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• W2042219673 startingPage "155" @default.
• W2042219673 abstract "Since the time of Freud, psychiatry has embraced the proposition that physiological and/or psychological stress precipitates various psychiatric disorders. To this effect, we propose that a continuum of liability obtains between stress, anxiety states and anorexia nervosa – a continuum which is grounded on a cytokine profile common to each of these conditions. For example, the biological response to stress, anxiety states and anorexia nervosa includes the elevation of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), and downregulation of interferon-γ (IFN-γ). Sustained elevation of IL-1β and TNF-α dysregulates both somatostatin and insulin secretion, the latter of which influences regional cerebral blood flow (rCBF) and brain energy metabolism. In addition, IL-1β and TNF-α influence the expression of certain crucial neuropeptides, which are known to be associated with anxiety states and anorexia nervosa. These neuropeptides include: β-endorphin, cholecystokinin (CCK), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP). β-endorphin effects glucose metabolism in the limbic system, CCK increases the release of β-endorphin from the anterior pituitary, NPY is a powerful anxiolytic that regulates β-endorphin and insulin, while VIP indirectly regulates the expression of TNF-α through the inhibition of interleukin-4 (IL-4)." @default.
• W2042219673 created "2016-06-24" @default.
• W2042219673 creator A5066908076 @default.
• W2042219673 creator A5080656438 @default.
• W2042219673 date "1999-02-01" @default.
• W2042219673 modified "2023-09-26" @default.
• W2042219673 title "Tumor necrosis factor-α: is there a continuum of liability between stress, anxiety states and anorexia nervosa?" @default.
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• W2042219673 doi "https://doi.org/10.1054/mehy.1997.0641" @default.
• W2042219673 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10340296" @default.
• W2042219673 hasPublicationYear "1999" @default.
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