For years cholesterol has been portrayed as the villain when it comes to heart disease, but it turns out it might have been in the wrong time place at the wrong time; thus inheriting all the blame. In order to understand why cholesterol got caught up in the heart disease mess, let’s first take a look at what cholesterol is and what roles it plays in the body.
Cholesterol is a waxy, fat-like substance that is present in every cell of the body. Our bodies need cholesterol to synthesize hormones, vitamin D, protect the cells, and make bile acids to digest foods. Simply put, we need cholesterol in order to function optimally.
Cholesterol transport in the body
In order for cholesterol to be delivered where it is needed in the body, it travels in small packages called lipoproteins. The two most known lipoproteins are high-density lipoprotein (HDL) and low-density lipoprotein (LDL), otherwise known as “good” and “bad” cholesterol, respectively (1).
What differentiates these two lipoproteins is that HDL is responsible for reverse cholesterol transport, meaning it carries cholesterol back to the liver for elimination, particularly the type that likes to hang around in the arteries. On the other had, LDL is responsible for carrying cholesterol where it is needed in the body. Nevertheless, it may spill some cholesterol in the arteries along the way depending on how much it’s carrying and/or in response to inflammation; thus creating a buildup of cholesterol and possibly leading to arterial obstruction and subsequently: heart disease.
But what’s important to consider is that not all cholesterol is created equal.
Particle size and number
The number and size of the particles matter. Think about the many ways in which you could make up a dollar using coins. You can do it with 4 quarters, 10 dimes, 20 nickels or 100 pennies, among many other ways. The smaller the particle (think pennies) and the higher the number, the more likely they are to get stuck in the arterial wall. In fact, a 5% smaller LDL diameter is linked to a 50% increase in the rate of uptake by the arterial wall.
But what causes these particles to become smaller in the first place?
If you guessed oxidative stress (free radicals) and inflammation, you are correct. The oxidized LDL promotes inflammation as macrophages (immune cells) engulf them in an attempt to control the situation, but instead end up creating even more inflammation.
So it would seem that addressing the free radical load and the inflammatory cascade would be a better approach than simply trying to lower cholesterol with prescription drugs, right?
Statins are among the most commonly prescribed drugs in the United States, yet heart disease remains the number 1 killer. Why would that be?
Statins do lower cholesterol by blocking the enzyme HMG-CoA reductase, which controls cholesterol synthesis in the liver. What they don’t do is address the cause of the elevated and/or oxidized cholesterol and inflammation, which we know to be the true culprit. Another thing they don’t do is help as many people as it’s often claimed.
In fact, it could be argued that statins usefulness has been greatly inflated.
One report published on the Expert Review of Clinical Pharmacology argued that statin research arrives at its impressive success rate numbers by using a statistical tool called relative risk reduction (RRR) that amplifies the beneficial effects of statins while minimizing the adverse effects (2). By using this tool, statins effectiveness translates to 30-50% benefit, whereas if you look at the absolute risk it would be more like 1%.
This means that 1 in 100 individuals would need to be treated in order to avoid cardiovascular events.
Another helpful way to assess statins effectiveness is by differentiating primary prevention from secondary prevention. Primary prevention aims to avert any cardiovascular event in otherwise healthy individuals, while secondary prevention aims to reduce the risk of a cardiovascular event in individuals with known heart disease.
For those who were prescribed statins as means of primary prevention, 98% saw no benefit; 0% were helped by being saved from death; 1.6% were helped by preventing a heart attack; and 0.4% were helped by preventing a stroke. Conversely, the usefulness of statins for secondary prevention increases only slightly: 96% saw no benefit; 1.2% were helped by being saved from death; 2.6% were helped by preventing a repeat heart attack; and 0.8% were helped by preventing a stroke (3).
In other words, if you’ve never had a cardiovascular event you have a 98% chance of NOT getting any benefits at all from taking a statin. Talk about putting things into perspective.
Last but certainly not least, statins are associated with a few mild side effects ranging from headaches, diarrhea, constipation and fatigue to more serious side effects including muscle pain, cramping and muscle damage, increased risk of diabetes, decreased antioxidant status (lower CoQ10 levels), cognitive decline, neuropathies and sexual dysfunction (4, 5, 6, 7).
So after looking at the “benefits” numbers above in conjunction with statins’ potential side effects, I pose the question – is it worth it?
Cholesterol is not the enemy and statins are not The Avengers. It is far more complex than that. In order to truly foster cardiovascular health and prevent heart-related events, a healthy lifestyle including diet, exercise and stress management (and natural supplementation when needed) can provide far better results than cholesterol reduction alone – and with a few side-benefits.