The following originally appeared on The Upshot (copyright 2016, The New York Times Company).
Billions of dollars are spent every year on medications that reduce the risk of heart disease — the No. 1 killer in the United States.
But some people feel powerless to prevent it: Many of the risk factors seem baked into the cake at birth. Genetic factors can have a huge impact on people’s chances of dying of heart disease, and it has long been thought that those factors are almost always outside of one’s control.
Recent research contradicts this, though, and that should give us all renewed hope.
Since the 1930s, we’ve recognized that heart disease runs in families. For the last decade, we’ve been able to identify specific genes that are linked to coronary artery disease. In fact, these genes seem to have a cumulative effect. People who have more of them are at greater risk.
Familial factors are some of the strongest arguments for using drugs like statins widely. After all, there’s only so much you can do about your cholesterol through diet and exercise changes. Some people can see reductions in cholesterol only through pharmacological intervention.
Still, we tend to treat those at low risk with lifestyle changes, while those at high risk get more intensive therapy. A new study in The New England Journal of Medicine argues that thinking may be wrong.
Researchers gathered data from four large prospective cohort studies that followed thousands of people for years, looking at the relationships between various risk factors and heart disease. The first began enrolling patients in 1987 and the last in 2008. Even though specific genes of interest weren’t known when these studies began, data were available that allowed scientists to evaluate genetic risk decades later. Using about 50 different variations — single-nucleotide polymorphisms (otherwise known as SNPs) — researchers created a risk score.
They also looked at how lifestyle factors were associated with outcomes. These included not smoking cigarettes, not being obese (having a B.M.I. less than 30), performing physical activity at least once a week and having a healthful diet pattern.
That last criterion was defined as doing at least half of the following recommendations: eating more fruits, nuts, vegetables, whole grains, fish and dairy products and eating less refined grains, processed meats, unprocessed red meats, sugar-sweetened beverages, trans fats and sodium. Every one of the four lifestyle factors was associated with a decreased risk of coronary events.
That’s the first bit of good news. Doing any one of these things makes a difference.
But the effect is cumulative. The researchers divided people into three groups based on these factors. “Favorable” required at least three of the four factors, “intermediate” required two of them, and “unfavorable” required one or none. Across all studies, those with an unfavorable lifestyle had a risk that was 71 percent to 121 percent higher than those with a favorable lifestyle.
More impressive was the reduction in coronary events — heart attacks, bypass procedures and death from cardiovascular causes — at every level of risk. Those with a favorable lifestyle, compared with those with an unfavorable lifestyle, had a 45 percent reduction in coronary events among those at low genetic risk, a 47 percent reduction among those with intermediate genetic risk, and a 46 percent reduction among those at high genetic risk.
What does this mean in real-world numbers? Among those at high genetic risk in the oldest cohort study, 10.7 percent could expect to have a coronary event over a 10-year period if they had an unfavorable lifestyle. That number was reduced to 5.1 percent if they had a favorable lifestyle. Among those at low genetic risk, the 10-year event rate was 5.8 percent with an unfavorable lifestyle and 3.1 percent with a favorable lifestyle. In the other cohort studies, similar relative reductions were seen.
These differences aren’t small. The risk of a coronary event in 10 years was halved. The absolute reduction, more than 5 percentage points in the genetic group at high risk, means that lifestyle changes are as powerful as, if not more powerful than, many drugs we recommend and pay billions of dollars for all the time.
There are caveats, of course. All of the participants in these analyses were white, because there are few well-validated genetic studies in black populations. But the researchers also saw similar findings in the black population of the oldest cohort. These aren’t randomized controlled trials, and there could be other factors at play that we aren’t measuring. But the results were consistent over a number of studies, and the effect size is large.
There are important lessons to be learned. These results should encourage us that genetics do not determine everything about our health. Changes in lifestyle can overcome much of the risk our DNA imposes.
Lifestyle changes are hugely important not only for those at low risk, but for those at high risk. The relative reductions in events were similar at all levels of genetic risk.
Moreover, given how changes in lifestyle will also reduce your risk of other diseases like cancer (the No. 2 killer), it’s clear that a healthier lifestyle could have huge implications for many, many more people.
It’s important to acknowledge that these lifestyle recommendations are even less constrictive than those I’ve discussed in the past. You need only be a current nonsmoker; past smoking doesn’t exclude you. You can also be overweight, just not obese. And in contrast with most physical activity recommendations, it requires only once-a-week exercise, not the 30 minutes for five days that most professional organizations like the American Heart Association endorse.