Sixteen Weeks of Exercise Reduces C-Reactive Protein Levels in Young Women

Arikawa, Andrea Y.; Thomas, William; Schmitz, Kathryn H.; Kurzer, Mindy S.

doi:10.1249/mss.0b013e3182059eda

Cited by 83 publications

(75 citation statements)

References 43 publications

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“…Nevertheless, the relationship among weight loss or exercise, inflammation, and depression or anxiety is only beginning to be established. For example, although a 16-week exercise program was shown to reduce peripheral blood concentrations of CRP in a sample of 319 sedentary women, changes in inflammation, which were especially pronounced in obese exercisers, were not associated with improvements in mood (Arikawa et al, 2011). Nevertheless, it should be noted that these women were not clinically depressed.…”

Section: Reviewmentioning

confidence: 95%

Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Miller

Haroon

Felger

2016

Neuropsychopharmacol

119

124

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A wealth of data has been amassed that details a complex, yet accessible, series of pathways by which the immune system, notably inflammation, can influence the brain and behavior. These data have opened the window to a diverse array of novel targets whose potential efficacy is tied to specific neurotransmitters and neurocircuits as well as specific behaviors. What is clear is that the impact of inflammation on the brain cuts across psychiatric disorders and engages dopaminergic and glutamatergic pathways that regulate motivation and motor activity as well as the sensitivity to threat. Given the ability to identify patient populations with increased inflammation, the precision of interventions can be further tuned, in conjunction with the ability to establish target engagement in the brain through the use of multiple neuroimaging strategies. After a brief overview of the mechanisms by which inflammation affects the brain and behavior, this review examines the extant literature on the efficacy of anti-inflammatory treatments, while forging guidelines for future intelligent clinical trial design. An examination of the most promising therapeutic strategies is also provided, along with some of the most exciting clinical trials that are currently being planned or underway.

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Section: Reviewmentioning

confidence: 95%

Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Miller

Haroon

Felger

2016

Neuropsychopharmacol

119

124

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“…However, the link between improvement in depressive symptoms and reductions in inflammatory measures has yet to be established. For example, although a 16-week exercise programme was shown to reduce the peripheral blood concentrations of CRP in a sample of 319 sedentary women, changes in inflammation, which were especially pronounced in obese exercisers, were not associated with improvements in mood (Arikawa et al, 2010). Nevertheless, subjects in this and other studies on the effects of exercise on the immune system have not included patients with major depression or patients at risk for depression.…”

Section: Weight Reduction and Dietary Manipulationsmentioning

confidence: 96%

Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior

Haroon

Raison

Miller

2011

Neuropsychopharmacol

837

596

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The potential contribution of chronic inflammation to the development of neuropsychiatric disorders such as major depression has received increasing attention. Elevated biomarkers of inflammation, including inflammatory cytokines and acute-phase proteins, have been found in depressed patients, and administration of inflammatory stimuli has been associated with the development of depressive symptoms. Data also have demonstrated that inflammatory cytokines can interact with multiple pathways known to be involved in the development of depression, including monoamine metabolism, neuroendocrine function, synaptic plasticity, and neurocircuits relevant to mood regulation. Further understanding of mechanisms by which cytokines alter behavior have revealed a host of pharmacologic targets that may be unique to the impact of inflammation on behavior and may be especially relevant to the treatment and prevention of depression in patients with evidence of increased inflammation. Such targets include the inflammatory signaling pathways cyclooxygenase, p38 mitogen-activated protein kinase, and nuclear factor-kB, as well as the metabolic enzyme, indoleamine-2,3-dioxygenase, which breaks down tryptophan into kynurenine. Other targets include the cytokines themselves in addition to chemokines, which attract inflammatory cells from the periphery to the brain. Psychosocial stress, diet, obesity, a leaky gut, and an imbalance between regulatory and pro-inflammatory T cells also contribute to inflammation and may serve as a focus for preventative strategies relevant to both the development of depression and its recurrence. Taken together, identification of mechanisms by which cytokines influence behavior may reveal a panoply of personalized treatment options that target the unique contributions of the immune system to depression.

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“…In contrast, hsCRP levels increased (65%) in the S1 group. The level of the inflammation marker hsCRP depends on factors such as age, sex, physical activity, nutrition, weight, BMI and smoking [38][39][40][41] and is strongly increased in response to mild infections and inflammations. 2,42 In the present study group, great fluctuations in hsCRP levels were found.…”

Section: Discussionmentioning

confidence: 99%