Fatigue, Inflammation, and ω-3 and ω-6 Fatty Acid Intake Among Breast Cancer Survivors

Alfano, Catherine M.; Imayama, Ikuyo; Neuhouser, Marian L.; Kiecolt‐Glaser, Janice K.; Smith, Ashley Wilder; Meeske, Kathleen; McTiernan, Anne; Bernstein, Leslie; Baumgartner, Kathy B.; Ulrich, Cornelia M.; Ballard‐Barbash, Rachel

doi:10.1200/jco.2011.36.4109

Cited by 135 publications

(98 citation statements)

References 55 publications

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“…This finding supported the results of a case study by the same group [270], which noted structural changes in the brain of a patient with chronic fatigue syndrome detected by NMR spectroscopy following a course of EPA supplementation [270]. There is also robust evidence demonstrating that EPA supplementation produces clinically significant reductions in the levels of severe intractable fatigue experienced by sufferers of cancer [271,272].…”

Section: Lipid Rafts Mlrs and N-3 Pufas In Chronic Fatigue Syndromesupporting

confidence: 74%

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders

Morris¹,

Walder

Puri

et al. 2015

Mol Neurobiol

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Oxidative and nitrosative stress (O&NS) is causatively implicated in the pathogenesis of Alzheimer's and Parkinson's disease, multiple sclerosis, chronic fatigue syndrome, schizophrenia and depression. Many of the consequences stemming from O&NS, including damage to proteins, lipids and DNA, are well known, whereas the effects of O&NS on lipoprotein-based cellular signalling involving palmitoylation and plasma membrane lipid rafts are less well documented. The aim of this narrative review is to discuss the mechanisms involved in lipid-based signalling, including palmitoylation, membrane/lipid raft (MLR) and n-3 polyunsaturated fatty acid (PUFA) functions, the effects of O&NS processes on these processes and their role in the abovementioned diseases. S-palmitoylation is a post-translational modification, which regulates protein trafficking and association with the plasma membrane, protein subcellular location and functions. Palmitoylation and MRLs play a key role in neuronal functions, including glutamatergic neurotransmission, and immune-inflammatory responses. Palmitoylation, MLRs and n-3 PUFAs are vulnerable to the corruptive effects of O&NS. Chronic O&NS inhibits palmitoylation and causes profound changes in lipid membrane composition, e.g. n-3 PUFA depletion, increased membrane permeability and reduced fluidity, which together lead to disorders in intracellular signal transduction, receptor dysfunction and increased neurotoxicity. Disruption of lipid-based signalling is a source of the neuroimmune disorders involved in the pathophysiology of the abovementioned diseases. n-3 PUFA supplementation is a rational therapeutic approach targeting disruptions in lipid-based signalling.

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Section: Lipid Rafts Mlrs and N-3 Pufas In Chronic Fatigue Syndromesupporting

confidence: 74%

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders

Morris¹,

Walder

Puri

et al. 2015

Mol Neurobiol

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“…We focused on two inflammatory markers, IL-6 and CRP, which have been associated with cancer-related fatigue (Schubert et al, 2007; Alfano et al, 2012) and with HRV (Sajadieh et al, 2004; Sloan et al, 2007). Plasma levels of IL-6 were determined by the Quantikine high-sensitivity ELISA kit (R&D Systems, Minneapolis, MN), with a lower detection limit of 0.039 pg/mL.…”

Section: Methodsmentioning

confidence: 99%

Low heart rate variability and cancer-related fatigue in breast cancer survivors

Crosswell

Lockwood

Ganz

et al. 2014

Psychoneuroendocrinology

101

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Cancer-related fatigue is a common and often long lasting symptom for many breast cancer survivors. Fatigued survivors show evidence of elevated inflammation, but the physiological mechanisms driving inflammatory activity have not been determined. Alterations in the autonomic nervous system, and particularly parasympathetic nervous system activity, are a plausible, yet understudied contributor to cancer-related fatigue. The goal of this study was to replicate one previous study showing an association between lower parasympathetic activity and higher fatigue in breast cancer survivors (Fagundes et al., 2011), and to examine whether inflammation mediates this association. Study participants were drawn from two samples and included 84 women originally diagnosed with early-stage breast cancer prior to age 50. Participants completed questionnaires, provided blood samples for determination of interleukin (IL)-6 and C-reactive protein (CRP), and underwent electrocardiography (ECG) assessment for evaluation of resting heart rate variability (HRV), a measure of parasympathetic activity. Results showed that lower HRV was associated with higher fatigue (p < .05), as predicted. In bivariate analyses, HRV was also correlated with circulating concentrations of IL-6 and CRP. However, path analyses did not support inflammation as a mediator of the association between HRV and fatigue; instead, associations among these variables appeared to be driven by age and BMI. These findings identify HRV as a potential contributor to cancer-related fatigue, but suggest that inflammation does not mediate this association in younger, healthy breast cancer survivors who are several years post-treatment. The autonomic nervous system merits additional attention in research on the etiology of cancer-related fatigue.

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“…The primary outcome of this randomized controlled trial was fatigue, and results showed improvements in fatigue and energy among women assigned to the yoga group relative to women assigned to the health education control condition (Bower et al, 2012). In addition to behavioral outcomes, the trial was designed to examine effects on inflammatory processes, which may underlie symptoms of cancer-related fatigue (Bower et al, 2002; Collado-Hidalgo et al, 2006; Orre et al, 2011; Bower et al, 2011b; Alfano et al, 2012). Based on preliminary work suggesting beneficial effects of yoga on inflammation (Pullen et al, 2008; Pullen et al, 2010), we hypothesized that women randomly assigned to the targeted Iyengar yoga intervention would show decreases in markers of inflammatory activity relative to health education controls.…”

Section: Introductionmentioning

confidence: 99%

Yoga reduces inflammatory signaling in fatigued breast cancer survivors: A randomized controlled trial

Bower¹,

Greendale²,

Crosswell³

et al. 2014

Psychoneuroendocrinology

229

231

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Background Yoga is a popular mind-body therapy that has demonstrated beneficial effects on psychological, behavioral, and functional outcomes. However, few studies have investigated effects on inflammatory processes. This study tested the hypothesis that an Iyengar yoga intervention specifically designed for fatigued breast cancer survivors would lead to decreases in inflammation-related gene expression and circulating markers of proinflammatory cytokine activity. Methods Breast cancer survivors with persistent cancer-related fatigue were randomized to a 12-week Iyengar yoga intervention (n = 16) or a 12-week health education control condition (n = 15). Blood samples were collected at baseline, post-intervention, and at a 3-month follow-up for genome-wide transcriptional profiling and bioinformatic analyses. Plasma inflammatory markers and salivary cortisol were also assessed. Results In promoter-based bioinformatics analyses, the yoga group showed reduced activity of the pro-inflammatory transcription factor nuclear factor kappa B (NF-κB), increased activity of the anti-inflammatory glucocorticoid receptor, and reduced activity of cAMP response element-binding protein (CREB) family transcription factors relative to controls (all ps < .05). There was also a significant intervention effect on the soluble tumor necrosis factor receptor type II (sTNF-RII), a marker of TNF activity; plasma levels of sTNF-RII remained stable in the yoga group, whereas levels of this marker increased in the health education group (p = .028). A similar, non-significant trend was observed for the interleukin 1 receptor antagonist (p = .16). No significant changes in C reactive protein (CRP), interleukin 6 (IL-6), or diurnal cortisol measures were observed. Conclusions A 12-week restorative Iyengar yoga intervention reduced inflammation-related gene expression in breast cancer survivors with persistent fatigue. These findings suggest that a targeted yoga program may have beneficial effects on inflammatory activity in this patient population, with potential relevance for behavioral and physical health. ClinicalTrials.gov identifier: NCT00727662.

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Fatigue, Inflammation, and ω-3 and ω-6 Fatty Acid Intake Among Breast Cancer Survivors

Cited by 135 publications

References 55 publications

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders

The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders

Low heart rate variability and cancer-related fatigue in breast cancer survivors

Yoga reduces inflammatory signaling in fatigued breast cancer survivors: A randomized controlled trial

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