Stroke and heart attacks are the end products of progressive damage to blood vessels supplying the heart and brain, a process known as atherosclerosis. Atherosclerosis progresses when there are high levels of chemicals in the body known as pro-inflammatory cytokines. It is thought that persisting stress increases the risk for atherosclerosis and cardiovascular disease by evoking negative emotions that, in turn, raise the levels of pro-inflammatory chemicals in the body. A team from the University of Pittsburgh (Pennsylvania, USA) has revealed the neural circuitry that drives anger, anxiety, and depression to raise the risks of stroke and heart attack. Peter Gianaros and colleagues enrolled 157 healthy adults, ages 30 to 54 years, who were asked to regulate their emotional reactions to unpleasant pictures while their brain activity was measured with functional imaging. The researchers also scanned the subjects’ arteries for signs of atherosclerosis to assess heart disease risk and measured levels of inflammation in the bloodstream, a major physiological risk factor for atherosclerosis and premature death by heart disease. The team found that individuals who show greater brain activation when regulating their negative emotions also exhibit elevated blood levels of interleukin-6, one of the body’s pro-inflammatory cytokines, and increased thickness of the carotid artery wall, a marker of atherosclerosis. The inflammation levels accounted for the link between signs of atherosclerosis and brain activity patterns seen during emotion regulation. The study authors submit that their study identifies: “The cognitive regulation of emotion might relate to [cardiovascular disease] risk through a pathway involving the functional interplay between the anterior cingulate region of the prefrontal cortex and inflammatory activity.”
Gianaros PJ, Marsland AL, Kuan DC, Schirda BL, Jennings JR, Sheu LK, Hariri AR, Gross JJ, Manuck SB. “An inflammatory pathway links atherosclerotic cardiovascular disease risk to neural activity evoked by the cognitive regulation of emotion.” Biol Psychiatry. 2014 May 1;75(9):738-45.
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