Sarosh J. Motivala,Ph.D.

Brief Biography
Sarosh Motivala received his doctorate in health-clinical psychology from the University of Miami in 2001. His master’s thesis focused on examining cardiovascular psychophysiology with measures of immune system activity in response to acute stress.
For his doctoral dissertation, he used structural equation modeling to examine

relationships between psychological distress, T cell counts and viral load in HIV spectrum disease. In 2001, after completing his clinical internship at UCLA, he began working at the Cousins Center for PNI, studying immune pathways related to stress and disease activity in rheumatoid arthritis.

Brief Description of Research Project

Rheumatoid arthritis is a chronic autoimmune condition in which pro-inflammatory cytokines play a major role in disease activity. The pathophysiology of RA may dysregulate interactions between hormones involved in the stress response and immune regulation (e.g. cortisol, epinephrine and norepinephrine). This in turn may make RA patients particularly vulnerable to stress-related flares in disease activity by stimulating expression of pro-inflammatory cytokines.
In our research project, we are examining whether individuals with RA have different patterns of stress responsivity compared to healthy control participants. In addition, we seek to determine whether responsivity is predictive of disease activity over a three month period. The study combines psychosocial interviews and self-report data with laboratory tests of psychological and physiological stress reactivity in an acute, laboratory-based setting. Acute stress paradigms provide a valuable platform for examining relationships between stress-responsive physiological systems. The two major mediators of the stress response are the hypothalamic-pituitary adrenocortical (HPAC) axis and the sympathetic nervous system/adrenal medullary (SAM) axis. The purpose of the study is to examine the relationships between these axes (by measuring catecholamine and cortisol levels in conjunction with psychophysiologically derived estimates of sympathetic and parasympathetic activity) with immunological parameters (circulating plasma levels and stimulated intracellular levels of Interleukin-6 and tumor necrosis factor) linked to disease activity in RA patients.