eLetters

60 e-Letters

published between 2017 and 2020

  • Inconsistent referencing and underlying conclusion issues

    If it's not too late. The authors may wish to correct their referencing throughout the paper. I noticed that the 3rd paragraph in the Introduction provides references that do not support the statements made. e.g. the Biswas et al paper did NOT assess the impact of PROLONGED sitting. Evidence on bouts of sitting is still very unclear, and none of these interventions have shown is has a meaningful impact.

    It is also unclear how the authors can make their statement about 30 min/day being “likely to be clinically meaningful” – when it probably depends on what the sitting was replaced with (i.e. with standing vs. movement, etc) and the isotemporal substitution paper that is cited to support this assertion is based on a ‘theoretical’ shift of sitting to light activity from a cross sectional study (with risk of reverse causation). This seems to be selling a story that really isn't there.

    A more reasoned conclusion might be that VERY SMALL reductions in TOTAL sitting per day seem possible (a drop in the bucket?) with interventions that require significant resources (notably, not too dissimilar to PA interventions), but whether or not such shifts in sitting per se would make any meaningful difference for health outcomes/biomarkers remains very unclear. Not much good if there is no efficacy for outcomes. The reducing sitting story comes across as more of an hypothesis and 'feel good' story, but the evidence upon which it is based (in terms of effic...

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  • The Author of the Inflammation and Heart Disease Theory Cautions - Cholesterol and Saturated Fat are an Integral part of the Inflammatory process we call Coronary Artery Disease.

    In the mid-1990s, as one of the reviewers for the American Heart Association, the first author of this letter, Dr Richard M Fleming (RMF) introduced a then controversial theory stating that Coronary Artery Disease (CAD) is the result of an inflammatory process, which builds up within the walls of the arteries (Figure 1) impairing their ability to dilate and increase coronary blood flow when needed; thus producing regional blood flow differences resulting in angina [1-3] and ultimately myocardial infarction (MI) and death.
    In recent years, people promoting various dietary and lifestyle practices – particularly those promoting LowCarb-Keto diets, have taken advantage of the obesity epidemic and focused everyone’s attention on obesity and weight loss. These individuals have not determined the actual impact their diets have on CAD - which would require more than just looking at changes in weight or serum blood tests. It would require measurement of changes occurring within the walls of the coronary arteries themselves – not some other artery - and the resulting change in coronary artery function [1,4].
    These individuals, including Dr. Aseem Malhotra [5] support their dietary recommendations by showing weight loss, and occasionally reductions in cholesterol levels – at least initially in some people. Over the years as it has been shown that cholesterol levels fail to fall, and frequently increase on such diets, their argument has changed and has been replaced with “...

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  • On editorials, access and bias at the BJSM

    In May 2018, the following tweet was posted from the BJSM twitter account:

    '115K views. via brave iconocolast @DrAseemMalhotra. Importantly, no rebuttals. Real food saturated fat does not clog arteries - beware processed food that causes hyperinsulinemia (& hypertension). #Rethink'

    Followed by signposting to a linked editorial(1)

    Several people responded, including Catherine Collins (https://twitter.com/RD_Catherine/status/1001707243828596737), pointing out that a number of rebuttals to the editorial in question had in fact been made, not least a 2017 PubMed Commons/PubPeer commentary (https://pubpeer.com/publications/8741FBE4D9D7A38A7802515B33302E), which form the precursor of our rebuttal here. In response to Catherine, the BJSM Editor in Chief (EIC) Karim Khan contacted the lead author here indicating he had missed his email a year previous regarding our commentary originally offered to the BJSM as a formal rebuttal [see PubPeer post]. The EIC indicated he would be happy to publish our PubPeer rebuttal in the BJSM. The lead author thanked the EIC and, with co-authors Duane Mellor, Nicola Guess, and Ian Lahart, submitted a revised version in July 2018.

    In the interest of fairness and open debate, we made a request to the EIC and BJSM editorial board that our manuscript be made o...

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  • Gate control pain modulation theory explains the effectiveness of prolotherapy
    Stavros Saripanidis

    Dear Editors,

    The dorsal horns are not merely passive transmission stations but sites at which dynamic activities (inhibition, excitation and modulation) occur. [18]

    Via a series of filters and amplifiers, the nociceptive message is integrated and analysed in the cerebral cortex, with interconnections with various areas. [1]

    The processing of pain takes place in an integrated matrix throughout...

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  • What an odd piece.

    I was quite surprised to see this piece in a BMJ journal. It is quite odd and doesn't appear to bear much relationship to the data. If any readers are interested I strongly suggest that the read the original peer reviewed lancet PACE trial paper and make up their own minds.
    https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(11)60096-2/abstract

  • Drugs do not Level the Playing Field

    Here is my simple response to this absurd proposal. If drugs help those who are not as genetically advantaged to be more competitive with those who are, shall we prohibit the genetically advantaged from taking them? Otherwise, you create the situation where all athletes must take these drugs just to maintain the status quo. Athletes who prefer not to use drugs would suffer the most. Since drug use monitoring will be required anyway for safety, let's prohibit their use as much as possible. Allowing their use only benefits the pharmaceutical companies who sell the drugs. Sports would becomes less about athletic ability and more about who can come up with the best drug formula for competitive success.

  • Exercise-associated hyponatraemia and medication

    I had been a sufferer of exercise-associated hyponatraemia for at least a year, when I was living on a farm, as a direct result of drinking bore water. Unlike most bores which are overmineralized and dirty, these ones tapped into deep aquifers, that sourced ultra purified water. Because the water is trapped under deep layers of dolomites and Saprolites, the only way it can travel deeper into the earth is by passing through the micro pores of rocks, which results in micro filtration and ultra purification.

    But humans are adaptable to drinking pure water and pure water alone isn't going to make a normal person hyponatraemic, I had at one stage performing a labour intensive job as a tree surgeon. Also, because I have ADHD, I am medicated with adder-all.

    My situation was quite rare because I was living on a farm, drinking bore water and had a job pruning trees in residential areas, in the city. There, one would sweat heavily and would be drinking city water, which is one recipe for water that has a good mineral trace element content to it, but going home later that evening meant a diet of pure drinking water or cooking foods in pure water. This messed me up and affected my clear state of mind, often its a state of delirium that you start to feel as one of the typical symptoms.

    But then I also go back to the adder-all, which may have some role in making me vulnerable, because its an amphetamine and similar to the way ecstasy makes people become wate...

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  • The ACWR model presented in the IOC consensus is flawed and not validated

    The BJSM recently rejected our request of retraction or errata corrige of the editorials by Blanch and Gabbett(1) and Gabbett (2) presenting the relation between the Acute:Chronic Workload Ratio (ACWR) and likelihood of injuries. The preprint and a list of some of the errors presented in that figure can be found here: https://osf.io/preprints/sportrxiv/gs8yu/. In challenging our request, it was underlined several times by the Editor in Chief of BJSM that the “model” was presented as illustrative only, and this seems to make errors acceptable like if the editorials are a “safe zone” where for illustrative purposes it is possible to bend and even break scientific rules and methods, presenting models using unpublished and uncontrollable data.

    However, the reason of this communication is to warn the members of the consensus (and readers) that the ACWR model published in the IOC consensus(3) as a validated model has in fact not been validated at all: [page 1034] “The model has currently been validated through data from three different sports (Australian football, cricket and rugby league)(187)”. The reference 187 is one of the two editorials(1) for which we asked the retraction. So on one side the Editor in Chief insists that it is just an illustrative (flawed) model, but on the other side the same Editor in Chief, co-author (with one of the proponents of the model) of the IOC consensus wrote and published that it...

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  • Agreed.

    For readers who are following the debate about how training load may relate to injury, Dr Johann Windt considers the implication of the correlation that is pointed out here. Thanks to all the authors. k2

    https://bjsm.bmj.com/content/early/2018/05/28/bjsports-2017-098925

  • Letter to the editor

    After careful appraisal and following our own investigations, we are concerned that the article “Is interval training the magic bullet for fat loss? A systematic review and meta-analysis comparing moderate-intensity continuous training with high-intensity interval training (HIIT)” [1] may have some data extraction and analysis errors that warrant further review by the editor and authors, and which more concerningly, may impact the original conclusions of the article.

    We were initially concerned about the reported results within the Thomas et al. paper [2], particularly the biological plausibility of a mean between-group fat-loss difference of 13.44 kg over 12 weeks. Given that the authors did not report any study-level data, we decided to investigate the effect size within this paper. However, this study [2] did not report any fat mass data, only % body fat data. Given that the authors of the review [1] reported “When studies provided insufficient data for inclusion in the meta-analysis (five studies), the corresponding authors were contacted via email to determine whether additional data could be provided; however, no corresponding authors responded.”, it is unclear how an unpublished mean difference of -13.44 kg in favour of HIIT/SIT could be presented within the fat mass analysis of this review. Furthermore, when reviewing another of the included studies [3], we found that fat mass data were reported, but not included in the current meta-analysis [1]. Given the m...

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