We know that a balanced diet, regular exercise, good sleep hygiene, and avoidance of certain kinds of stress (distress vs. eustress) will prolong our lives. Despite frequent advice regarding these habits, we do not always make beneficial choices. Yet capitulation is not inevitable. For example, stop-smoking campaigns, supported by science and aggressive public health policies, have been remarkably successful by many measures, reversing trends and changing behavior around tobacco. Determining how lifestyle affects our biology is important for at least two reasons. First, revealing a particular habit’s biological impact can inform specific public health policies. Second, such work may help identify tissular, cellular, and molecular mechanisms central to how the body adapts to environmental stressors. These insights can teach us nature’s patterns, which we can then adapt and widen to improve our lives.

On one hand, stress is a vital physiological mechanism that alerts us to possible danger. Acute stress can save our lives by eliciting a fight, flight, or freeze response. On the other hand, acute and chronic stress elevate the risk of developing cardiovascular disease. Chronic psychosocial stress also often overlaps with confounding unhealthy habits including smoking, alcohol consumption, irregular sleep, and a sedentary lifestyle. Stress has multiple, interdependent impacts on health.

Though the neuroscience of stress is vast and complex, the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) are key physiological effectors. A growing body of work has demonstrated that the bone marrow’s capacity to produce and mobilize immune cells is partly mediated by the SNS. More broadly, the central nervous system can influence hematopoietic cell function through either direct innervation or secreted factors. However, multiple questions remain concerning communication networks linking the nervous and immune systems. Various labs at Mount Sinai’s CVRI use chemogenetics, optogenetics, and acute stress models to test the hypothesis that distinct brain regions control anticipatory and tailored leukocyte function in response to acute stress. The inflammatory response to infection or injury varies widely and can be a matter of life and death. Understanding how stress shapes that response, therefore, is critical.