Inflammatory markers and negative mood symptoms following exercise withdrawal.

Posted on March 3, 2012 by Maurice Preter MD

Brain Behav Immun. 2008 Nov;22(8):1190-6. Epub 2008 Jul 10.
Inflammatory markers and negative mood symptoms following exercise withdrawal.
Kop WJ, Weinstein AA, Deuster PA, Whittaker KS, Tracy RP.
Source

Department of Medicine, University of Maryland Medical Center, 22 South Greene Street, S3B04, Baltimore, MD 21201, USA. wkop@medicine.umaryland.edu
Abstract
OBJECTIVE:

Physical inactivity is associated with elevated inflammatory markers, but little is known about the time trajectories of reduced physical activity and inflammatory markers. Changes in inflammatory markers in response to withholding regular aerobic exercise were prospectively examined and correlated with increased negative mood symptoms and fatigue that accompany exercise withdrawal.
METHODS:

Participants with regular exercise habits (N=40, mean age of 31.3+/-7.5 years, 55% women) were randomized to aerobic exercise withdrawal or to continue regular exercise for 2 weeks. Protocol adherence was documented using ambulatory actigraphy. Inflammatory markers (interleukin-6, C-reactive protein, fibrinogen and soluble intercellular adhesion molecule-1) were assessed at weekly intervals. Negative mood was measured with the Profile of Mood States (POMS) and the Beck Depression Inventory (BDI), and fatigue with the Multidimensional Fatigue Inventory (MFI). Autonomic nervous system activity was examined using heart rate variability-based indices.
RESULTS:

Changes in inflammatory markers did not differ between exercise withdrawal and control groups (multivariate p interaction=0.25). Exercise withdrawal resulted in increased negative mood symptoms and fatigue from baseline to day 14 compared to controls (p DeltaPOMS=0.008, p DeltaBDI=0.002; p DeltaMFI=0.003), but these responses were not associated with changes in inflammatory markers (p-values >0.10). Inflammatory markers were also not correlated with autonomic nervous system dysregulation (p-values >0.10).
CONCLUSION:

Inflammatory markers were not increased following 2 weeks of exercise withdrawal. Negative mood symptoms and fatigue were not accounted for by changes in inflammatory markers. Compensatory feedback mechanisms may operate among healthy individuals to promote resilience from the effects of reduced exercise.

PMID:
18619772
[PubMed – indexed for MEDLINE]

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Depressive symptoms and metabolic syndrome: is inflammation the underlying link?

Posted on March 3, 2012 by Maurice Preter MD

Biol Psychiatry. 2008 Nov 15;64(10):896-900. Epub 2008 Jul 2.
Depressive symptoms and metabolic syndrome: is inflammation the underlying link?
Capuron L, Su S, Miller AH, Bremner JD, Goldberg J, Vogt GJ, Maisano C, Jones L, Murrah NV, Vaccarino V.
Source

Laboratory of Psychoneuroimmunology, Nutrition and Genetics, INRA-University Victor Segalen Bordeaux 2, Bordeaux, France. lucile.capuron@bordeaux.inra.fr
Abstract
BACKGROUND:

Behavioral alterations, including depression, are frequent in individuals with the metabolic syndrome (MetS). Recent findings suggest that chronic activation of innate immunity might be involved. The objective of this study was to examine the relationship between MetS and depressive symptoms and to elucidate the involvement of inflammation in this relationship.
METHODS:

Participants were 323 male twins, with and without MetS and free of symptomatic cardiovascular disease, drawn from the Vietnam Era Twin Registry. Depressive symptoms were measured with the Beck Depression Inventory (BDI). Inflammatory status was assessed using C-reactive protein (CRP) and interleukin-6 (IL-6); twins with both CRP and IL-6 levels above the median were classified as having an elevated inflammatory status. Factor analysis was performed on individual BDI items to extract specific symptom dimensions (neurovegetative, mood, affective-cognitive).
RESULTS:

Subjects with MetS had more depressive symptoms than those without. Depressive symptoms with neurovegetative features were more common and more robustly associated with MetS. Both the BDI total score and each symptom subscore were associated with inflammatory biomarkers. After adjusting for age, education, and smoking status, the MetS was significantly associated with the BDI total score and the neurovegetative score. After further adjusting for inflammation, the coefficient for MetS decreased somewhat but remained statistically significant for the BDI neurovegetative subscore. When controlling for the MetS, inflammation remained significantly associated with the BDI mood subscore.
CONCLUSIONS:

The MetS is associated with higher depressive symptomatology characterized primarily by neurovegetative features. Inflammation is one determinant of depressive symptoms in individuals with MetS.

PMID:
18597739
[PubMed – indexed for MEDLINE]
PMCID:
PMC2621309

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Relationship between inflammation and cognitive function in obstructive sleep apnea.

Posted on March 3, 2012 by Maurice Preter MD

Sleep Breath. 2009 Mar;13(1):35-41. Epub 2008 Jun 13.
Relationship between inflammation and cognitive function in obstructive sleep apnea.
Haensel A, Bardwell WA, Mills PJ, Loredo JS, Ancoli-Israel S, Morgan EE, Heaton RK, Dimsdale JE.
Source

Department of General Internal Medicine, University Hospital Berne, Berne, Switzerland.
Abstract
OBJECTIVES:

Obstructive sleep apnea (OSA) can have adverse effects on cognitive functioning, mood, and cardiovascular functioning. OSA brings with it disturbances in sleep architecture, oxygenation, sympathetic nervous system function, and inflammatory processes. It is not clear which of these mechanisms is linked to the decrease in cognitive functioning. This study examined the effect of inflammatory parameters on cognitive dysfunction.
MATERIALS AND METHODS:

Thirty-nine patients with untreated sleep apnea were evaluated by polysomnography and completed a battery of neuropsychological tests. After the first night of evaluation in the sleep laboratory, blood samples were taken for analysis of interleukin 6, tumor necrosis factor-alpha (TNF-alpha), and soluble TNF receptor 1 (sTNF-R1).
RESULTS:

sTNF-R1 significantly correlated with cognitive dysfunction. In hierarchical linear regression analysis, measures of obstructive sleep apnea severity explained 5.5% of the variance in cognitive dysfunction (n.s.). After including sTNF-R1, percentage of variance explained by the full model increased more than threefold to 19.6% (F = 2.84, df = 3, 36, p = 0.05). Only sTNF-R1 had a significant individual relationship with cognitive dysfunction ( = 0.376 t = 2.48, p = 0.02).
CONCLUSIONS:

sTNF-R1 as a marker of chronic inflammation may be associated with diminished neuropsychological functioning in patients with OSA.

PMID:
18551328
[PubMed – indexed for MEDLINE]
PMCID:
PMC3175694

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Predictors of fatigue in obstructive sleep apnea.

Posted on March 3, 2012 by Maurice Preter MD

Sleep Breath. 2008 Nov;12(4):397-9. Epub 2008 May 31.
Predictors of fatigue in obstructive sleep apnea.
Mills PJ, Kim JH, Bardwell W, Hong S, Dimsdale JE.
Source

Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA. pmills@ucsd.edu
Abstract
OBJECTIVE:

The objective of this study was to determine potential inflammatory predictors of fatigue in obstructive sleep apnea (OSA).
MATERIALS AND METHODS:

Fifty-six women and men untreated OSA patients had their sleep monitored with polysomnography. Fatigue was assessed by the Multidimensional Fatigue Symptom Inventory-Short Form. Depressed mood was assessed by the Center for Epidemiologic Studies-Depression Scale. Blood was drawn to assess circulating levels of Interleukin-6 (IL-6) and soluble tumor necrosis factor receptor I (sTNF-RI). Age, gender, body mass index (BMI), blood pressure, OSA severity, depressed mood, and inflammatory biomarkers were entered into a hierarchical multiple linear regression analysis predicting self-reported fatigue.
RESULTS:

Approximately 42% of the patients reported significant amounts of fatigue. Higher BMI (p = 0.014), greater depressed mood (p = 0.004), and higher sTNF-RI levels (p = 0.033) were independent predictors of fatigue in the final model (full model R2 = .571; p = .003). Age, gender, blood pressure and apnea severity were unrelated to fatigue.
CONCLUSION:

The findings suggest that in addition to depressed mood, fatigue in OSA may be associated with increased body weight and elevated levels of the proinflammatory cytokine receptor sTNF-RI. The findings support a linkage between the widely reported fatigue in OSA and a sleep-related component of inflammation.

PMID:
18516635
[PubMed – indexed for MEDLINE]
PMCID:
PMC2633300

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Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids.

Posted on March 3, 2012 by Maurice Preter MD

Altern Med Rev. 2007 Sep;12(3):207-27.
Omega-3 DHA and EPA for cognition, behavior, and mood: clinical findings and structural-functional synergies with cell membrane phospholipids.
Kidd PM.
Source

University of California, Berkeley, California, USA.
Abstract

The omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are orthomolecular, conditionally essential nutrients that enhance quality of life and lower the risk of premature death. They function exclusively via cell membranes, in which they are anchored by phospholipid molecules. DHA is proven essential to pre- and postnatal brain development, whereas EPA seems more influential on behavior and mood. Both DHA and EPA generate neuroprotective metabolites. In double-blind, randomized, controlled trials, DHA and EPA combinations have been shown to benefit attention deficit/hyperactivity disorder (AD/HD), autism, dyspraxia, dyslexia, and aggression. For the affective disorders, meta-analyses confirm benefits in major depressive disorder (MDD) and bipolar disorder, with promising results in schizophrenia and initial benefit for borderline personality disorder. Accelerated cognitive decline and mild cognitive impairment (MCI) correlate with lowered tissue levels of DHA/EPA, and supplementation has improved cognitive function. Huntington disease has responded to EPA. Omega-3 phospholipid supplements that combine DHA/EPA and phospholipids into the same molecule have shown marked promise in early clinical trials. Phosphatidylserine with DHA/EPA attached (Omega-3 PS) has been shown to alleviate AD/HD symptoms. Krill omega-3 phospholipids, containing mostly phosphatidylcholine (PC) with DHA/EPA attached, markedly outperformed conventional fish oil DHA/EPA triglycerides in double-blind trials for premenstrual syndrome/dysmenorrhea and for normalizing blood lipid profiles. Krill omega-3 phospholipids demonstrated anti-inflammatory activity, lowering C-reactive protein (CRP) levels in a double-blind trial. Utilizing DHA and EPA together with phospholipids and membrane antioxidants to achieve a triple cell membrane synergy may further diversify their currently wide range of clinical applications.

PMID:
18072818
[PubMed – indexed for MEDLINE]

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