Relationship between musculoskeletal symptoms and blood markers of oxidative stress in patients with chronic fatigue syndrome

doi:10.1016/S0304-3940(02)01058-3

Neuroscience Letters

Volume 335, Issue 3, 2 January 2003, Pages 151-154

https://doi.org/10.1016/S0304-3940(02)01058-3 Get rights and content

Abstract

In 21 patients with chronic fatigue syndrome (CFS) versus 20 normal subjects, we investigated the oxidant/antioxidant balance and its correlation with muscle symptoms. Patients versus controls showed significantly: lower Lag Phase and Vitamin E (Vit E) concentrations in plasma and low-density lipoproteins (LDL), higher LDL thiobarbituric acid reactive substances (TBARS), higher fatigue and lower muscle pain thresholds to electrical stimulation. A significant direct linear correlation was found between fatigue and TBARS, thresholds and Lag Phase, thresholds and Vit E in plasma and LDL. A significant inverse linear correlation was found between fatigue and Lag Phase, fatigue and Vit E, thresholds and TBARS. Increased oxidative stress and decreased antioxidant defenses are related to the extent of symptomatology in CFS, suggesting that antioxidant supplementation might relieve muscle symptoms in the syndrome.

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Central sensitisation in chronic fatigue syndrome and fibromyalgia; a case control study
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However, there was no statistical difference between case groups for the thermal tests. A previous case-controlled study has shown that PPTs, including at non-painful locations, and pain thresholds to electrical stimulation of muscles but not skin, are reduced in people with CFS [32–34]. Reduced pain thresholds in FM have been demonstrated in response to pressure, heat [35,36], cold [37] and electrical [36,38] induced pain.
Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are both complex conditions that are challenging to treat. This may be related to an incomplete understanding of their pathophysiology, itself obfuscated by their heterogeneity. The symptomatic overlap between them and their common comorbidity suggests a shared vulnerability, which might be explained by central sensitisation.
19 CFS cases, 19 FM cases and 20 age and sex matched healthy controls (HC) were recruited primarily from secondary care clinics in London. Those with other pain disorders, psychiatric diagnoses and those taking centrally acting or opiate medications were excluded. Participants were asked to abstain from alcohol and over the counter analgaesia 48 h prior to assessment by static and dynamic quantitative sensory tests, including measures of temporal summation (TS) and conditioned pain modulation (CPM).
CS, as defined by the presence of both enhanced TS and inefficient CPM, was present in 16 (84%) CFS cases, 18 (95%) FM cases, and none of the HC (p < 0.001). Pressure pain thresholds were lower in CFS (Median222kPaIQR 146–311; p = 0.04) and FM cases (Median 189 kPa; IQR 129–272; p = 0.003) compared to HC (Median 311 kPa; IQR 245–377). FM cases differed from HC in cold-induced (FM = 22.6 °C (15.3–27.7) vs HC = 14.2 °C (9.0–20.5); p = 0.01) and heat-induced (FM = 38.0 °C (35.2–44.0) vs HC = 45.3 °C (40.1–46.8); p = 0.03) pain thresholds, where CFS cases did not.
Central sensitisation may be a common endophenotype in chronic fatigue syndrome and fibromyalgia. Further research should address whether central sensitisation is a cause or effect of these disorders.
Efficacy of Korean red ginseng (Panax ginseng) for middle-aged and moderate level of chronic fatigue patients: A randomized, double-blind, placebo-controlled trial
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Chronic fatigue (CF) is unexplained fatigue lasting more than 6 months. Korean red ginseng (KRG) is known to have higher anti-fatigue substance than white ginseng. However, its efficacy and safety for CF is unknown. The purpose of this study was to investigate the effect of KRG on CF by various measurements and objective indicators.
A randomized, double-blind, clinical trial was conducted on 50 patients with CF.
Participants were allocated to KRG or placebo group (1:1 ratio) and visited hospital every 2 weeks during taking 3 g KRG or placebo for 6 weeks and followed up 4 weeks after the treatment.
The primary outcome measurement was fatigue VAS. Secondary outcome measurements included FSS, CFSQ, SRI, scales of various fields (Depression: BDI; Sleep: ISI; Quality of life: EQ-5D 5 L), biochemical test (Antioxidants: d-ROMs, TBARS, BAP, and SOD; Cortisol concentration: salivary cortisol), blinding assessment, and adverse events.
The fatigue VAS declined significantly in each group, but there were no significant differences between the groups. The 2 groups also had no significant differences in the secondary outcome measurements and there were no adverse events. Sub-group analysis indicated that patients with initial fatigue VAS below 80 mm and older than 50 years had significantly greater reductions in the fatigue VAS if they used KRG rather than placebo.
By our study, KRG did not show absolute anti-fatigue effect but provided the objective evidence of fatigue-related measurement and the therapeutic potential for middle-aged individuals with moderate fatigue.
Role of mitochondrial dysfunction on rheumatic diseases
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Although the etiology of this disease is still unknown, recent studies have indicated the implication of oxidative stress, mitochondrial dysfunction and inflammation in the pathophysiology of FM [213,214]. For instance, different studies have observed increased oxidative stress and deregulated antioxidative parameters in patients with FM [37,213,215], events that have been associated with musculoskeletal manifestations like fatigue and pain [216]. Likewise, levels of altered lipid peroxidases were correlated with clinical symptoms and severity of FM [213].
Rheumatic and musculoskeletal diseases are a heterogeneous group of disorders affecting joint tissues and in some cases even organs, some of them being among the most common diseases worldwide. Mitochondria are the organelles considered as powerhouse of cells providing energy to the organism mainly through oxidative phosphorylation. However, mitochondria are also involved in crucial pathways responsible for maintaining cell physiology, such as the activation of metabolic and survival signaling, and innate and adaptive immune response. As consequence of the pivotal role of mitochondria in cell homeostasis, an impairment of mitochondrial function has been associated with activation of pathological events, including oxidative stress and subsequently damaged protein and DNA, deregulation of programmed cell death, and over-activation of inflammatory responses modulated by redox-sensitive signaling or direct activation of the inflammasome. Thus, a growing amount of evidence emphasizes the role of mitochondria in aging and inflammatory-related diseases, including rheumatic disorders. In this regard, emerging findings suggest that targeting of the pathways involved in the maintenance of mitochondrial metabolism may control cell homeostasis, and in turn delay ageing and prevent or improve articular pathologies. In this review we will focus on the importance of mitochondria in metabolic homeostasis of articular cells, as well as their influence on the activation of pathological signaling pathways, as a result of a genetic predisposition, damage, decline or impairment of their function. Finally, we will discuss some of the most important evidences of involvement of mitochondria in the onset and progression of rheumatic diseases.
Relationship Between Exercise-induced Oxidative Stress Changes and Parasympathetic Activity in Chronic Fatigue Syndrome: An Observational Study in Patients and Healthy Subjects
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Citation Excerpt :
However, oxidative stress may reasonably be proposed as one of the underlying mechanisms. Higher levels of oxidative stress have been reported in people with ME/CFS,23,24 and studies found that oxidative stress occurs earlier during exercise in people with ME/CFS compared to healthy controls.25,26 In addition, people with ME/CFS present a delayed antioxidant response following exercise.25,26
Oxidative stress has been proposed as a contributor to pain in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). During incremental exercise in patients with ME/CFS, oxidative stress enhances sooner and antioxidant response is delayed. We explored whether oxidative stress is associated with pain symptoms or pain changes following exercise, and the possible relationships between oxidative stress and parasympathetic vagal nerve activity in patients with ME/CFS versus healthy, inactive controls.
The present study reports secondary outcomes from a previous work. Data from 36 participants were studied (women with ME/CFS and healthy controls). Subjects performed a submaximal exercise test with continuous cardiorespiratory monitoring. Levels of thiobarbituric acid–reactive substances (TBARSs) were used as a measure of oxidative stress, and heart rate variability was used to assess vagal activity. Before and after the exercise, subjects were asked to rate their pain using a visual analogic scale.
Significant between-group differences in pain at both baseline and following exercise were found (both, P < 0.007). In healthy controls, pain was significantly improved following exercise (P = 0.002). No change in oxidative stress level after exercise was found. Significant correlation between TBARS levels and pain was found at baseline (r = 0.540; P = 0.021) and after exercise (r = 0.524; P = 0.024) in patients only. No significant correlation between TBARS and heart rate variability at baseline or following exercise was found in either group. However, a significant correlation was found between exercise-induced changes in HRV and TBARS in healthy controls (r = −0.720; P = 0.001).
Oxidative stress showed an association with pain symptoms in people with ME/CFS, but no exercise-induced changes in oxidative stress were found. In addition, the change in parasympathetic activity following exercise partially accounted for the change in oxidative stress in healthy controls. More research is required to further explore this link.
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Relationship between musculoskeletal symptoms and blood markers of oxidative stress in patients with chronic fatigue syndrome

Abstract

Free Radic. Biol. Med.

Pain

Neurosci. Lett.

Low density lipoprotein cholesterol, lipoprotein(a), and apo(a) isoforms in the elderly: relationship to fasting insulin

Assoc. Med. Sabin Nutr. Metab. Cardiovasc. Dis.

Measurement of pain

Effect of thyroid function on LDL oxidation

Arterioscler. Thromb. Vasc. Biol.

Continuous monitoring of in vitro oxidation of human low density lipoprotein

Free Radic. Res. Commun.

The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group

Ann. Intern. Med.