Understanding Statins, Cholesterol and Heart Disease
Lipoproteins are the taxis that carry cholesterol around our bodies
According to the NHS Choices website, “statins are a group of medicines that can help lower the level of LDL (low-density lipoprotein) cholesterol in the blood. “ It goes on to explain that LDL cholesterol is often referred to as “bad cholesterol” and that statins reduce the production of it inside the liver.
In my opinion, explanations such as this give rise to confusion. There is no such thing as ‘good’ or ‘bad’ cholesterol. There is only one type of cholesterol, made up of 27 carbon atoms, 45 hydrogen atoms and an oxygen-hydrogen pair. You can search as hard as you like but you will never find any other type of cholesterol.
So where does the Good/Bad confusion come from?
Cholesterol consists of three parts. Two of the three cannot be dissolved in water. This means cholesterol is incapable of dissolving in blood. In order to get to the cells where it is needed, it has to be transported throughout the bloodstream. This is where lipoproteins come in. Lipoproteins are vehicles that transport cholesterol around the blood. Lipoproteins are a combination of various fats (lipo) and protein. Unlike cholesterol, of which there is only one type, there are different types of lipoprotein. Lipoproteins are classified according to their density. Two of the most important, in terms of cardiovascular disease, are high-density lipoproteins (HDLs) and low-density lipoproteins (LDLs).
- HDLs transport cholesterol from the cells and tissue back to the liver. HDLs are considered ‘good’ as they take cholesterol out of cells and the blood thus helping to prevent excess cholesterol. HDLs also remove cholesterol deposited in the walls of blood vessels.
- The production of cholesterol takes place in every single cell in your body. Cholesterol is VITAL for cellular survival. Your liver is a manufacturing plant and one of the many ‘commodities’ it manufactures is cholesterol. If your cells need extra cholesterol, your liver is where the extra cholesterol is made. This cholesterol then has to get to the cells that require it. This is where LDLs come into the picture. LDLs are the 'taxis' that collect cholesterol from the liver and take it around the body, depositing it where it is needed. It is LDLs that are often referred to as ‘bad’ cholesterol.
There is only one type of cholesterol, made up of 27 carbon atoms, 45 hydrogen atoms and an oxygen-hydrogen pair.
So why do LDL's get such bad press?
The transportive functionality of LDLs is absolutely vital to the health and survival of every cell in your body. If LDLs have such a vital role, why are they called ‘bad?’ The fact is, LDLs are not bad, per se. They only become a problem when they become entrenched in arterial walls, thereby clogging up your arteries. This is where the size and number of LDL particles matter. LDL particles exist in different sizes – large, fluffy, cotton-ball like molecules and small dense molecules. Studies are showing that people whose LDL particles are predominantly small and dense have a greater risk of coronary heart disease.
Today we are learning to differentiate between LDL-C and LDL-P. LDL-C represents total cholesterol count (i.e. the cholesterol mass within the LDL particles), whereas LDL-P represents the number of LDL particles transporting the cholesterol in your body. Cholesterol shares its LDL 'taxi' with other fats, such as triglycerides and apolipoprotein Bs (ApoBs) (high levels of which represent a higher risk for cardiovascular disease than cholesterol). The more space these other fats take up, the less space is available for cholesterol, and so more LDL taxis will be required to transport the cholesterol from the liver where it is produced, to the cells where it is needed. This appears to be where the true problem lies. The higher your LDL-P levels (the number of LDL particles in your blood), the higher your triglyceride levels. Put more simply, scientists used to believe that the number of passengers in the 'taxi' (i.e the concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies suggest that it’s the number of 'taxis' on the road (LDL-P) that matters most. In other words, the more 'taxis' there are on the road, the more likely some will 'crash' into the fragile lining of the artery.
A cholesterol molecule
The transportive functionality of LDLs is absolutely vital to the health and survival of every cell in your body. If LDLs have such a vital role, why are they called ‘bad?’ The fact is, LDLs are not bad, per se. They only become a problem when they become entrenched in arterial walls, thereby clogging up your arteries. This is where the size and number of LDL particles matter. LDL particles exist in different sizes – large, fluffy, cotton-ball like molecules and small dense molecules. Studies are showing that people whose LDL particles are predominantly small and dense have a greater risk of coronary heart disease.
Today we are learning to differentiate between LDL-C and LDL-P. LDL-C represents total cholesterol count (i.e. the cholesterol mass within the LDL particles), whereas LDL-P represents the number of LDL particles transporting the cholesterol in your body. Cholesterol shares its LDL 'taxi' with other fats, such as triglycerides and apolipoprotein Bs (ApoBs) (high levels of which represent a higher risk for cardiovascular disease than cholesterol). The more space these other fats take up, the less space is available for cholesterol, and so more LDL taxis will be required to transport the cholesterol from the liver where it is produced, to the cells where it is needed. This appears to be where the true problem lies. The higher your LDL-P levels (the number of LDL particles in your blood), the higher your triglyceride levels. Put more simply, scientists used to believe that the number of passengers in the 'taxi' (i.e the concentration of cholesterol in the LDL particle) is the driving factor in the development of heart disease. More recent studies suggest that it’s the number of 'taxis' on the road (LDL-P) that matters most. In other words, the more 'taxis' there are on the road, the more likely some will 'crash' into the fragile lining of the artery.
If a person only has their cholesterol measured, and not their LDL particle number, they will be led to believe they are at a low risk of heart disease.
The importance of this in terms of heart disease risk is profound. When you go to a doctor to get your cholesterol levels tested, chances are it’s your total LDL and HDL cholesterol levels that are being tested. This tells you the concentration of cholesterol (passengers) inside the lipoproteins (taxis), which is not the driving factor behind plaque formation and heart disease. Instead, what should be measured is the number of LDL particles in your blood. Often, LDL cholesterol levels and LDL particle numbers are concordant (i.e when one is high, the other is high and vice versa). This is the most likely explanation for the association between LDL cholesterol and heart disease. But it is very possible to have a high number of LDL particles and normal/low cholesterol (e.g. 4 taxis each carrying 1 passenger will give you a low cholesterol of 4mmol/L, or 4 passengers, but a high LDL-P 4, or 4 taxis). If a person only has their cholesterol measured, and not their LDL particle number, they will be led to believe they are at a low risk of heart disease. Worse still, it is often the patients with high LDL particle number who present with some or more of the components of metabolic syndrome – such as abdominal obesity, hypertension, insulin resistance, high triglycerides and low HDL – and who are at higher risk of heart disease. Compare this to two taxis carrying 3 passengers each. This will mean a LDL- P of 2 (2 “taxis” on the road) but a high cholesterol level of 6mmol/L. More and more research is showing that patients with high LDL cholesterol (LDL-C) and low LDL particle number (LDL-P) are not at high risk of heart disease and in fact have a lower risk than patients with low LDL-C and low LDL-P.[1]
LDL particles, as mentioned, are not a problem per se, but rather become a problem when they oxidise. All lipids (fats) can be damaged by exposure to heat and oxygen. Some LDLs are of very small size and can pass through artery walls. Free radicals can then cause oxidation and rancidity, triggering the inflammatory response. The important question to ask is “what is causing these LDLs to oxidise?” Consuming artificial, partially hydrogenated oils (trans fats), a diet high in refined sugars and refined carbohydrates, alcohol and smoking cigarettes will cause LDL particles to oxidise. When there is oxidation in the body, there tends to be free radical activity in the tissues, Consuming a diet high in antioxidants such as vitamins C and E helps to prevent oxidative free radical damage.
The higher the number of LDL particles in your body, the higher your triglyceride levels will tend to be. If you have elevated triglycerides it is important to avoid a high carbohydrate diet, alcohol, sugary and refined carbohydrates, including sugar, honey, sugary drinks, and anything made with white refined flour. A diet low in carbohydrates and high in healthy fats, high fibre, non-starchy vegetables, seeds, nuts and with good-quality grass fed animal protein will help to reduce LDL particle number and optimise lipid levels.
The most common side effects of statin drugs are loss of physical strength, sexual dysfunction, changes in mood and myopathy.
Statins
This brings us to the issue of statins. Many in the conventional medical establishment have hailed statins as a wonder drug. Statins are a class of medicines that are frequently used to lower blood cholesterol levels. They do this by blocking the action of a specific chemical in the liver that is necessary for making cholesterol. The main problem with this is the failure of the medical world to treat each person as unique and to instead adopt a ‘one size fits all approach.’ We know that cholesterol has many important functions in the body. Without cholesterol, for example, pregnenolone cannot be made. Pregnenolone is often referred to as the ‘master hormone’ as, without it, numerous other hormones cannot be synthesized. Cortisol is an important stress hormone, which is also a powerful anti-inflammatory hormone. If a person is going through a particularly stressful period, the liver may very well be called upon to make additional cholesterol. Statins interfere with this cholesterol-making process in the liver. All cholesterol-lowering drugs, such as statins, diminish hormone function. The most common side effects of statin drugs are loss of physical strength, sexual dysfunction, changes in mood and myopathy.
Statins deplete the body of CoQ10
This is an enzyme necessary for the production of energy by every cell in the body. It is vital for good health, high energy levels, longevity and a good quality of life. The reduced form of CoQ10, ubiquinol, is a critical component of the production of your adenosine triphosphate molecules (ATP). Muscle cells need ATP like a car needs petrol. And guess what? Your heart is the most energy-demanding organ in the body. You can therefore understand how potentially devastating it can be to deplete your body of its main source of cellular energy. Thus when you read that statins can actually increase your risk of acute heart failure, this can be due to the depletion of CoQ10.
If you are on a statin, make sure you discuss with a health care practitioner the need to take coenzyme Q10 as a supplement (in the form of ubiquinol if you are over 40, as in this form it will be far more effectively absorbed by your body). Ubiquinol actually helps keep your LDL levels reduced, as it’s an exceptionally potent antioxidant. LDL cholesterol only becomes a problem when it is oxidised. By reducing CoQ10 production in your body you are also removing the mechanism that keeps LDL cholesterol from doing harm in your body.
Are statins ever beneficial?
Yes. To summarise the scientific research on statins:
- The only section of the population that statins extend life in are men under the age of 80 who already have pre-existing heart disease.
- Statins have not been shown to extend lifespan in men under 80 without pre-existing heart disease, men over 80 with or without heart disease, and women of any age with or without disease.
- Statins do reduce the risk of cardiovascular events in all populations but these reductions are more modest than most assume and statins have been shown to cause a number of side effects.
- In fact, today the anti-inflammatory effects of statins on the vascular wall are more widely accepted. Randomized clinical trials have demonstrated that, further to their lipid-lowering properties, statins also reduce cardiovascular risk by exerting anti-inflammatory effects.[2] Since other cholesterol-lowering drugs have had little or no effect on heart disease, it is possibly the anti-inflammatory effects of statin drugs that are reducing this risk, particularly in light of the fact that chronic, low-grade inflammation is now accepted as being closely linked to all stages of atherosclerosis.
- However, due to the many side effects of statins and with our better understanding that it is not necessarily cholesterol by itself that leads to heart disease, but a process that begins with inflammation resulting in oxidation of cholesterol particles, it is important to incorporate a diet rich in anti-inflammatory foods.
Other (often overlooked) factors implicated in heart disease
- Magnesium deficiency. This is a commonly overlooked risk factor for cardiovascular disease. Even a moderate magnesium deficiency can cause profound changes in how the heart functions. Because magnesium is essential for the healthy control of blood vessel function, blood pressure regulation and normal heart contractions, a magnesium deficiency increases the risk of conditions such as endothelial dysfunction, hypertension and cardiacarrythmias.[3]
- Vitamin K2 deficiency. Vitamin K2 is as important as vitamin D for protecting your health. It is essential for activating enzymes involved in transporting calcium from your arterial walls to your bone.
- Calcium, vitamin K2, magnesium and vitamin D work together synergistically, and should ideally be taken in combination. According to top cardiologist, Dr Dennis Goodman, the importance of vitamin K2 in cardiovascular health is its ability to remove calcium from the lining of blood vessels.
- Calcium in the arteries is a key indicator of heart attack or stroke risk. In fact, measuring calcium build-up in the arteries is believed to be a better indicator of the likelihood of heart disease than measuring blood cholesterol levels. Vitamin D helps the body absorb calcium. Vitamin K2 (in the form of mk7) directs calcium out of the blood and to the bones. Taking too much calcium to prevent osteoporosis may increase your risk of myocardial infarction or heart attack, particularly if accompanied by a vitamin D and/or vitamin K deficiency.
- Elevated homocysteine. Studies of the general population have suggested that high homocysteine levels are associated with cardiovascular morbididy and mortality.[4]
What a traditional diet tells us
Cultural studies provide the most relevant research for cholesterol and fat in the diet. Some of the fattiest diets in the world (such as in Austria, France, Greece and Switzerland) are low in processed, refined and hydrogenated fats and high in saturated fats such as butter, eggs, cream, cheeses and organic meats, yet these countries have lower rates of heart disease than the USA. In fact the diets of the countries that line the Mediterranean Sea have received a lot of attention lately. Saturated fats make up 70% of the caloric intake in these diets and yet traditionally they have some of the lowest rates of heart disease in the world. For more information, please read my article on the benefits of the Mediterranean diet on heart health.
[1] Davidson MH, Ballantyne CM, Jacobson TA et al.; (2011) Clinical utility of inflammatory markers and advanced lipoprotein testing: advice from an expert panel of lipid specialists. Journal of Clinical Lipidol 5(5): 338-367.
[2] Bu DX, Griffin G, Lichtman AH (2011) Mechanisms for the anti-inflammatory effects of statins. Current Opinion on Lipidology 22(3): 165-170.
[3] Geiger H, Wanner C (2012) Magnesium in disease. Clinical Kidney Journal 5(Suppl 1): i25-i38.
[4] Marcus J, Samak M, Menon V (2007) Homocysteine lowering and cardiovascular risk: Lost in translation. The Canadian Journal of Cardiology 23(9): 707-710.