If I took a stroll down a busy city street today and asked 100 people what comes to their minds when I mention the word ‘cholesterol’, I doubt many of the answers would be positive. For most people, cholesterol is thought of as a harmful substance in their body that can cause heart disease and stroke. This demonized view of cholesterol is not only misguided, but can also cause significant harm to your health when it leads to an unnecessarily restricted diet or the potentially unnecessary consumption of pharmaceutical drugs that can have significant adverse health effects.
Cholesterol is crucial for health
The majority of cholesterol found in the body is produced by the liver (around 75%) with the remainder coming from diet, and its levels are tightly regulated according to the body’s needs. This is because cholesterol plays a vital role in many cellular processes, from the production of hormones and vitamin D, to maintaining the stability of cellular membranes, aiding neurological function, and forming the bile acids which help in the absorption of dietary fats. We cannot live without cholesterol, and this alone should call into question the practice of drastically lowering your cholesterol in the belief it will negate your risk for cardiovascular disease.
The evolution of serum cholesterol markers: Total cholesterol, LDL, VLDL, HDL, LDL-C & LDL-P
Wow that’s quite a list isn’t it? There was a time in the not too recent past when the only serum marker deemed important to determine cardiovascular risk was your total cholesterol. Then there was a discernment made between two types of cholesterol carriers: LDL (low density lipoprotein) and HDL (high density lipoprotein). LDL was painted as the bad guy who delivered cholesterol into the bloodstream and thus caused plaque formation and subsequent heart disease, and HDL was seen as the good guy who removed cholesterol from circulation and lowered your risk of plaque formation. Relative risk could be determined by examining the ratio of LDL to HDL. If your LDL was up, and your HDL down, then your risk of heart disease was deemed high. If your LDL was up, but your HDL was also nice and high, your relative risk of heart disease was still pretty low (unfortunately there are still practitioners who only assess the LDL number without taking into account the amount of HDL). Then a further discernment was made between two types of LDL: your standard run-of-the-mill low density lipoprotein, and a smaller denser variety termed VLDL (very low density lipoprotein). If LDL was still considered a bad guy, then VLDL was the arch villain. The theory ran that the smaller and denser the particle, the greater its ability to infiltrate the blood vessel wall and oxidise, thus triggering inflammation and plaque formation.
The underlying assumption behind most of these measurements is that the concentration of cholesterol bound to these lipoproteins (particulartly LDL, termed LDL-C in this instance) is the most specific measure of heart disease risk. Recently, however, there has been a shift in research that strongly suggests it is the number of LDL and VLDL particles in the bloodstream (called LDL-P), rather than the amount of cholesterol that they carry, that gives the most accurate measure of a persons cardiovascular disease risk. The best way to understand this idea is to use an analogy: Lipoproteins are like vehicles that can carry cholesterol and other fats (the passengers) around the body. The old assumption was that the number of passengers in the vehicles influenced disease risk – the more passengers, the greater the risk. However it now seems that it is actually the number of vehicles that is the greatest risk factor. Imagine your blood vessels as a series of transport tunnels. If the traffic in these tunnels is light (a low LDL-P), then there is a decreased risk of a collision between the tunnel wall and the vehicle. If there is heavier traffic (a high LDL-P), there is a greater risk of collision which would result in damage to the tunnel wall and the possible formation of a plaque.
Triglycerides and the true underlying cause of heart disease
So up to this point you may be thinking “Ok I’m with you that an increased number of LDL and VLDL particles can increase risk for heart disease, but aren’t they both elevated because of increased cholesterol in the body?”. That is a sensible question, and to answer it you need to understand the relative sizes of all of the particles carried by lipoprotein molecules. Of all the lipid components that these lipoproteins carry, triglycerides (the primary fat delivery molecules in the body) have by far the greatest size and molecular weight. The lipoproteins can only carry a limited amount of materials, so to increase the amount of triglycerides that they must carry will (in relation to other molecules such as cholesterol and fat soluble vitamins) disproportionately drive up the number of lipoprotein particles in circulation. And guess what? Triglyceride volumes in the body are predominantly driven up by the dietary consumption of calories that are surplus to requirements, and the greatest contributor to these surplus calories are refined and processed carbohydrates i.e. sugar. Your body has an amazingly efficient mechanism for converting simple sugars into these triglyceride forms for later use, as opposed to the consumption of healthy fats and proteins that tend to be used preferentially for energy production or structural function.
The damage of the low fat food movement
Now you are probably beginning to see just how misguided our beliefs have been in relation to cholesterol, dietary fat consumption, and heart disease. The huge push for lowering our intake of dietary fats has resulted in a plethora of low fat products in the marketplace. These products typically contains large volumes of sugar to compensate for the lack of taste enhancing fats, and thus drive up serum triglycerides and increase LDL-P. The very strategy that has been employed to lower the incidence of heart disease in the population has achieved the exact opposite. Focusing on cholesterol as the cause of heart disease is like blaming the firefighters who arrive at the scene of a blaze to put out the fire. They are there help repair the damage (remember that cholesterol is a crucial component in every cellular membrane), damage already instigated by an increased LDL-P which is in turn driven up by a high carbohydrate, low fat diet.
Inflammation and C-reactive protein
Remember the analogy of the lipoprotein ‘vehicles’ only causing damage to the blood vessel ‘tunnels’ when there is a sufficiently high volume of traffic to cause a collision? There is another layer to this, and another condition that will generally need to be in place for this collision to cause damage. The blood vessel wall in its natural healthy state is relatively smooth and robust. Think of a tunnel made of reinforced and smooth steel. When a lipoprotein particle collides with this well structured wall, it will generally glance off its surface harmlessly and continue on its merry way. However if there is a roughening of the blood vessel lining, then the lipoprotein has a surface to which is can stick and become embedded. Once in this state, the particle can oxidise and attract a range of inflammatory chemicals that now see it as a threat. The body’s natural response to a threat is to contain it, thus the formation of what is called a ‘foam cell’ which can eventually form a hardened plaque and possibly occlude the blood vessel. So what can cause this initial roughening of the blood vessel? In a word: inflammation. And the main cause of this inflammation: excess consumption of refined sugar. Because the body regulates the volume of sugar in the blood within a very narrow range, any level beyond this range is quickly cleared from circulation by the hormone insulin and is driven into the cells. When the cells are full, the excess sugar is converted to triglycerides for storage (as discussed above). However when you constantly consume refined sugars, you overwhelm your insulin response and a cascade of reactions occur which cause the formation of blood vessel damaging complexes – imagine rubbing sandpaper on the inside of you blood vessels day in day out and you get the picture of how a typical Western diet effects our cardiovascular system. C-reactive protein is a marker used for determining systemic inflammation in the body. Couple high LDL-P with high C-reactive protein and you have a recipe for heart disease. The good news is that both of these markers are most effectively lowered by dietary interventions. It is important to note that there are many other possible contributors to blood vessel inflammation, including the consumption of unhealthy fats in the form of easily oxidised vegetable oils, as well as bacterial, viral and fungal infections. For a detailed list of foods and additives that can contribute to blood vessel inflammation, please sign up to my newsletter to receive my ten part series on living your healthiest life – this topic is covered in part one.
Statins and their effectiveness at lowering heart disease risk
I feel it is important to state that the use of statin drugs does have a place in lowering the risk of heart disease, however in a much smaller population segment than the broad spectrum approach in which it is currently applied. Those that have familial risk for heart disease and high cholesterol may benefit from the use of statin therapies to lower this risk. The use of dietary interventions would not be as effective for these individuals due to an inherent inability to remove cholesterol from circulation. Also those with a very high LDL-P may benefit from short term statin use to help lower this marker, but the majority of benefit and effectiveness will still be derived from a dietary shift away from processed carbohydrate dense food to one of higher protein and healthy fat consumption (again refer to part one of my ten part series on living your healthiest life). For pretty much everybody else, a focus on dietary intervention (working alongside a qualified health practitioner) will have a tremendously higher likelihood of decreasing heart disease risk. The myriad side effects of statins (including muscle pain, liver damage, cataracts, kidney failure, cognitive impairment, impotence and diabetes) should suggest an approach with no side effects and far greater effectiveness such as dietary intervention should be employed as a first line measure.
I hope this gives you some valuable information on the true causes of heart disease, and empowers you to have a healthy discussion with your doctor or health care professional regarding the various measures you can employ to lower your risk. Look out for my specific recommendations for lowering your risk of heart disease in a future post.
In wellness,
James
