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Alan Breier, MD
Maryland Psychiatric Research Center Outpatient Department Box 21247 Baltimore, MD 21228

Prince K. Arora, Phd
National Institute of Child Health and Human Development Laboratory of Developmental and Molecular Immunity Bldg 6, Room 416 9000 Rockville Pike Bethesda, MD 20892

Owen M. Wolkowitz, MD
Langley-Porter Psychiatry Institute University of California, San Francisco Box 391 401 Parnassus Ave San Francisco, CA 94143

David Pickar, MD; Steven M. Paul, MD
The Clinical Neurosciences Branch National Institutes of Mental Health Bldg 10, Room 4N212 9000 Rockville Pike Bethesda, MD 20892

Arch Gen Psychiatry. 1987;44(12):1108-1109.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

A growing number of preclinical and clinical studies^1-4 have shown that exposure to stress results in suppression of immune function. In humans, reductions in cell-mediated immunity have been associated with depression and bereavement^3,4; however, the mechanisms involved in stress-induced immunosuppression are not fully understood. An experimental stress paradigm that reliably produces alterations in immune function in humans could be an important tool in helping to assess the mechanism(s) underlying stress-related immunosuppression.

Our laboratory is involved in a series of studies examining the behavioral and neurobiologic effects of 2-deoxy-D-glucose (2-DG), a metabolic stressor, on normal volunteers and psychiatric patients. 2-DG is a glucose analogue that competitively inhibits glucose-6phosphate, resulting in disruption of intracellular glucose utilization. The behavioral and physiological effects of 2-DG administration include fatigue, hypothermia, increased hunger, diaphoresis, tachycardia, increased sympathetic nervous system activity, and increased cortisol secretion.⁵ We now report that 2-DG administration . . . [Full Text PDF of this Article]

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