Taking depression to heart

In his new book Treating the Aching Heart (Vanderbilt University Press, 2007), American psychiatrist Lawson Wulsin offers a clear description of the latest thinking. Depression along with related anxiety disorder, he says, is a disease not just of the mind but of the brain and the body too. While most of us define depression as a mental illness linked to a cluster of feelings and ways of thinking, it is also a disease that sets off hormonal, immune and nervous system changes that are first triggered in the brain and then spread throughout the whole body. When you think about it, such a progression makes sense.

As Wulsin puts it, “Depression begins in the brain, specifically the emotional brain or the limbic system, and disrupts other systems in the body, including the circulatory system.”

The most direct pathway from depression to heart disease, says Wulsin, is through the body’s stress response system. People who are depressed release higher levels of cortisol in the adrenal glands. Cortisol is the fight-or-flight hormone the body produces to manage acute stress. Chronic high levels will send heart rates and blood pressure soaring and cause disruption in all major systems in the body, including the cardiovascular system.

Depression also plays havoc with our autonomic nervous system. This system controls our heart rate at a fixed rate of between 50 and 90 beats a second. But stimuli from inside and outside the body can increase or decrease heart rate as well. And depression, which has been shown to cause dysfunction in the autonomic nervous system, can lead to an elevated heart rate and arrhythmia, putting strain on the heart by making it work harder.

Depression also increases the risk of atherosclerosis, or hardening of the arteries. The traditional view of atherosclerosis was that excessive levels of cholesterol circulating in the bloodstream stopped up the blood flow and formed plaque at narrowed openings that eventually broke loose and resulted in a heart attack or stroke. Hardening of the arteries was viewed as a plumbing problem.

But new thinking describes atherosclerosis as an inflammation problem, where plaque builds up over time to protect the artery walls from low-density lipoprotein, or “bad” cholesterol. When the body’s immune system is working well, the immune system clears the inflammation before that buildup can happen. Depression, which can disrupt this immune response, allows inflammation to continue. Currently, the best way to measure inflammation in the vascular system is by measuring a protein called C-reactive protein (CRP). And studies have shown that people suffering from depression have higher levels of CRP.

Montreal cardiologist and Heart and Stroke Foundation spokesperson Jacques Genest says that while the links between depression and heart disease are becoming clearer, the evidence is not strong yet to show that treating depression reduces the risk of developing heart disease. “We don’t have a huge amount of solid data to say antidepressants are life-saving,” he says. “We have some data but not a lot.” The reason may have more to do with the nature of depression itself in that it can be a transient condition and more difficult to measure effectively than other diseases. However, that doesn’t stop Genest from pointing out the importance of managing stress and treating depression and anxiety as an important step to heart health.