Inflammation worsens all psychiatric symptoms

Dr. Weeks Comment: The title of this post is irrefutable, but so is the converse: Psychiatric symptoms resulting from adrenalin (with a negative cognitive spin on it) cause inflammation. This helpful video interview from Thailand explains the relationship. Either way, inflammation and all psychiatric suffering, (even depression which seems devoid of adrenalin) are causally linked so anti-inflammatory agents can facilitate recovery from all psychiatric ailments. This relationship was first broadcast in in Psychiatric Times January 2014 entitled The Potential for Rational Adjunctive Anti-inflammatory Therapy in Schizophrenia: Quenching the Fire? A follow up article the Psychiatric Annals in May 2015 in a big review article entitled Inflammation and Psychiatric Disorders – Exploring the pathophysiology of Major psychiatric and neurological disorders; Now we get down to the details of mitochondrial function in the article shared below – but the answer is simple: use safe and effective anti-inflammatory diet to minimize the difficulties of all psychiatric illnesses.

Proc Natl Acad Sci U S A. 2015 Dec 1; 112(48): E6614–E6623.

Published online 2015 Nov 16. doi: 10.1073/pnas.1515733112

Mitochondrial functions modulate neuroendocrine, metabolic, inflammatory, and transcriptional responses to acute psychological stress

Martin Picard,a,b,1 Meagan J. McManus,a,b Jason D. Gray,c Carla Nasca,c Cynthia Moffat,d Piotr K. Kopinski,a,b Erin L. Seifert,d Bruce S. McEwen,c and Douglas C. Wallacea,b,2


In humans and animals, stress triggers multisystemic physiological responses that vary in nature and magnitude. The organism’s response to stress, rather than actual stressors, leads to allostatic load that predisposes to disease. This study in mice demonstrates that a specific cellular component that sustains life via energy transformation and intracellular signaling—the mitochondrion—influences the organism’s integrated response to psychological stress. Each component of the stress response assessed was modified by at least one mitochondrial defect. When analyzed collectively, stress-induced neuroendocrine, inflammatory, metabolic, and transcriptional responses coalesced into unique signatures that distinguish groups based on their mitochondrial genotype. This work shows that mitochondria can regulate complex whole-body physiological responses, impacting stress perception at the cellular and organismal levels.


The experience of psychological stress triggers neuroendocrine, inflammatory, metabolic, and transcriptional perturbations that ultimately predispose to disease. However, the subcellular determinants of this integrated, multisystemic stress response have not been defined. Central to stress adaptation is cellular energetics, involving mitochondrial energy production and oxidative stress. We therefore hypothesized that abnormal mitochondrial functions would differentially modulate the organism’s multisystemic response to psychological stress. By mutating or deleting mitochondrial genes encoded in the mtDNA [NADH dehydrogenase 6 (ND6) and cytochrome c oxidase subunit I (COI)] or nuclear DNA [adenine nucleotide translocator 1 (ANT1) and nicotinamide nucleotide transhydrogenase (NNT)], we selectively impaired mitochondrial respiratory chain function, energy exchange, and mitochondrial redox balance in mice. The resulting impact on physiological reactivity and recovery from restraint stress were then characterized. We show that mitochondrial dysfunctions altered the hypothalamic–pituitary–adrenal axis, sympathetic adrenal–medullary activation and catecholamine levels, the inflammatory cytokine IL-6, circulating metabolites, and hippocampal gene expression responses to stress. Each mitochondrial defect generated a distinct whole-body stress-response signature. These results demonstrate the role of mitochondrial energetics and redox balance as modulators of key pathophysiological perturbations previously linked to disease. This work establishes mitochondria as stress-response modulators, with implications for understanding the mechanisms of stress pathophysiology and mitochondrial diseases.

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