AM I GOING TO HAVE A HEART ATTACK?

This is the question everyone wants to know. It boils down to “risk.” Just what is my likelihood of dropping dead of a massive heart attack and leaving my family to fare without me?

My question is…why? If we’re honest, from a mainstream medical standpoint, the risk is predicted purely to decide when to medicate. Do we start Lipitor at a cholesterol of 230, 208 or 260?? 

From a personal standpoint, we want to know risk so we can put into perspective healthier lifestyle choices. Our doctor determines we’re at very low risk? McDonalds on the way home follow by an evening as a couch potato. High risk?  Maybe get the salad and go for a walk when we get home…

Sound too simplistic? For me, the perfect world would have no estimation of risk because everyone would be living a life free of processed food and stress and exercising consistently. We don’t need to know our risk, and we could care less because we’re going to do the right things anyway.

But alas, McDonald’s and Kraft still exist.

So, why this topic? Because if we use our estimated risks to determine how our lifestyles should be lived, we may be way off the mark. I’ve covered the concept of surrogate end markers and how this is a house of cards in medicine in previous posts. This particular study compared the relationship between risk factors identified in observational studies and cardiovascular disease and the same relationship seen in actual clinical studies.

As an example, let’s say that, when we looked at a population of 100,000 people, cholesterol levels are determined to be associated with cardiovascular disease. So we then decide to use cholesterol to determine someone’s risk of having a heart attack. So someone with elevated cholesterol now thinks they are at high risk of having a heart attack and makes a decision to take a statin drug to “protect” themselves.

But what happens when we then look at the studies used to determine if these drugs work at lowering the rates of heart attacks? Turns out, in many cases, the risk was not quite so strong as we thought. On average, the risk was actually about 25% lower than was seen in the observational studies.

What does this mean? It means that we use medications to treat what we think are risk factors for disease states (in this case cardiovascular disease). We use the medication when that lab value creeps high enough. But, in reality, what we are doing is using drugs to lower the risk of a disease based on overblown data. The result? Not quite the protection we were looking for, but at great cost.

The beauty of lifestyle changes is that they cut across a single risk factor. That group in the observational study that had lowered risk of a heart attack not only had lower cholesterol, but had higher HDL, lower triglycerides, an ideal body weight, lower hsCRP, low blood pressure, low uric acid, lower liver enzymes… You get the idea.