Heart rate is the product of many factors working in concert, all converging on the sinus node, the heart's natural pacemaker. It generates an electrical impulse that travels through the atria and, eventually, to the ventricles. The electrical impulse is the trigger for the heart muscles to contract and pump blood to body and brain.
One of the prime influences on heart rate is the autonomic nervous system, the bureau that runs the routines of breathing, pumping blood and digestion so that we can focus attention on finding jobs, mates and food, raising kids, and generally engaging with the world around us.
The autonomic nervous system achieves fine regulation of body functions much the way you drive a car. There's an accelerator, a network of nerves that feed the system; this is the sympathetic pathway. It's gassed up by such heady hormones as adrenaline (epinephrine) and norepinephrine. These are the hormones stirred up by the fight-or-flight response, flagship of the stress system. Depression elevates stress hormone levels. The autonomic nervous system also has a built-in brake, the parasympathetic pathway. When engaged, it dampens sympathetic function and allows for moment-to-moment modulation of autonomic activity.
In both anxiety and depression, which more often than not co-exist, there is some dysfunction of autonomic tone. Something goes awry in the balance of sympathetic and parasympathetic activity. The evidence so far points to hyperactivity of the sympathetic channel. Whether there is also failure in the parasympathetic braking system is unknown.
A team of researchers at Yale and at Emory universities examined the role of HRV in 50 pairs of identical male twins free of symptomatic heart disease. One twin in each pair, however, had a history of depression. Even in apparently heart-healthy people, the researchers found, low HRV accompanies depression, but only in the presence of active depression. The more severe current symptoms of depression, the lower the HRV, reflecting more severe autonomic dysfunction. Even low levels of depression compromised HRV.
The study was the first to look at HRV in people free of heart disease, reports Viola Vaccarino, M.D., associate professor of cardiology at Emory. "We controlled for smoking, hypertension and diabetes; the relationship between current depression and low HRV still persisted." She next plans to look at subclinical heart disease, "to make sure the depression is not the result of heart disease we are unaware of."
That HRV is impaired in depression suggests that depression too is a direct risk factor for cardiac mortality. As ominous as diminished HRV is, however, it's by no means the only way that depression influences the risk of heart disease.
Blood platelets. Depression alters the propensity of the blood to form clots. There's evidence that depression activates blood platelets so that they become stickier ready to clump into thrombi that choke the supply of blood to the heart or brain.
The problem is, activated platelets are drawn to those spots in artery walls that have accumulated cholesterol-laden plaque. There they adhere and rope in more platelets. Under the right conditions, clotting can occur quickly, leading to heart attack.
Here's where the plot, well, thickens. Many factors influence platelet activation—including the autonomic nervous system. "Think of the fight or flight response," suggests Carney. "It's paradoxical, but depression is marked by superaroused physiology." In the event of attack by tiger, the stress response prepares the body for rapid repair of wounds. Platelets become trigger-responsive to staunch the flow of blood. "The coagulation processes may be especially harmful if you have existing heart disease," he notes.
But wait. Platelets also contain large quantities of the neurotransmitter serotonin and receptors for it. It's not clear how platelet serotonin relates to brain serotonin, and in fact, they may have no relationship at all.
While the complexities of platelet activation are yet to be unraveled, there is evidence that antidepressants known to affect serotonin levels, the SSRIs, reduce blood platelet activity in depressed patients. "Sertraline has the same effect as aspirin," says Duke's Krishnan. "We don't know whether it's of benefit because it is a better aspirin or because it reduces depression. It could do both—and it probably does."
Metabolism. The cortisol increases that typify depression reshuffle the body's energy resources and affect the way the body handles insulin. Specifically, they reduce sensitivity to insulin, known as insulin resistance. Insulin is the hormone that controls blood sugar, the brain's preferred fuel. Insulin resistance encourages a particularly pernicious form of weight gain. There is an increase in abdominal fat deposits.
Storing fat on the belly gives it a privileged position, close to the liver, where, in the event of an emergency—remember, fight or flight—it can be quickly converted to glucose and rushed to muscles. Unfortunately, abdominal fat wasn't meant for more than short-term parking. It puts a direct load on the heart, as does the high circulating level of cortisol that prompted it in the first place.
The metabolic tilt towards abdominal fat is injury enough. What adds a special insult is that depression often encourages weight gain. It makes people inactive, even inert. And a common form of depression, so-called atypical depression, is characterized by increased appetite and substantial weight gain, as well as profound lethargy. Physiology and behavior collide, perhaps fatally.
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