Chronic stress alters our genetic immune response

MOST people would agree that stress increases your risk for illness and this is particularly true for severe long-term stresses, such as caring for a family member with a chronic medical illness.
However, we still have a relatively limited understanding of exactly how stress contributes to the risk for illness. In the August 15th issue of Biological Psychiatry, researchers shed new light on one link between stress and illness by describing a mechanism through which stress alters immune function.
In a very promising preliminary study, Miller and colleagues found that the pattern of gene expression differed between caregivers of family members with cancer relative to a matched group of individuals who did not have this type of life stress. They found that among the caregivers, even though they had normal cortisol levels in their blood, the pattern of gene expression in the monocytes, a type of white blood cell involved in the body’s immune response, was altered so that they were relatively less responsive to the anti-inflammatory actions of cortisol, but relatively more responsive to pro-inflammatory actions of a transcription factor called nuclear factor-kappa B, or NF-?B.
Gregory Miller, Ph.D., corresponding author, explains more simply that, although “caregivers have similar cortisol levels as controls, their cells seem to be ‘hearing’ less of this signal. In other words, something goes awry in caregivers’ white blood cells so they are not able to ‘receive’ the signal from cortisol that tells them to shut down inflammation.”
Thus, the current findings might help to explain why the caregivers would seem to be in a chronic pro-inflammatory state, a condition of immunologic activation. This activated state could contribute to the risk for a number of medical illnesses, such as depression, heart disease, and diabetes.