Nijs is pretty much a mystery to me. Can't predict what he'll be saying next.
Chronic fatigue syndrome: lack of association between pain-related fear of movement and exercise capacity and disability.
Nijs J, Vanherberghen K, Duquet W, De Meirleir K.
Phys Ther. 2004 Aug;84(8):696-705
Still, there is currently no evidence that having “high fear” has any functional relevance in patients with CFS, especially given that fear of movement has not been shown to be related to either disability (as measured by the CFS-APQ) or exercise capacity in the types of patients we studied.
Conclusion: In a subgroup of patients with CFS, namely those who were experiencing widespread pain as defined by the 1990 American College of Rheumatology criteria for fibromyalgia,
26 measurements of pain-related fear of movement were neither correlated with exercise capacity data nor correlated with data obtained for activity limitations and participation restrictions. Future studies regarding these associations are needed in different subgroups of people with CFS or in a sample that is more likely to reflect people with CFS in general.
cf with:
Exercise performance and chronic pain in chronic fatigue syndrome: the role of pain catastrophizing.
Nijs J, Van de Putte K, Louckx F, Truijen S, De Meirleir K.
Pain Med. 2008 Nov;9(8):1164-72. Epub 2007 Oct 3.
CONCLUSIONS: These data provide evidence favoring a significant association between pain catastrophizing, bodily pain, exercise performance, and self-reported disability in female patients with CFS who experience widespread pain. Further prospective longitudinal studying of these variables is required.
How to explain central sensitization to patients with 'unexplained' chronic musculoskeletal pain: practice guidelines.
Nijs J, Paul van Wilgen C, Van Oosterwijck J, van Ittersum M, Meeus M.
Man Ther. 2011 Oct;16(5):413-8. Epub 2011 May 31.
Central sensitization provides an evidence-based explanation for many cases of 'unexplained' chronic musculoskeletal pain. Prior to commencing rehabilitation in such cases, it is crucial to change maladaptive illness perceptions, to alter maladaptive pain cognitions and to reconceptualise pain.
This can be accomplished by patient education about central sensitization and its role in chronic pain, a strategy known as pain physiology education. Pain physiology education is indicated when: 1) the clinical picture is characterized and dominated by central sensitization; and 2) maladaptive illness perceptions are present. Both are prerequisites for commencing pain physiology education.
Face-to-face sessions of pain physiology education, in conjunction with written educational material, are effective for changing pain cognitions and improving health status in patients with various chronic musculoskeletal pain disorders. These include patients with chronic low back pain, chronic whiplash, fibromyalgia and chronic fatigue syndrome.
cf with:
Intracellular immune dysfunction in myalgic encephalomyelitis/chronic fatigue syndrome: state of the art and therapeutic implications.
Nijs J, Frémont M.
Expert Opin Ther Targets. 2008 Mar;12(3):281-9. Review.
RESULTS/CONCLUSION: From the scientific literature it is concluded that proteolytic cleavage of the native RNase L enzyme is characteristic of the dysregulation of intracellular immunity in people with ME/CFS, but the origin of the dysregulation is speculative. There is increasing evidence for immune cell apoptosis and upregulation of various aspects of the 2'-5' oligoadenylate (2-5A) synthetase/RNase L pathway in ME/CFS. This review provides the theoretical rationale for conducting studies examining the effectiveness of direct or indirect drug targeting of the 2-5A synthetase/RNase L pathway in ME/CFS patients.
Disability evaluation in chronic fatigue syndrome: associations between exercise capacity and activity limitations/participation restrictions.
Nijs J, De Meirleir K, Wolfs S, Duquet W.
Clin Rehabil. 2004 Mar;18(2):139-48.
RESULTS: A statistically significant correlation between the score obtained with the CFS-APQ and the body weight-adjusted peak oxygen uptake (Spearman rho = -0.32; p = 0.005), functional aerobic impairment (rho = 0.33; p = 0.004), workload/body weight (rho = -0.30; p = 0.009), exercise duration (rho = -0.30; p = 0.008), and the percentage of target heart rate achieved (rho = -0.33; p = 0.004) was observed. The correlations between the remaining exercise capacity parameters and the scores obtained with the CFS-APQ all indicated a trend towards association (0.01 <p<0.05).
CONCLUSIONS: These results suggest a moderate association between exercise capacity and activity limitations/participation restrictions in patients with CFS. The observed correlations lack strength to predict activity limitations/ participation restriction based on exercise capacity parameters. Disability evaluation in CFS should therefore encompass both exercise capacity testing and measurements at the activity/participation dimension.
cf with "How to Exercise People with Chronic Fatigue Syndrome"
Immunological similarities between cancer and chronic fatigue syndrome: the common link to fatigue?
Meeus M, Mistiaen W, Lambrecht L,
Nijs J.
Anticancer Res. 2009 Nov;29(11):4717-26. Review.
Besides fatigue, certain aspects of immune dysfunctions appear to be present in both illnesses. In this regard, a literature review of overlapping immune dysfunctions in CFS and cancer is provided. Special emphasis is given to the relationship between immune dysfunctions and fatigue.
example para with annoying bits:
The cause may yet not be clear, but fatigue is the hallmark of CFS. Several hypotheses as to the cause of the fatigue have been proposed in the literature. Most rely on a biopsychosocial model with possible contributing factors such as neuroendocrine abnormalities, neuropsychological dysfunctions, autonomic dysregulations, environmental factors, psychological processes and personality traits, abnormal exercise response, overactive or passive lifestyle, infections and immune dysfunctions. Many reviews are available on these possible contributing or predisposing factors. But then again, CFS, with the hallmark fatigue, can only be diagnosed in the absence of a clear medical cause for the fatigue.
some interesting bits from the
full text
CFS patients. One of the major intracellular immune dysfunctions in CFS is the dysregulation of the RNase L antiviral pathway. .... By regulating viral and cellular RNA expression, RNase L plays an important role in the antiviral and antiproliferative activities of IFN and contributes to innate immunity and cell metabolism.
In consequence [of some cell biology stuff it discussed], the LMW RNase L fragments in CFS patients are responsible for the uncontrolled degradation of ribosomal and mitochondrial RNA, leading to apoptosis. Apoptosis triggers the production of elastase and calpain (
37), which are, in turn, considered to be responsible for the proteolytic cleavage of a number of structurally and functionally vital proteins, including the authentic RNase L (
35), leading to an apoptopic vicious circle (
37). In addition, the LMW RNase L may disturb proper ion flux through cell membranes by binding to the ion channels. The subsequent channelopathy causes inefficient ion transport, possibly leading to several of the CFS symptoms (
38).
Cancer patients. Besides antiviral activity, RNase L has been suggested to function as a tumour suppressor based on its roles in mediating apoptosis and antiproliferative activity of IFN (
40).
[which interferon?]
The R462Q variant of RNASEL, having about 3-fold reduced catalytic activity in vitro, is the most prevalent genetic marker for prostate cancer.
It remains to be seen if mutated
RNASEL predisposes to any other forms of cancer. Bartsch and colleagues (
46) showed that the
RNASEL R462Q variant might be associated with an increased risk for sporadic pancreas cancer and with more aggressive tumours in familial pancreatic cancer. Furthermore, the occurrence of elevated levels of RNase L seems to be an early event in colorectal tumourigenesis, suggesting that control of RNA turnover is an important step in tumour progression (
47).
CFS patients. NF-κB, as well as inducible nitric oxide synthetase and NO have been shown to be increased in CFS (
50-
52). The production of NF-κB is significantly correlated to the severity of illness and symptoms, such as fatigue and pain. These correlations suggest that the symptoms of CFS, such as fatigue, pain, muscular tension and depressive symptoms reflect a genuine inflammatory response in those patients (
50).
The produced NO, in turn, has an immunological function: it is cytotoxic by inhibiting the mitochondrial electron transport and the DNA synthesis and by influencing iron metabolism (important for the proliferation of viruses) (
49,
53). Excessive or persistent NO production as reported in CFS (
52), is, however, detrimental for physiological functions, as explained in earlier studies on intracellular immune dysfunctions in CFS (
34,
54,
55).
Cancer patients. Aberrant activation of NF-κB has been observed in many cancer types (
56-
58).
...
Based on the evidence describing the role of NF-κB, it is evident that NF-κB plays a pivotal role in suppression of apoptosis, promotion of cell proliferation and inflammation, and is closely associated with cancer development (
61).
Curiously, the low NK syndrome itself is characterized by an uncomfortable chronic fatigue, malaise and reduced interest in physical or mental activities. In addition, long-lasting low-grade fever is often reported and most of the sufferers are disabled or even bedridden. These symptoms are almost identical to those associated with CFS (
66). Observations suggest that individuals with chronically low NK activity may be genetically predisposed to the development of CFS (
65).
Cancer patients. Natural cytotoxic receptors (
e.g. NKp46, NKp44, NKp30) are displayed on the surface of NK cells and trigger NK cytotoxicity against tumour cells (
67). Tumour cells appear continuously, but in healthy people they are cleared by NK cells. This is accomplished by perforins, stored in the cytoplasm of NK cells and capable of destroying the cell membrane of tumour cells (
67). Alternatively, activated NK cells produce tumour necrosis factor α, which in turn initiates tumour cell apoptosis (
68).
In general, the level of NK activity is a stable individual trait, which fluctuates within a low, middle, or high normal range characteristic for each individual. Therefore it is not surprising that both CFS and cancer often occur in the same family (
65).
Physical activity (
i.e. aerobic exercise) is known to have positive effects on the number and cytotoxicity of natural killer cells in healthy humans (
78-
80), but this interaction is currently unexplored in people with cancer or CFS.
Finally, increased oxidative stress, apparent in CFS patients (as reviewed in
81) and also in cancer survivors due to the aftercare (
82), can reduce NK cytotoxicity (reviewed in
83) and cause fatigue (
82).
These authors hypothesize that the fatigue [of CFS] may be the consequence of a chronic inflammatory response due to reduced NK activity.
including chanellopathy, mitochondrial dysfunction, etc.
It is proposed that cancer-related symptom clusters, which include fatigue, share common cytokine-based neuroimmunological mechanisms. The review of Lee
et al. (
90) provides evidence for a correlation between the altered cytokine profile and cancer-related symptoms. The expression of coexisting symptoms such as fatigue could thus be linked to the dysregulated activity of NF-κB.
As presented in
Figure 1, there is already evidence for the relation between immune dysfunctions and fatigue in CFS, but in cancer this relation is far less understood.
characteristic solution proposed:
Since, for example, RNase L and NK cells may play a role in both the disabling fatigue and the protection of cancer patients against cancer reoccurrence, it would be important to target treatment approaches at improving functioning of these immune aspects.
Several pharmacological therapies could offer a solution, but rehabilitation might also be beneficial. Given the fact that appropriate amounts of physical activity have positive effects on the number and cytotoxicity of NK cells in both healthy humans (
72) and cancer patients (
91), sufficient physical activity could be an important item in rehabilitation, especially since both CFS and cancer patients seems to be rather passive (
92-
96). A lack of physical activity might not only predispose cancer patients to experience severe fatigue, it might even decrease NK cell functioning and hence make them prone to cancer reoccurrence (
97,
98). In addition, in CFS patients, light physical activity is associated with better well-being (unpublished data).
hahahahaha, being better is associated with being better! imagine that #tautology
In consequence, exercise is currently recommended as a conservative intervention for both fatigued cancer patients and CFS patients. However, with regard to these immunological abnormalities, prudence is called concerning exercise during the rehabilitation of these patients. Based on literature findings and our own results, we know that intracellular immune dysfunctions restrict exercise capacity, but also that too vigorous exercise may further worsen the immune system (
99,
100) and the complaints in CFS patients (
1). The exercise response to intensive activity in cancer patients is less understood. Several conditions during cancer treatment and recovery can preclude any physical activity,...
rather thin discussion on the risks of exercise in ME or CFS, but immunology is acknowledged