when your body produces insulin you can’t store any fat you might have eaten so what happens the levels of fat in your blood (triglycerides) goes up. Keep eating more carbs than you can burn for long enough and in the end your body starts to become resistant to the insulin. This means you need to produce more and more to have the same effect and this chronic cycle causes inflammation throughout your body, which in turn causes the plaque to build up.
Don’t believe me here’s a bunch of real science that shows the link, not between saturated fat and CVD, but between inflammation and CVD.
P Libby, PM Ridker, A Maseri – Circulation, 2002 – Am Heart Assoc
Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing
inflammatory response. Recent advances in basic science have established a fundamental role
for inflammation in mediating all stages of this disease from initiation through progression …
Cited by 5784 – Related articles – BL Direct – All 36 versions
Inflammation and atherosclerosis
GK Hansson, AKL Robertson, C Söderberg-Nauclér – 2006 – Annual Reviews
Abstract Atherosclerosis, the cause of myocardial infarction, stroke, and ischemic gangrene,
is an inflammatory disease. The atherosclerotic process is initiated when cholesterol-containing
low-density lipoproteins accumulate in the intima and activate the endothelium. …
Cited by 177 – Related articles – BL Direct – All 3 versions
Inflammation and atherosclerosis
EA Kaperonis, CD Liapis, JD Kakisis, D … – European journal of …, 2006 – Elsevier
An initial chemical, mechanical or immunological insult induces endothelial dysfunction. This
triggers a cascade of inflammatory reactions, in which monocytes, macrophages, T lymphocytes
and vascular smooth muscle cells participate. Leukocyte adhesion molecules, cytokines, …
MH Shishehbor, DL Bhatt – Current Atherosclerosis Reports, 2004 – Springer
Introduction Atherosclerosis, a chronic inflammatory condition charac- terized by the accumulation
of lipids and fibrous elements in subendothelial space, is the leading cause of death in the United
States [1•]. As we understand the mechanistic path- ways responsible for atherogenesis, …
Cited by 36 – Related articles – BL Direct – All 5 versions
[PDF] Inflammation and Atherosclerosis
I Atherosclerosis, A Reprint – 2004 – stacommunications.com
… Processes of Atherogenesis: The Role of Inflammation The link between inflammation and
atherosclerosis has been explored in detail in recent reviews.7-9 This review described how,
even in the earliest stages of the atherosclerotic process, the endothelium becomes more …
Related articles – All 2 versions
And here’s the first 3 out of 106,000 from a Google search for “Inflammation and insulin resistance”
Inflammation and insulin resistance
SE Shoelson, J Lee, AB … – Journal of Clinical …, 2006 – Am Soc Clin Investig
Over a hundred years ago, high doses of salicylates were shown to lower glucose levels in diabetic
patients. This should have been an important clue to link inflammation to the pathogenesis of
type 2 diabetes (T2D), but the antihyperglycemic and antiinflammatory effects of …
Cited by 475 – Related articles – BL Direct – All 13 versions
Inflammation and insulin resistance
C de Luca, JM Olefsky – FEBS letters, 2008 – Elsevier
Obesity-induced chronic inflammation is a key component in the pathogenesis of insulin resistance
and the Metabolic syndrome. In this review, we focus on the interconnection between
obesity, inflammation and insulin resistance. Pro-inflammatory cytokines can cause …
Cited by 84 – Related articles – All 12 versions
ZT Bloomgarden – Diabetes Care, 2003 – Am Diabetes Assoc
Renu Virmani (Washington, DC) discussed aspects of the pathology of atherosclerosis. C-reactive
protein (CRP) staining of plaques is a prominent histologic finding, and CRP levels are elevated
in patients who die suddenly (1). Thin-capped fibroatheromas (“vulnerable plaques”) are …
Cited by 67 – Related articles – BL Direct – All 8 versions