Columbia University Medical Center

Is Stress Really Bad for Your Heart?

Most people, including most cardiologists, would say yes to that question. But what’s the evidence behind the claim?

“The impact of stress on cardiovascular disease is one of the bedrocks of psychosomatic medicine,” says Donald Edmondson, PhD, assistant professor of behavioral medicine at P&S and the Center for Behavioral Cardiovascular Health.

“But like a lot of things we think we know, it turns out that no one had gone back and systematically looked at the literature to see what’s really true.”

Edmondson and his colleagues decided to review the evidence behind two common beliefs about stress and heart disease: that long-term stress increases heart disease and intense emotions trigger heart attacks.

Perceived Stress Is a Risk Factor, but Only a Moderate One

The first thing the researchers learned when they examined the literature is that most studies that claim to measure stress do not.

“When you dig into these studies, you discover that they’re really asking about anxiety, depression or other disorders that are already well-established risk factors,” Edmondson says.

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The researchers also omitted studies that relied on more objective measures of stress, such as demanding occupations or caring for relatives. “You don’t to work 80 hours a week to be stressed in your life,” Edmondson says. “We picked studies that simply asked participants: how stressed are you?”

Edmondson and his colleagues Safiya Richardson, MD, a 2012 P&S graduate, and Jonathan Shaffer, PhD, assistant professor of clinical medicine, found six such studies between 1948 and 2011 – with a combined 118,000 participants.

The results show that people who feel a high degree of stress in their lives are 27 percent more likely to develop heart disease or die from heart disease. That makes long-term stress a moderate risk factor for heart disease, comparable to smoking five cigarettes a day, or a small increase in blood pressure or cholesterol.

“High stress is not a huge factor in heart disease, but it’s not nothing. Negative emotions accumulate and are corrosive over time,” Edmondson adds. “The good news is that we know there are things people can do to reduce stress, things like exercise, yoga, or time with good friends.”

 

Emotional Triggers Are Not Very Common

At first glance, the research seems to back up the common belief that sudden, intense emotions trigger heart attacks. Recent studies suggest anger and depression nearly triple the risk, and grief raises the risk an incredible 21 times over the average.

Again, Edmondson and his colleagues dug deeply into these studies and asked how the numbers came about.

“The answer is: People have a heart attack or cardiac arrest, they go to the hospital, they survive, and then a researcher comes by and asks if they had any negative emotions before the event,” he explains. “As a psychologist I know that when something negative happens, people are much more likely to recall that preceding events were also negative.”

If you're really worried about your heart, avoiding anger would be down the list.That “recall” bias means very little is really known about the true prevalence and severity of emotional triggers, although it is unlikely to account for more than 2 or 3 percent of all heart attacks or arrests.

But identifying those 2 to 3 percent is important. The researchers suggest that animal studies could provide more insight into the physiology of negative emotions and help identify people who may be most prone to emotional triggers.

In the meantime, Edmondson says people shouldn’t try to stifle strong emotions. “If you’re really worried about your cardiovascular health, avoiding anger would be far down the list,” he says. “Exercise, smoking, blood pressure, and cholesterol have much bigger effects on heart health, and that’s where people should start.”

 

The findings were published in the Dec. 15 issue of the American Journal of Cardiology and Nov. 23 in advanced access section of the European Heart Journal. The research was supported by the NIH (grants HL088117, HL47540, HL101663, HL84034, HL007854, CA156709, and Columbia University’s CTSA grant RR024156).

 

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