Sally S. Dickerson ¹ , Shelly L. Gable ² , Michael R. Irwin ³ , Najib Aziz ⁴ , and Margaret E. Kemeny ⁵

  ¹ Department of Psychology and Social Behavior, University of California, Irvine;   ² Department of Psychology, University of California, Santa Barbara;   ³ Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience, David Geffen School of Medicine, University of California, Los Angeles;   ⁴ Department of Pathology and Laboratory Medicine, University of California, Los Angeles; and   ⁵ Department of Psychiatry, University of California, San Francisco

 Address correspondence to Sally S. Dickerson, Department of Psychology and Social Behavior, University of California, Irvine, 3340 Social Ecology II, Irvine, CA 92697-7085, e-mail: sdickers@uci.edu.

Copyright © 2009 Association for Psychological Science

ABSTRACT

ABSTRACT—This study experimentally tested whether a stressor characterized by social-evaluative threat (SET), a context in which the self can be judged negatively by others, would elicit increases in proinflammatory cytokine activity and alter the regulation of this response. This hypothesis was derived in part from research on immunological responses to social threat in nonhuman animals. Healthy female participants were assigned to perform a speech and a math task in the presence or absence of an evaluative audience (SET or non-SET, respectively). As hypothesized, stimulated production of the proinflammatory cytokine tumor necrosis factor-α (TNF-α) increased from baseline to poststressor in the SET condition, but was unchanged in the non-SET condition. Further, the increases in TNF-α production correlated with participants' cognitive appraisals of being evaluated. Additionally, the ability of glucocorticoids to shut down the inflammatory response was decreased in the SET condition. These findings underscore the importance of social evaluation as a threat capable of eliciting proinflammatory cytokine activity and altering its regulation.

Insulin resistance linked to ulcer bacteria

July 21st, 2009 The Yomiuri Shimbun -->

Helicobacter pylori bacteria, which can cause gastric ulcers, have been linked to type B insulin resistance syndrome in diabetics, researchers reported in the British medical journal The Lancet.

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A diabetic patient was found to have completely recovered from insulin resistance after the bacteria were killed with antibiotics. The discovery was made by Prof. Hideki Katagiri of the Center for Translational and Advanced Animal Research at Tohoku University Graduate School of Medicine in Japan and others.

When a person develops type B insulin resistance syndrome diabetes, insulin is prevented from functioning properly by the immune system. The syndrome, thought to occur in only one in every thousand to tens of thousands of people, does not respond to common diabetes treatments.

Katagiri and others examined a patient with type B insulin resistance who had become thrombocytopenic -- a condition characterized by a low level of blood platelets _ and found they were infected with pylori bacteria. After eradicating the bacteria with antibiotic treatments used for treating thrombocytopenia in March last year, the patient reportedly showed no further symptoms of either diseases.

Katagiri said the eradication of the bacteria could completely cure type B insulin resistance, theorizing that the pylori bacteria are affecting patients' immune systems and contributing to the development of diabetes.