The Stress-Susceptible Individual and the Risk for Inflammatory Diseases

Stress Susceptible Individual Risk Inflammatory Diseases

In this recent editorial Gailen Marshall, Editor-in-Chief of Annals of Allergy, Asthma & Immunology, discusses the topic of identifying and stratifying stress-susceptible individuals and established patients, and the relevance of correlating this susceptibility to the presence and/or progression of immune-mediated inflammatory conditions.

An increasing body of evidence suggests stress is a confounder of therapeutic response, as well as a risk factor for common human inflammatory diseases. As stated elsewhere (cf. JAOA, 104, suppl., May 2004: 1-6), by the same author, various sources have estimated that up to 75% of all visits to physicians’ offices are stress-related.

This estimate appears to be particularly true in relation to immune-based dysfunctions. Because of an inappropriate rather than deficient immune response, otherwise healthy individuals may, at times of significant stress, have one or a combination of the following: increased incidence, severity, and duration of multiple distinct conditions.

For example, psychological stress has known adverse effects on existing allergic and asthmatic diseases, and there is also an association between higher rates of allergic disorders and depression or anxiety.

Psychological stress and allergy and asthma incidence are both steadily increasing in our society, and the value of exploring and addressing their interrelationship is clear – from an economic standpoint, an estimated 40 million Americans (nearly 25% of the population) have allergic diseases with associated annual medical costs estimated at $3.4 billion and about 28 million days of decreased productivity (in school and work) from either symptoms or medication side effects (JAOA, 104, suppl., May 2004: 1-6).

Thus, in this editorial Gailen Marshall discusses the need for translational research in the field of neuroendocrine-immunology and psychoneuroimmunology as a means of identifying specific risk factors and developing scientifically sound rationales for interventions in specific disease states.

To achieve this goal the author believes that a crucial step would be establishing validated criteria to identify stress-susceptible individuals, and delineating techniques to identify how much of stress susceptibility is genetic or conditional (environmental).

This will involve microarray technology, single nucleotide polymorphisms for various neuroendocrine-immune pathways, neuroendocrine methods to evaluate various stressors, or several modifiers able to alter the susceptibility of the individual to a perceived stress, as well as validated laboratory tools that can predict immune profiles, responsiveness and disease activity.

As stated by the author – the answer to these and any other important translational research questions are not likely to reside in any single discipline of genetics, immunology, endocrinology or psychology, but rather all four disciplines combined into a interdisciplinary conceptual framework or ‘profile’ that can be used to identify risk. Such ‘profiles’ would be undoubtedly useful for identifying stress-susceptible individuals and altering their risk with specific therapeutic, and hopefully prophylactic interventions.

Expert Rev Clin Immunol 2009, 5: 119
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