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...
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 open access in line with the original editorial that was granted open access status by the EIC. The EIC informed us that the board decided to prioritise other articles for open access. We expressed our disappointment at the board’s decision and added a footnote to our article, the subject of which forms the content of this letter. The addition of our footnote was prohibited but we were invited to submit it for discussion as an e-letter in response to our own editorial.
At this point it is important to highlight the BMJ groups editorial process in relation to publishing articles that are free or open access (OA). The main difference between "free" and "open access" is the license the article is published under. For example, an article that is free to access would still require permission to be sought if someone wanted to reuse the content whereas an article that is published under the OA license would not require this.
Articles published under an OA license are indicated by an open padlock symbol and denotes that costs for publication and licensing of the article have been paid for by the authors, their institution(s) and or the funder if relevant. Articles published under the “free” license denote that costs have been waivered. We have been informed by the journal publisher that the EIC has control over decisions to grant articles with a free license.
The EIC can, therefore, choose which articles will be published under the “free” license. This subjectivity clearly presents a risk of bias if not managed appropriately. We feel it has become apparent that bias has entered this process within the BJSM. Here we provide evidence for this observation in relation to a particular narrative, one that finds an unexpected home in a sport and exercise journal, around dietary guidelines, a specific dietary approach, and statins.
The original editorial(1)—to which we provide a rebuttal—received a large amount of attention, both in the press and social media, partly because it was available free via the 'Editors choice' status granted by the EIC. It was and continues to be widely tweeted by the BJSM twitter account which is managed at least in part by the BJSM EIC. Key narratives of the editorial are the denigration of current dietary guidelines and the promotion of a low-carbohydrate, high-fat diet of which the editorial’s lead author is a well-known advocate.
In the past 3 years, the BJSM has also published 10 articles (https://docs.google.com/spreadsheets/d/1VaPB0Tl9RUrGntkWeaNwIX-CIK4Z6SaJ...) with a similar and related focus including criticism of current (and past) nutritional guidelines and the evidence base around dietary fat, dietary management of type 2 diabetes, physical activity for the management of obesity, and statins. The majority of these articles also promote a low-carbohydrate, high-fat diet and of these types of articles, all are authored by known advocates of this dietary approach. Some authors, including the author of the highlighted editorial, have published two or more of the 10 articles.
All 10 articles were published under the “free” license as granted by the EIC. They were also widely tweeted and retweeted by the BJSM twitter account and some have also been accompanied by podcasts and/or blogs with their respective author(s). Of these articles, only one(2) has had any formal rebuttal published in the BJSM in the form of three responses from different groups, including one from our group(3). None of the rebuttals were made available “free” by the editors, were tweeted only once by the BJSM account with no accompanying blog or podcasts. Therefore, there has not been an open and balanced discourse to any of the 10 articles at the time of their publication in the BJSM.
Finally, on the day our editorial was published Online First, there were no linked tweets from the BJSM account. However, there were several in relation to a BJSM podcast with the lead author of 3 of the 10 articles who makes a living from promoting low carb, high fat diets and dismissing any role of saturated fat in heart disease.
The EBM manifesto is a call to arms against to systematic bias, wastage, error, and fraud in research underpinning patient care(4). It points to the pivotal role of journal editors in safeguarding against communication of over-hyped, inaccurate or misinterpreted evidence. To make fair and informed judgements on the value and relevance of evidence, people must have access to it the manifesto stresses. We believe there is sufficient evidence of bias towards a specific narrative within the editorial group at the BJSM that impedes this important goal. The latest rebuttal is another in a familiar line of missed opportunities to redress this and reaffirms the importance of trustworthiness in key gate-keepers tasked with ensuring open and fair scientific, evidence-based discourse on diet and health.
1) Malhotra A, Redberg RF, Meier P. Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions. Br J Sports Med 2017;51:1111-1112. https://bjsm.bmj.com/content/51/15/1111
2) Malhotra A, Noakes T, Phinney S. It is time to bust the myth of physical inactivity and obesity: you cannot outrun a bad diet.Br J Sports Med 2015;49:967–968. https://bjsm.bmj.com/content/49/15/967
3) Mahtani KR, McManus J, Nunan D. Physical activity and obesity editorial: is exercise pointless or was it a pointless exercise? Br J Sports Med 2015;49:969-970. https://bjsm.bmj.com/content/49/15/969
4) Heneghan C, Mahtani KR, Goldacre B, Goldee F, Macdonald H, Jarvies D. Evidence based medicine manifesto for better healthcare. BMJ 2017;357:j2973. https://www.bmj.com/content/357/bmj.j2973
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...
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
the neuroaxis and occurs on at least three levels, at peripheral, spinal,
and supraspinal sites. [9]
Knowledge of the modalities of pain control is essential to correctly
adapt treatment strategies (drugs, neurostimulation, psycho-behavioural
therapy, etc.).
Dysfunction of pain control systems causes neuropathic pain. [1]
Spinal Cord Stimulation modalities evolved from the gate-control
theory postulating a spinal modulation of noxious inflow. [16] [2] [7]
[11] [12] [15] [17] [20] [22] [23] [24] [25] [26]
It has been demonstrated in multiple studies that dorsal horn
neuronal activity caused by peripheral noxious stimuli could be inhibited
by concomitant stimulation of the dorsal columns. [8]
Pain relief was more prominent at pain ascending through C fibers
than pain ascending through Adelta fibers. [21]
Many theories on the mechanism of action of Spinal Cord Stimulation
have been suggested, including activation of gate control mechanisms,
conductance blockade of the spinothalamic tracts, activation of
supraspinal mechanisms, blockade of supraspinal sympathetic mechanisms,
and activation or release of putative neuromodulators. [14]
At present, Spinal Cord Stimulation is a well established form of
treatment for failed back surgery syndrome, complex regional pain
syndromes (CRPS), low back pain with radiculopathy and refractory pain due
to ischemia. [4] [3] [8] [13]
Stimulation produced analgesia can provide a level of analgesia and
efficacy that is unattainable by other treatment modalities. [19]
Spinal Cord Stimulation for the treatment of chronic pain is cost-
effective when used in the context of a pain treatment continuum. [14]
Precise subcutaneous field stimulation is targeted to specific areas
of neuropathic pain. [6]
We aim at attenuation or blockade of pain through intervention at the
periphery, by activation of inhibitory processes that gate pain at the
spinal cord and brain. [9]
Segmental noxious stimulation produces a stronger analgesic effect
than segmental innocuous stimulation. [10]
That is exactly what intradermal sterile water injections do!
This therapeutic approach should not be limited only to elite
athletes.
It can work for every patient with back pain.
References
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Department of Physical and Rehabilitation Medicine, Linhartova 51, SI-1000
Ljubljana, Slovenia.
http://www.ncbi.nlm.nih.gov/pubmed/20042866
[3] Conf Proc IEEE Eng Med Biol Soc. 2009;2009:2033-6.
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Shrivastav M, Musley S.
Medtronic Neuromodulation, 7000 Central Ave NE, Minneapolis, Minnesota,
55432 USA.
http://www.ncbi.nlm.nih.gov/pubmed/19964771
[4] J Clin Monit Comput. 2009 Oct;23(5):333-9.
Spinal cord stimulation: principles of past, present and future practice:
a review.
Kunnumpurath S, Srinivasagopalan R, Vadivelu N.
St George's School of Anaesthesia, Tooting, London, UK.
http://www.ncbi.nlm.nih.gov/pubmed/19728120
[5] Brain Res Rev. 2009 Apr;60(1):149-70. Epub 2008 Dec 31.
Chloride regulation in the pain pathway.
Price TJ, Cervero F, Gold MS, Hammond DL, Prescott SA.
University of Arizona, Department of Pharmacology, USA.
[6] Curr Pain Headache Rep. 2008 Jan;12(1):28-31.
Peripheral nerve stimulation for chronic pain.
Henderson JM.
Stereotactic and Functional Neurosurgery, Stanford University School of
Medicine, 300 Pasteur Drive, Edwards Building/R-227, Stanford, CA 94305,
USA.
http://www.ncbi.nlm.nih.gov/pubmed/18417020
[7] Schmerz. 2007 Aug;21(4):307-10, 312-7.
From Descartes to fMRI. Pain theories and pain concepts.
Handwerker HO.
Institut fur Physiologie und Pathophysiologie, Universitat
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[8] Pain Physician. 2002 Apr;5(2):156-66.
Spinal cord stimulation.
Stojanovic MP, Abdi S.
Interventional Pain Program, MGH Pain Center, Department of Anesthesia and
Critical Care, Massachusetts General Hospital, Harvard Medical School,
Cambridge, MA 02135, USA.
http://www.ncbi.nlm.nih.gov/pubmed/16902666
[9] J Bone Joint Surg Am. 2006 Apr;88 Suppl 2:58-62.
Basic science of pain.
DeLeo JA.
Dartmouth-Hitchcock Medical Center, Dartmouth Medical School, Neuroscience
Center at Dartmouth, Department of Anesthesiology, Lebanon, NH 03756, USA.
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[10] Pain. 2005 May;115(1-2):152-60.
Segmental noxious versus innocuous electrical stimulation for chronic pain
relief and the effect of fading sensation during treatment.
Defrin R, Ariel E, Peretz C.
Department of Physical Therapy, School of Allied Health Professions,
Sackler Faculty of Medicine, Tel-Aviv University, 69978 Ramat Aviv,
Israel.
http://www.ncbi.nlm.nih.gov/pubmed/15836978
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Craig AD.
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[12] Sports Med. 2002;32(4):251-67.
Return-to-work interventions for low back pain: a descriptive review of
contents and concepts of working mechanisms.
Staal JB, Hlobil H, van Tulder MW, K?ke AJ, Smid T, van Mechelen W.
Department of Social Medicine and Research Centre on Work, Physical
Activity and Health, VU University Medical Center, Van der Boechorststraat
7, Amsterdam, The Netherlands.
http://www.ncbi.nlm.nih.gov/pubmed/11929354
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[14] Curr Rev Pain. 1999;3(6):419-426.
Spinal Cord Stimulation: Indications, Mechanism of Action, and Efficacy.
Krames E.
Pacific Pain Treatment Centers, 2000 Van Ness Avenue, Suite 402, San
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http://www.ncbi.nlm.nih.gov/pubmed/10998699
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Department of Clinical Neuroscience, Karolinska Institute, Stockholm,
Sweden.
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[17] Pain. 1999 Aug;Suppl 6:S149-52.
Regulation of spinal nociceptive processing: where we went when we
wandered onto the path marked by the gate.
Yaksh TL.
Department of Anesthesiology, University of California, San Diego, USA.
http://www.ncbi.nlm.nih.gov/pubmed/10491984
[18] Pain. 1999 Aug;Suppl 6:S121-6.
From the gate to the neuromatrix.
Melzack R.
Department of Psychology, McGill University, Montreal, Quebec, Canada.
http://www.ncbi.nlm.nih.gov/pubmed/10491980
[19] J Clin Neurophysiol. 1997 Jan;14(1):46-62.
Stimulation of the central and peripheral nervous system for the control
of pain.
Stanton-Hicks M, Salamon J.
Anaesthesia Pain Management Center, Cleveland Clinic Foundation, OH 44195,
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http://www.ncbi.nlm.nih.gov/pubmed/9013359
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An investigation of the gate control theory of pain using the experimental
pain stimulus of potassium iontophoresis.
Humphries SA, Johnson MH, Long NR.
Department of Psychology, Massey University, Palmerston North, New
Zealand.
http://www.ncbi.nlm.nih.gov/pubmed/8710448
[21] J Peripher Nerv Syst. 1996;1(3):189-98.
Pain relief by various kinds of interference stimulation applied to the
peripheral skin in humans: pain-related brain potentials following CO2
laser stimulation.
Kakigi R, Watanabe S.
Department of Integrative Physiology, National Institute for Physiological
Sciences, Okazaki, Japan.
http://www.ncbi.nlm.nih.gov/pubmed/10970109
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Davis P.
http://www.ncbi.nlm.nih.gov/pubmed/8398721
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pain.
Cambier J.
http://www.ncbi.nlm.nih.gov/pubmed/2620243
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Benabid AL, Henriksen SJ, McGinty JF, Bloom FE.
http://www.ncbi.nlm.nih.gov/pubmed/6652483
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http://www.ncbi.nlm.nih.gov/pubmed/441227
[26] GATE CONTROL OF ION FLUX IN AXONS.
GOLDMAN DE.
J Gen Physiol. 1965 May;48:SUPPL:75-7.
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
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.
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...
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 water intoxicated. One good article to that effect is "MDMA Impairs Response to Water Intake in Healthy Volunteers".
Yes, water intoxication is real. It's a possible danger that people should be aware of. That delirious state of mind isn't a pleasant
feeling. For me, drinking only city water is essential, I only need to drink half a litre of bore water, and following a 2 hour time period, a
sickness would occur. I've also come to realize bottled spring water from the shop had similar sickening results.
Medication makes you vulnerable to dilutional hyponatremia, heavy exercise plays a part, so its important to be aware of what liquids you're re hydrating yourself with, because not all water is the same, it has a mineral content that determines its tonicity, it comes in different formulas so to speak.
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...
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 was a validated model. There is something of great concern here. The publication of this figure in your consensus has given that model the credit it does not deserve. Other than not being validated, the errors in developing that figure are evident and I am sure the members can easily realize this by reading the original editorials proposing the model in the first place or by reading the problems in our request of retraction or errata. I believe that the consensus members gave too much credit to some participants involved in the consensus that proposed the model as validated. I further underline that the ACWR model you have presented also shows that if you taper before a competition or you complete a recovery week (i.e. you are outside the “sweet spot”), you are at higher risk of injuries. This is, unfortunately, an exemplificative “practical” translation of one part of the model you have contributed (unknowingly) to be popularized through including it in a consensus statement. The problem is that the metric (ACWR) is also deceptive and the members probably did not realize the meaning and hence interpretation of the ratio and figure. Furthermore, the ACWR-injury relation it is not established and in the literature various and contrasting relations can be found. Clearly more studies, hopefully with lower risk of bias, are needed. Therefore, since I value your contribution to better science and evidence-based recommendations, it would be appreciated to know whether at least the IOC panel will acknowledge and advise the reader the fact that the model has not been validated and potentially misleading.
References
1. Blanch P, Gabbett TJ. Has the athlete trained enough to return to play safely? The acute:chronic workload ratio permits clinicians to quantify a player's risk of subsequent injury. Br J Sports Med 2016;50(8):471-5. doi: 10.1136/bjsports-2015-095445
2. Gabbett TJ. The training-injury prevention paradox: should athletes be training smarter and harder? Br J Sports Med 2016;50(5):273-80. doi: 10.1136/bjsports-2015-095788
3. Soligard T, Schwellnus M, Alonso JM, et al. How much is too much? (Part 1) International Olympic Committee consensus statement on load in sport and risk of injury. Br J Sports Med 2016;50(17):1030-41. doi: 10.1136/bjsports-2016-096581
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
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...
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 marginal level of significance for the fat mass outcome in the review (MD, CI; -2.28, [-4.00, -0.56]), it is possible that if these data had been excluded/included the primary conclusion of this article (that HIIT training resulted in superior fat mass loss compared to moderate intensity aerobic training), may be altered.
Additionally, upon review of the first two data points in the % body fat plot, we also have concerns regarding the calculated effect sizes. We are unable to confirm the accuracy of the calculations, given the lack of study-level data reported and the absence of effect size (ES) calculation methods in either the review article methods or the registered protocol on PROSPERO (CRD42018089427). Whilst the Thomas et al. [2] paper reported % body fat data graphically, and we acknowledge there may be some minor differences in data points depending on which graph analysis tool was used, the Trapp et al. [3] paper reported all pre- and post- mean and standard error data, so our ES and CI calculations should be identical to those in the review if the same calculation method was used. However, our calculated ES using the pooled baseline SD for ES calculation (-3.30 [-13.36, 6.76]) varied significantly from that reported by the Viana et al (-9.59 [-16.97, -2.20]). Presuming that the authors are presenting mean difference data (as suggested in their forest plot figures), there should be no disputing this value as -3.30, based solely on study-level data. Our analyses only examined data from these two studies, so we can neither verify nor refute the results presented for the remaining 34 included studies.
Finally, we question the inclusion of one of the studies in the review. Viana et al. have included the study by Boer and Moss [4] that used 70-80% VO2peak for their moderate intensity exercise. This is outside the 40-60% VO2max ‘criteria’ for moderate intensity provided by the authors.
In conclusion, we have grave concerns about the accuracy of the data extraction and analysis, as well as study selection in the Viana et al review [1]. We would ask the editors therefore to request clarification and transparency in the methods used to derive the statistical comparisons presented in the published review. At minimum, a published correction of the article is needed, given the likelihood that this review will be highly cited by others who do not have the time or the statistical knowledge to question the findings. However, if the conclusions of the article are in fact driven by the errors in data extraction and analysis noted above, then full retraction may be indicated.
[1] Viana RB, Naves JPA, Coswig VS, et al 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) Br J Sports Med. Published Online First: 14 February 2019.
[2] Thomas TR, Adeniran SB, Etheridge GL. Effects of different running programs on VO2max, percent fat, and plasma lipids. Can J Appl Sport Sci 1984;9:55–62.
[3] Trapp EG, Chisholm DJ, Freund J, et al. The effects of high-intensity intermittent exercise training on fat loss and fasting insulin levels of young women. Int J Obes 2008;32:684–91.
[4] Boer PH , Moss SJ . Effect of continuous aerobic vs. interval training on selected anthropometrical, physiological and functional parameters of adults with Down syndrome. J Intellect Disabil Res 2016;60:322–34
We would like to thank you for your insightful and interesting comment.
Regarding the first point, we presented the 28.5% to illustrate the relative difference in total absolute fat (kg) change between interventions, so the reader could have information about the relative difference between groups. We would like to highlight that it was only possible to perform this analysis using the within group changes, since the change between group analysis was showed in absolute values.
About the second point, it was not our purpose to analyse lean body mass; however, we agree that this topic is very important for health and athletic performance purposes. This is an unanswered question and we are performing studies to test the effects of interval training on lean body mass to help shedding light in the topic.
In this article the authors discuss their analysis of 21 female and 22 male athletic events. Testing all 43, they find 3 events significant with p<0.05. When testing 43 events, the expectation is that a well-calibrated statistical test will produce 2 false positives with random data, on average, due to the definition of the p-value. The odds of producing 3 false positives are also rather high; for normally distributed simulated data under the null, I found 3 or more false positives approximately 1/3 of the time such an analysis is performed, see here for a simulation notebook: https://github.com/davidasiegel/False-Positive-Rate-for-Multiple-Tests-i....
This is why adjustments for multiple comparisons needs to be performed. It was neglected in their initial study and neglected again in this study. In the 2017 study they state, "These different athletic events were considered as distinct independent analyses and adjustment for multiple comparisons was not required." This doesn't make sense to me; if the analyses are distinct, then all the more reason to correct for multiple comparisons. If a Bonferroni correction were performed, none of the p-values would test significant at the level of the study (p<0.05/43 = 0.001). Therefore I do not see why there is any reason to reject the null hypothesis for any of these results.
In this article the authors discuss their analysis of 21 female and 22 male athletic events. Testing all 43, they find 3 events significant with p<0.05. When testing 43 events, the expectation is that a well-calibrated statistical test will produce 2 false positives with random data, on average, due to the definition of the p-value. The odds of producing 3 false positives are also rather high; for normally distributed simulated data under the null, I found 3 or more false positives approximately 1/3 of the time such an analysis is performed, see here for a simulation notebook: https://github.com/davidasiegel/False-Positive-Rate-for-Multiple-Tests-i....
This is why adjustments for multiple comparisons needs to be performed. It was neglected in their initial study and neglected again in this study. In the 2017 study they state, "These different athletic events were considered as distinct independent analyses and adjustment for multiple comparisons was not required." This doesn't make sense to me; if the analyses are distinct, then all the more reason to correct for multiple comparisons. If a Bonferroni correction were performed, none of the p-values would test significant at the level of the study (p<0.05/43 = 0.001). Therefore I do not see why there is any reason to reject the null hypothesis for any of these results.
Performing a series of tests and then re-testing the subset of events with the most significant results is also poor statistical practice that doesn't add meaning to the study.
In conclusion, taking into account the total number of tests that were performed (43), the results fail to be significant at the level of the study.
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...
Show MoreDear 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...
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
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.
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...
Show MoreThe 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...
Show MoreFor 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
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...
Show MoreDear Dr. Anoop Balachandran
We would like to thank you for your insightful and interesting comment.
Regarding the first point, we presented the 28.5% to illustrate the relative difference in total absolute fat (kg) change between interventions, so the reader could have information about the relative difference between groups. We would like to highlight that it was only possible to perform this analysis using the within group changes, since the change between group analysis was showed in absolute values.
About the second point, it was not our purpose to analyse lean body mass; however, we agree that this topic is very important for health and athletic performance purposes. This is an unanswered question and we are performing studies to test the effects of interval training on lean body mass to help shedding light in the topic.
Best regards.
In this article the authors discuss their analysis of 21 female and 22 male athletic events. Testing all 43, they find 3 events significant with p<0.05. When testing 43 events, the expectation is that a well-calibrated statistical test will produce 2 false positives with random data, on average, due to the definition of the p-value. The odds of producing 3 false positives are also rather high; for normally distributed simulated data under the null, I found 3 or more false positives approximately 1/3 of the time such an analysis is performed, see here for a simulation notebook: https://github.com/davidasiegel/False-Positive-Rate-for-Multiple-Tests-i....
This is why adjustments for multiple comparisons needs to be performed. It was neglected in their initial study and neglected again in this study. In the 2017 study they state, "These different athletic events were considered as distinct independent analyses and adjustment for multiple comparisons was not required." This doesn't make sense to me; if the analyses are distinct, then all the more reason to correct for multiple comparisons. If a Bonferroni correction were performed, none of the p-values would test significant at the level of the study (p<0.05/43 = 0.001). Therefore I do not see why there is any reason to reject the null hypothesis for any of these results.
Perfor...
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