An important finding?
This study is important, both because it was done as part of the International CFS Group that came up with the 2003 modified Fukuda definition, and because of its startling conclusion that everything from prolonged fatigue (more than one month) through chronic fatigue (6 months+) and CFS have the same types of symptoms - and probably the same underlying pathophysiology:
We suggest that this international study supports the proposition that chronic fatigue states [prolonged fatigue, chronic fatigue and CFS] share a common and stereotyped set of symptom domains, and that these can be readily identified in the community and at all levels of health care. Consequently, it is likely that they share common risk factors, are underpinned by a common pathophysiology, and may respond to common treatment strategies.
The authors don't report the evidence needed to back up their argument
The study used Factor Analysis, a statistical technique that tries to find underlying but hidden commonalities between variables, in this case symptoms. According to this study, the symptoms clustered into 5 factors common to all fatigue states:
musculoskeletal pain/fatigue, neurocognitive difficulties, inflammation, sleep disturbance/fatigue and mood disturbance
So you might imagine that they ran separate factor analyses on each of Prolonged Fatigue patients, Chronic Fatigue pateints and CFS patients - and found the same 5 factors in each case. But they didn't do this. Instead they analysed all 3 types of fatigue together - 88% of the total sample were prolonged fatigue cases and only 5% were CFS cases. Since almost all the cases were prolonged fatigue the only conclusions that can safely be drawn are those about prolonged fatigue. The study tells us nothing about the factors underlying CFS so the conclusion that CFS share the same 5 clusters of symptoms as other fatigue states is not supported by the evidence presented in this paper.
But maybe they did run the relevant analysis...
Interestingly, what appears to be an earlier version of this paper (by the same authors on the same dataset with much identical text) did include a separate analysis of CFS patients - and these patients had a different factor solution to that for the sample as a whole.
Finally, the 1,387 subjects specifically diagnosed as CFS in secondary/tertiary referral clinics were examined... In this sub-sample, the least satisfactory model was generated. It yielded four symptom factors that were less coherent than the factors in the earlier models, utilized 25 individual items and explained [only] 41% of the variance.
The first factor labelled as general physical health, was unique to this group of subjects. It included a large number of non-specific symptom items that had no outstanding clinical features and manifested diffuse item loadings. The other three factors were labelled similarly to those found in the broader community and healthcare settings. However, the mood disturbance factor included items such as headaches and chills or shivers as well as more typical items such nervous or tense / wound up? And look forward with enjoyment to things? - reflecting heterogeneity in the construct. Interestingly, although fatigue was notionally the central element of the clinical diagnoses, the most pertinent symptom items for fatigue (e.g. feeling tired after rest or relaxation or prolonged tiredness after activity) did not contribute to the factor solution. This suggests that although this group of subjects was drawn from the most homogeneous section of the healthcare system (specialized referral centres), they actually have varied illness experiences, which were not dominated by fatigue and were less uniform than in population and primary care settings.
Thanks to Dolphin for digging out this unpublished information.
So it appears that CFS does not have the same factor structure as other forms of fatigue, though this analysis has never been formally published.
The lack of a coherent factor structure ties in with an earlier paper by Hickie (which also contributed about half the patients used in the CFS-only analysis above) that concluded:
Criteria-based approaches to the diagnosis of [CFS] do not select a homogeneous patient group.
Also, the authors didn't evaluate more specific criteria
The other striking omisson in this study is that they didn't attempt to evaluate more specific criteria, or even (it appears) include Post Exertional Fatigue/Malaise as a symptom. Given that the main criticism of Fukuda is that it's too broad, and that they had accounted for less than half the variance with their own factor structure (which suggests there are better explanations they hadn't discovered), it's bizarre the authors go on to conclude that:
there is little to be gained by further reorganization of the diagnostic criteria
There are numerous other issues with the paper but I'm not sure it's worth going into the detail."
" The editorial claims that:
we previously demonstrated that chronic
fatigue states regardless of exactly how they are defined,
share a common and relatively stereotyped set
of symptom domains which can be readily identified
in the community, at all levels of health care, and
across cultures .
The sampe paper  also concludes:
"We also suggest thatthere is little to be gained by further reorganization of
the diagnostic criteria, or the related diagnostic entities."
24 Hickie I, Davenport T, Vernon SD et al. Are chronic fatigue and
chronic fatigue syndrome valid clinical entities across countries
andhealthcare settings?AustNZ JPsychiatry2009;43:2535.
However, it turns out that this paper doesn't include the relevant analysis to support these claims. Actually, it seems this analysis was done and included in an earlier draft of the paper, but the analysis contradicts the authors claims, which might explain why it was omitted from the final version.
The differential gene expression signature of Lyme disease following the acute phase of infection persisted for at least 3 weeks
No differential gene expression signature was observed between Lyme disease patients with resolved illness to those with persistent symptoms at 6 months post-treatment
We review recent findings suggesting that the success of the population-based approach is derived from the possibility of collecting much larger samples than in the clinic-based setting even at the risk of introducing phenotypic and genetic heterogeneity.
The most interesting part? People with the TRK mutation did not all have the same type of cancer. Some had sarcoma, while others had gastrointestinal stromal tumor cancer, salivary cancer, thyroid cancer, or non-small cell lung cancer. That means that, unlike most traditional cancer drugs, the medication didn't just work based on cancer type, but rather it worked on a genetic level.
Evolution has yielded multiple complex and complementary mechanisms to detect environmental danger and protect tissues from damage. The nervous system rapidly processes information and coordinates complex defense behaviors, and the immune system eliminates diverse threats by virtue of mobile, specialized cell populations. The two systems are tightly integrated, cooperating in local and systemic reflexes that restore homeostasis in response to tissue injury and infection. They further share a broad common language of cytokines, growth factors, and neuropeptides that enables bidirectional communication
Appreciating the immune and nervous systems as a holistic, coordinated defense system provides both new insights into inflammation and exciting opportunities for managing acute and chronic inflammatory diseases
A possible explanation for the negative results could be reduced power to detect an association based on diagnostic inaccuracy, because diagnoses were rendered based on questionnaires rather than the gold-standard of direct specialist–patient interviews. Another explanation offered by the authors is the heterogeneity of the population-based sample, with a less severe phenotype and consequently a lower genetic risk compared with patients seen in clinical practice.
. We recognise the need to update the Cochrane policy in respect of academic conflicts, and this process is in the pipeline – however current policy states that:
“Authors of primary studies should not extract data from their own study or studies. Instead, another author(s) or an editor(s) should extract these data, and check the interpretation against the study report and any available study registration details or protocol.
Also, the relevant authorship of the primary studies should be disclosed in Cochrane's disclosure of potential conflicts of interest form and therefore the Cochrane Review.”
We believe that our editorial processes also safeguard against reviews being unduly influenced by individuals with conflict of interest.
Coyne notes that the current review author team for the IPD review includes the trialists of the studies where individual patient data has been provided. This seems to be common practice in the world of individual patient data systematic reviews, although it is also important that all authors within a review team meet the requirements of the International Committee of Medical Journal Editors (ICMJE) in relation to authorshi
Professor Paul Glasziou has confirmed to me that the trialists involved in the review fully meet the ICMJE criteria for authorship, and that this is in line with standard practice - acknowledging the important role trialists can play in support of the IPD review to agree common methods and definitions to apply across all trials.
Cochrane is a strong supporter and founding member of the AllTrials initiative and is committed to clinical trials transparency. Cochrane does not believe that sharing data with its researchers is an appropriate rationale for withholding the data from alternative researchers.
Ioannadis may be correct that the primary purpose of evidence synthesis is to demonstrate the flaws in the available primary research. He may also be correct that in the future systematic reviews “should become primary research, where studies are designed with the explicit anticipation that they are part of an overarching planned cumulative meta-analysis.” However, in the meantime I believe that Cochrane Reviews characteristically present a more skeptical and balanced view of the evidence than is presented elsewhere, whether in primary or secondary research – something for which we receive much criticism from all the predictable quarters
In summary, Cochrane recognises the importance of conflict of interest as a potential source of bias in its reviews.
In relation to the CFS reviews, we are extremely aware of the heightened scrutiny that the IPD review will attract. We will therefore ensure that the author team is fully compliant with our conflict of interest policies, and ICMJE guidance on authorship, and that our editorial and peer review processes lead to the publication of a review that is robust and credible.
But as we move to wider data-sharing new questions arise. In particular, who should have access to the data? The simplest answer is everyone: the scientist could just put their data out there, and anyone and everyone could view it. In many areas, this is unproblematic, but some scientists have reservations about completely free access, even if they agree in principle with open data.
In some cases, there are concerns that data may be misused by people with conflicted interests or a specific ideological agenda.
A particular danger comes from unrestricted data-trawling of the kind that was evident in the CDC analysis. Although these dangers are especially serious when those doing the analysis are determined to find a particular result, they are not negligible when reputable and relatively open-minded scientists do secondary analyses.
Large datasets allow for analytic flexibility, and it is all too tempting to trawl a dataset for “significant” associations
An alternative is to require those analysing the data to specify in advance what analyses they plan to do – this is directly parallel to the idea of pre-registration of yet-to-be-done studies, which is beginning to gain traction in many areas of science as a way of improving reproducibility by distinguishing hypothesis-testing from exploratory analyses.
But how would we keep everyone honest? If we place restrictions on who has access to the data and what they do with it, we could end up with those who collected the data acting as gatekeepers. This runs the risk that if scientists themselves have conflict of interest or ideological agendas, they might deny access to others on spurious grounds.
The intermediary, who would be an expert in statistics and methods, would evaluate this, and if satisfied it was reasonable, would obtain the data from the originator, and conduct and make public the analysis
A scientist is part of what the Polish philosopher of science Ludwik Fleck called a “thought collective”: a group of people exchanging ideas in a mutually comprehensible idiom. The group, suggested Fleck, inevitably develops a mind of its own, as the individuals in it converge on a way of communicating, thinking and feeling.
This makes scientific inquiry prone to the eternal rules of human social life: deference to the charismatic, herding towards majority opinion, punishment for deviance, and intense discomfort with admitting to error. Of course, such tendencies are precisely what the scientific method was invented to correct for, and over the long run, it does a good job of it. In the long run, however, we’re all dead,
The UN’s Food and Agriculture Organisation, in a 2008 analysis of all studies of the low-fat diet, found “no probable or convincing evidence” that a high level of dietary fat causes heart disease or cancer.
Gary Taubes is a physicist by background. “In physics,” he told me, “You look for the anomalous result. Then you have something to explain. In nutrition, the game is to confirm what you and your predecessors have always believed.”
It’s difficult to square this theory with the dramatic rise in obesity since 1980, or with much other evidence. In America, average calorific intake increased by just a sixth over that period. In the UK, it actually fell. There has been no commensurate decline in physical activity, in either country – in the UK, exercise levels have increased over the last 20 years
Insulin-Carbohydrate” model of obesity. According to this model, an excess of refined carbohydrates interferes with the self-balancing equilibrium of the metabolic system.
The NIH study is the latest of more than 50 similar studies, which together suggest that low-carbohydrate diets are better than low-fat diets for achieving weight loss and controlling type 2 diabetes. As a body of evidence, it is far from conclusive, but it is as consistent as any in the literature.
Hi, I just fixed mine. The problem is with the little magnet on the filter. It is not strong enough to allow the unit to recognize that it is there. I placed a tiny but strong round flat magnet on top of the existing magnet. Put the filter back in, and Presto - it works perfectly!
Re: I have a dyson hand held that shuts off after just a...
- Level 1:
An expert who has achieved level 1.
- 1 Answer
Hi dc16 totaly agree its the magnet,but no need to strip or go soldering,look where pigk up is in the filter and you will see it flex's into housing so when vac on it pulls filter away,simply mark housing(the orange part)and pack with blue tac to stop filter pulling away from magnet regards steve
Posted on Oct 16, 201
DC16 was cutting out after less than 2 secs. Fixed with blue tac in seconds. Put tiny piece in hole in plastic filter housing. Works perfectly now.
Posted on Jan 25, 2015
Good solution, works a treat Steve.
I siliconed a piece of thin rubber on the same place.