Psychological Stress and Mitochondria
Published on: 02.02.2018
Associated with: Psychosomatic Medicine. 80(2):126-140, February/March 2018Psychosomatic Medicine. 80(2):141-153, February/March 2018
The integration of biological, psychological, and social factors in medicine has benefited from increasingly precise stress response biomarkers. Mitochondria, a subcellular organelle with its own genome, produce the energy required for life and generate signals that enable stress adaptation. An emerging concept proposes that mitochondria sense, integrate, and transduce psychosocial and behavioral factors into cellular and molecular modifications. Mitochondrial signaling might in turn contribute to the biological embedding of psychological states.
Cellular ‘powerhouses’ may explain health effects of stress
- February 2, 2018
- Wolters Kluwer Health
- How does psychological stress translate into physical health effects? A key piece of the puzzle may be found in specialized cellular structures known as mitochondria, according to a pair of new articles.
The articles present an update on current evidence and a conceptual framework of the role of mitochondria in understanding how psychosocial factors — either negative or positive — may affect human health. “Ultimately, the successful integration of mitochondria in psychosomatic research should foster a more comprehensive understanding of the forces that influence our health across the lifespan, and of the factors that hinder our ability to heal from disease,” write Martin Picard, PhD, of Columbia University and Bruce S. McEwen of The Rockefeller University, New York.
Mitochondria, Stress, and Health — New Evidence and Interactions
Mitochondria are subunits of cells throughout the body with their own DNA. Mitochondria are found in nearly every type of cell. Sometimes called cellular “powerhouses,” mitochondria generate the energy and signals required for life. When mitochondria do not work properly, they can cause severe diseases affecting many different body systems.
Research points to mitochondria as “a potential intersection point between psychosocial experiences and biological stress responses,” Drs. Picard and McEwen write. In 23 experimental studies in animals that have been conducted by researchers in laboratories across the world, acute and chronic stress influenced specific aspects of mitochondrial function — particularly in the brain. Mitochondrial vulnerability to stress may be influenced by a wide range of factors, including behavior, genes, and diet.
The authors also outline a conceptual framework by which mitochondria may transduce the effects of psychological stress on physical health. A growing body of evidence suggests that mitochondria “sense, integrate, and signal information about their environment.” This includes various stress-induced mediators, which cause structural and functional “recalibration” of the mitochondria.
The authors introduce the concept of mitochondrial allostatic load (MAL), describing the structural and functional changes that mitochondria undergo in response to chronic stress. In turn, these changes may lead to widespread health effects: for example, increased inflammation leading to disease risk, or cellular DNA damage leading to accelerated aging.
Mitochondria also appear to be involved in regulating the body’s stress reactivity systems, including the brain, as well as controlling immunity and inflammation. Damage to mitochondrial DNA has long been suggested to represent a biological “aging clock.” Recent studies have unequivocally shown that mitochondria affect the rate of aging in mammals, possibly through increased inflammation. However, it’s still unclear whether this is the case in humans.
The findings are especially exciting for the field of psychosomatic medicine, with its traditional focus on re-integrating the mind (“psyche”) and body (“soma”). Emerging evidence on the role of mitochondria in translating the effects of stress on health “extend the reach of mind-body research into the cellular-molecular domain that is the core foundation of current biomedical training and practice,” Drs. Picard and McEwen write. They emphasize the need for further studies to test various elements of their model, especially in humans. “Future research should consider the dynamic bi-directional interactions between mitochondria and other important physiological systems,” the authors conclude.
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Wolters Kluwer Health. “Cellular ‘powerhouses’ may explain health effects of stress.” ScienceDaily. ScienceDaily, 2 February 2018. <www.sciencedaily.com/releases/201
Psychological Stress and Mitochondria: A Conceptual Framework
Background The integration of biological, psychological, and social factors in medicine has benefited from increasingly precise stress response biomarkers. Mitochondria, a subcellular organelle with its own genome, produce the energy required for life and generate signals that enable stress adaptation. An emerging concept proposes that mitochondria sense, integrate, and transduce psychosocial and behavioral factors into cellular and molecular modifications. Mitochondrial signaling might in turn contribute to the biological embedding of psychological states.
Methods A narrative literature review was conducted to evaluate evidence supporting this model implicating mitochondria in the stress response, and its implementation in behavioral and psychosomatic medicine.
Results Chronically, psychological stress induces metabolic and neuroendocrine mediators that cause structural and functional recalibrations of mitochondria, which constitutes mitochondrial allostatic load. Clinically, primary mitochondrial defects affect the brain, the endocrine system, and the immune systems that play a role in psychosomatic processes, suggesting a shared underlying mechanistic basis. Mitochondrial function and dysfunction also contribute to systemic physiological regulation through the release of mitokines and other metabolites. At the cellular level, mitochondrial signaling influences gene expression and epigenetic modifications, and modulates the rate of cellular aging.
Conclusions This evidence suggests that mitochondrial allostatic load represents a potential subcellular mechanism for transducing psychosocial experiences and the resulting emotional responses—both adverse and positive—into clinically meaningful biological and physiological changes. The associated article in this issue of Psychosomatic Medicine presents a systematic review of the effects of psychological stress on mitochondria. Integrating mitochondria into biobehavioral and psychosomatic research opens new possibilities to investigate how psychosocial factors influence human health and well-being across the life-span.
Objective Mitochondria are multifunctional life-sustaining organelles that represent a potential intersection point between psychosocial experiences and biological stress responses. This article provides a systematic review of the effects of psychological stress on mitochondrial structure and function.
Methods A systematic review of the literature investigating the effects of psychological stress on mitochondrial function was conducted. The review focused on experimentally controlled studies allowing us to draw causal inference about the effect of induced psychological stress on mitochondria.
Results A total of 23 studies met the inclusion criteria. All studies involved male laboratory animals, and most demonstrated that acute and chronic stressors influenced specific facets of mitochondrial function, particularly within the brain. Nineteen studies showed significant adverse effects of psychological stress on mitochondria and four found increases in function or size after stress. In humans, only six observational studies were available, none with experimental designs, and most only measured biological markers that do not directly reflect mitochondrial function, such as mitochondrial DNA copy number.
Conclusons Overall, evidence supports the notion that acute and chronic stressors influence various aspects of mitochondrial biology, and that chronic stress exposure can lead to molecular and functional recalibrations among mitochondria. Limitations of current animal and human studies are discussed. Maladaptive mitochondrial changes that characterize this subcellular state of stress are termed mitochondrial allostatic load. Prospective studies with sensitive measures of specific mitochondrial outcomes will be needed to establish the link between psychosocial stressors, emotional states, the resulting neuroendocrine and immune processes, and mitochondrial energetics relevant to mind-body research in humans.