Thursday, June 09, 2005

From Science News, Vol. 167, No. 22, May 28, 2005, p. 341.

Positive Jolt: Electroshock therapy may have side benefit
Nathan Seppa

People with depression have high concentrations of norepinephrine, a nervous system hormone that signals blood vessels to constrict and ratchets up blood pressure, researchers report. Treating these individuals with electroshock therapy lowers their norepinephrine concentrations—and their heart rate and blood pressure too, scientists find.

A fast pulse, vessel constriction, and high blood pressure are valuable tools in a person's fight-or-flight response. But if high norepinephrine concentrations chronically keep a person in that state, it puts a strain on the heart, says Mitchel A. Kling, a psychiatrist at the National Institute of Mental Health in Bethesda, Md. Excess norepinephrine, he says, could partly explain the long-standing connection between depression and heart failure, which is a weakening of the heart. Depression doubles the risk of death in people with heart failure, as do high norepinephrine concentrations.

"Depression is not good for your heart, basically," says Kling.

He and his colleagues conducted standard clinical tests on 22 people with the most severe form of depression and 23 people free of depression. The groups were similar in age. Volunteers with depression had a higher average pulse rate and higher blood pressure than did people in the comparison group. Blood and spinal-fluid samples revealed higher concentrations of three stress hormones—norepinephrine, cortisol, and epinephrine—in study participants with depression than in the others. The stress-hormone differences showed up even during sleep.

Next in the study, eight of the depressed patients volunteered to receive a series of electroshock treatments, which are also called electroconvulsive therapy. Among psychiatrists, electroshock treatment remains controversial. Many depressed people show gains from it, but some complain of memory loss and other side effects. Its benefit sometimes lasts only a few days and, at other times, endures for months or years, Kling says.

The eight patients in Kling's study averaged nine electroshock treatments apiece over roughly 3 weeks. Four weeks after the last treatment, the patients again provided blood and spinal-fluid samples. These showed a clear drop in the concentration of norepinephrine, but not cortisol or epinephrine, the researchers report in an upcoming Proceedings of the National Academy of Sciences.

"To my knowledge, no one has ever looked at the effect of electroconvulsive therapy on the levels of norepinephrine," says cardiologist Inder S. Anand of the Veterans Affairs Medical Center and University of Minnesota in Minneapolis. Combined with other work, this research is "pretty convincing" that stress chemicals such as norepinephrine are being overproduced in the depressed brain, he says.

Even more interesting, he says, is that electroshock can change conditions in the brain to the point of reversing norepinephrine's oversupply.

Made by nerve cells, norepinephrine carries signals between the cells. Electroshock therapy might "reset" overzealous nerve cells in the brain and reduce their norepinephrine production, Kling hypothesizes. But the therapy's long-term benefits in this regard are unknown, he says.

Suppressing norepinephrine might nevertheless offer benefits for patients with heart failure, Kling says. Some of the many antidepression drugs on the market may reduce norepinephrine concentrations too, he says, "but there is surprisingly little data on that."
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References:

Gold, P.W. . . . and M.A. Kling. In press. Cardiac implications of increased arterial entry and reversible 24-h central and peripheral norepinephrine levels in melancholia. Proceedings of the National Academy of Sciences. Abstract available at http://www.pnas.org/cgi/doi/10.1073/pnas.0503069102.

Further Readings:

Aggarwal, A., et al. 2002. Norepinephrine turnover is increased in suprabulbar subcortical brain regions and is related to whole-body sympathetic activity in human heart failure. Circulation 105(March 5):1031-1033. Available at http://circ.ahajournals.org/cgi/content/full/105/9/1031.

Anand, I.S., et al. 2003. Changes in brain natriuretic peptide and norepinephrine over time and mortality and morbidity in the Valsartan Heart Failure Trial (Val-HeFT). Circulation 107(March 11):1278-1283. Available At http://circ.ahajournals.org/cgi/content/full/107/9/1278.

Carney, R.M., et al. 1999. Major depression, heart rate, and plasma norepinephrine in patients with coronary heart disease. Biological Psychiatry 45(Feb. 15):458-463. Abstract available at http://dx.doi.org/10.1016/S0006-3223(98)00049-3.


Sources:

Inder S. Anand
University of Minnesota, Minneapolis
Veterans Affairs Medical Center
1 Veterans Drive
Minneapolis, MN 55417

Mitchel A. Kling
National Institute of Mental Health
National Institutes of Health
Building 10, Room 2D-46
10 Center Drive
Bethesda, MD 20892-1284

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