Tagged: heart disease

In poverty, is your heart your stress ball?

University of Pittsburgh researcher Peter Gianaros speaks on poverty and stress for the last CNS Public Talk of the academic year. Image from the CNS

This year’s CNS Public Talk Series wrapped up April 4 with a foray into poverty, stress and heart disease — not the usual suspects for a neuroscience lecture. But speaker Peter Gianaros’ goal was to address health inequalities as a problem for neuroscience, and he started by explaining his own journey from studying cardiovascular disease risk to studying the brain.

That journey began with a decision to address the “elephant in the room” for health research: the fact that those living in poverty suffer more chronic illness across the board, including heart disease. Since stress affects cardiovascular responses, and low socioeconomic status individuals experience more stress, Gianaros focused on those two links.

Gianaros and colleagues have used behavioral paradigms to track factors like stress and emotional reactions, and they’ve turned to brain imaging to examine the corresponding brain systems. They’ve also tracked subjects’ education level, income and occupation — three factors the social science literature has shown tap into distinct aspects of social standing. Finally, to gauge effects on the heart, they looked at intima media thickness. IMT measures thickness of the arterial wall, with higher thickness indicating greater risk for heart disease.

Sifting through all these elements, the research has so far pointed to surprising connections, which help explain the greater vulnerability of low SES individuals to cardiovascular disease. SES shows an inverse relationship with IMT — that is, those with low SES have thicker arteries. The likely culprit?  Stress. As indicated by higher amygdala response to threat, these individuals are also more reactive to stress. And separate studies have found that higher amygdala response to threat in turn correlates with higher IMT, highlighting the relevant connection between the heart and the brain.

As Gianaros acknowledged, this work is very much associational — messy for determining cause and effect. After his talk, audience discussion focused on other factors that can alter stress levels, like social support and traumatic incidents. There’s a seemingly unending list of possible mediators. That helps explain why many researchers shy away from SES: it adds complicating layers in a discipline whose MO is to strip the most causal layers away possible.

But Gianaros’ point was that these complications are exactly what seem to drive chronic illness. He ended by calling for neuroscientists to pay more attention to health inequalities, and for inequalities researchers to pay more attention to neuroscience. In that respect, the CNS is already on board.

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