In their International Olympic Committee consensus statement, Maughan et al. reviewed the evidence for dietary supplements for high-performance athletes .
They wrote in regard to zinc that “Cochrane review shows benefit of [using] zinc acetate lozenges (75 mg) to decrease duration of URS [upper respiratory symptoms]” [1, Table 4]. This statement was based on their reading of the Cochrane review (2013) by Singh and Das , which was withdrawn in 2015 because of plagiarism . In addition, the same Cochrane review had a large number of other severe problems . In the above statement, Maughan et al. imply that only zinc acetate lozenges are effective; however, a recent meta-analysis showed that, up until 2017 at least, there was no evidence that zinc gluconate lozenges are less effective than zinc acetate lozenges .
When discussing treatment effects, the size of the effect and its confidence interval should be considered . Thereby a critically-minded reader can form his or her own opinion about whether the treatment effect is relevant. The data of 7 placebo-controlled double-blind RCTs showed that zinc acetate and zinc gluconate lozenges shortened common cold duration on average by 33% (95% CI 21% to 45%) . Individual-patient data were available for 3 zinc acetate lozenge trials and on the basis of these findings, zinc lozenges shortened the duration of colds by 2.7 days (95% CI 1.8 to 3.3 days) , and increased the rate of recovery by RR = 3....
When discussing treatment effects, the size of the effect and its confidence interval should be considered . Thereby a critically-minded reader can form his or her own opinion about whether the treatment effect is relevant. The data of 7 placebo-controlled double-blind RCTs showed that zinc acetate and zinc gluconate lozenges shortened common cold duration on average by 33% (95% CI 21% to 45%) . Individual-patient data were available for 3 zinc acetate lozenge trials and on the basis of these findings, zinc lozenges shortened the duration of colds by 2.7 days (95% CI 1.8 to 3.3 days) , and increased the rate of recovery by RR = 3.1 (95% CI 2.1 to 4.7) . So far, there is no published evidence to assume that the effects of zinc lozenges are less in athletes compared with the general population.
Maugham et al. wrote that many published studies had low quality, “specifically, small samples, poor controls and unclear procedures for randomization and blinding were commonplace” [1, p. 443]. To support this statement, they cited the above-mentioned Cochrane review  that was withdrawn in 2015 . However, that Cochrane review  did not point out any relevant methodological problems in the 7 placebo-controlled double-blind zinc lozenge RCTs mentioned above in which colds were shortened by 33% .
Furthermore, Maugham et al. did not mention at all the effect of vitamin C on exercise-induced bronchoconstriction [EIB]. Three double-blind placebo-controlled cross-over RCTs found that vitamin C decreased exercise-induced FEV1 decline by 48% (95% CI 33% to 64%) [9,10]. Only some athletes suffer from EIB, yet for them it may be worthwhile to test on an individual basis whether vitamin C has efficacy.
In our Cochrane review, we pooled 5 placebo-controlled double-blind RCTs on marathon runners, skiers and soldiers on subarctic exercises, and found that vitamin C reduced the risk of colds by 52% (95% CI 36% to 65%) . Maugham et al. opined that there is only “moderate support for preventing URS”. Given that the 5 RCTs conducted by 4 different research groups over 3 different decades found highly consistent results with I-square = 0% , it is quite puzzling as to what kind of evidence Maugham et al. would require to conclude strong support over and above any moderate support. Evidently, more research is needed. However, vitamin C is a cheap and safe essential nutrient, thus those athletes who often have upper respiratory symptoms associated with exercise may test whether the vitamin might be beneficial for them personally.
Maugham et al. further wrote that for vitamin C, “immune measures [are] no different from placebo” [1, Table 4]. This statement is misleading for readers. A search of the PubMed for reviews on vitamin C and immunity identifies dozens of reports. Reviews have shown that there is a large number of studies indicating that vitamin C does have effects on the immune system, three of which I cite here [12-14]. The published effects on the immune system do not indicate whether vitamin C has practical relevance, but it is misleading to claim that the effects of vitamin C on immune measures are no different from placebo .
Finally, Maugham et al. wrote that “Cochrane reviews show no benefit of initiating vitamin C supplementation (>200 mg/day) after onset of URS” and they cited refs 100,101 in their review [1, Table 4]. First, Maugham’s reference 101 is not a Cochrane review. Second, absence of evidence is not evidence of absence .
In our Cochrane review (ref. 100 in Maugham’s paper), we wrote that from a methodological perspective, therapeutic trials are much more complicated than regular supplementation trials . We gave examples of factors that may influence the efficacy of vitamin C, such as the timing of supplementation initiation, the duration of supplementation, and the dosage. Inappropriate selection of any of these factors might give rise to false negative findings in a therapeutic trial. We should therefore be cautious in the interpretation of the published therapeutic trials. Furthermore, we pointed out that “The larger effect observed using 8 g [of vitamin C] compared with 4 g as a single dose in the Anderson 1974f trial and the dose dependency in the Karlowski 1975a trial suggest that future therapeutic trials with adults should use doses of at least 8 g/day” ; see also .
It thus misleads readers to claim that our Cochrane review (ref. 100 in Maugham’s paper) “show[s] no benefit of initiating vitamin C supplementation after [the] onset of URS” . In contrast, we conclude in our abstract that “given the consistent effect of vitamin C on the duration and severity of colds in the regular supplementation studies, and the low cost and safety, it may be worthwhile for common cold patients to test on an individual basis whether therapeutic vitamin C is beneficial for them. Further therapeutic RCTs are warranted” .
I would like to raise some comments regarding the paper ‘Foot orthoses for plantar heel pain: a systematic review and meta-analysis.’ Whittaker et al, 2018, Br J Sports Med. 52(6): 322-328, and the editorial ‘Foot orthoses research: identifying limitations to improve translation to clinical knowledge and practice’, Griffiths & Spooner 52(6) in the same edition.
I would like to applaud the intention of the paper by Whittaker et al, to try and establish a conclusion to the question of foot orthoses efficiency in treating heel pain symptoms. This same praise I also give to the editorial in bring into the discussion the potential issue of the validity of random control trials as a research method to test foot orthoses efficiency. However, some key issues with the paper need exploring beyond the issues raised in the editorial in regarding how orthoses may work.
There are several key issues with the paper by Whittaker et al, which overall is a noble attempt to make sense of the present research on using orthoses for plantar heel pain. The issues are; plantar heel pain is a symptom not a diagnosis (therefore some of these studies may include multiple conditions); the studies are subject to potential bias (addresses by the authors); the studies do not compare like with like studies and seemed to have been shoe horned together to achieve a conclusion; and finally, foot orthoses do not logically conform to randomised control trials. Despite the best efforts of th...
There are several key issues with the paper by Whittaker et al, which overall is a noble attempt to make sense of the present research on using orthoses for plantar heel pain. The issues are; plantar heel pain is a symptom not a diagnosis (therefore some of these studies may include multiple conditions); the studies are subject to potential bias (addresses by the authors); the studies do not compare like with like studies and seemed to have been shoe horned together to achieve a conclusion; and finally, foot orthoses do not logically conform to randomised control trials. Despite the best efforts of the researchers to correlate the results to present a conclusion, reading the paper only shows that the paper was challenging statistically to produce. The studies so far published on this subject are so full of issues that any attempt to achieve coherence and a conclusion is potentially meaningless no matter how many attempts at statistical manipulation are thrown at the problem.
Despite this statistical need to achieve a result from poor data, the main problem must be that no attempt was given to provide the symptom of plantar heel pain a diagnosis in some of the studies involved in the review. This immediately invalidates the whole premise that these studies be included. We can hardly expect the same treatment to work for plantar fasciopathy, porta pedis nerve entrapment, Baxter’s neuroma or osteoarthritis of the subtalar joint. Each can cause plantar heel pain, but the mechanism of injury is different. Randomly sticking in insoles will give random results, perhaps the only conclusion we can take from these types of papers.
The editorial by Griffiths and Spooner discusses some of the issues in regards foot orthoses research used in random control trials. The authors of the editorial discuss the way the foot and the orthosis must interplay within the fundamentals of the laws of mechanics. These are principles of mechanics not unique to orthoses, but for anything that creates an interface between the foot and the ground. This is why a sham (placebo) orthosis in a study has potentially the same chance of influencing biomechanics as a so-called ‘real orthosis’. The difference in effects between the sham and the orthosis under test will be dependant on the difference between the shape and materials used in the two insole types.
The manufacture technique to produce the orthosis is probably irrelevant (22.214.171.124). Sadly some studies have failed to establish significant difference between insole types, picking a sham that is very close in design and material to the orthoses under test. Others studies pick custom orthoses of a much more robust design compared to the preform comparison orthosis (5.6). Bias is a serious problem in many studies.
The authors of the editorial claim that foot orthoses “can only exert their effect via placebo effect and/or directly modifying ground reaction forces at the foot-orthosis interface”. Kinematic and realignment effects are dismissed as “unlikely”. This statement is difficult to substantiate when compared to a wealth of published-research where much data on kinematic changes are reported (primarily in the foot) with foot orthoses (126.96.36.199.10.11.12). Similar kinematics changes occur when footwear and lack of footwear are compared (13.14).
Different kinematic effects have also been shown with different prescription additions on orthoses (15.16), which indicates how important individual prescription addition is to get a particular desired effect. However, data in regards to foot orthoses producing kinematic changes in sports related studies are less conclusive (17). This is likely to be in part because the contact time for the foot in running is reduced to around 40% (dependant on running pace) resulting in a significant float phase where neither foot is in ground contact. During float phase the orthosis has no mechanical influence except on increasing the foot segment mass in swing. Orthoses cannot redirect forces if there is no ground reaction force to interact with. Other issues such as preferred movement pathways (18) might over ride the effect of the orthosis or shoes especially in studies conducted on healthy asymptomatic runners.
The issue in sport is different to orthopaedics, in that most commonly in sportspeople, issues of mal-alignment and joint dysfunction are usually small. Sports medicine is largely about treating the ‘fit and well’, pushing their tissues to fatigue. In sport poor lower limb function or mal-alignment of a significant nature enough to significantly influence energetics, is rare. Such dysfunction would prevent a patient from being normally active. In orthopaedics serious postural mal-alignments that cause, or are a cause of dysfunction, are commonly found in patient contacts, and here changes with foot orthoses are likely to be more significant.
Griffiths & Spooner’s editorial proposes that the effects of orthoses are most likely to be due to kinetic changes within the tissues. This leads to the suggestion that for research, orthoses must be chosen that equally change the tissue stresses within specific tissues in different individuals, rather than picking the same prescription.
Sadly as we have no way of routinely assessing internal body kinetics within tissues dynamically, this suggested research pathway is not yet readily open to us. If possible, such an approach would also raise complications in that individual variance in morphology and body tissue composition would still make subject selection as well as prescription selection quite challenging. Orthoses requirements to achieve the same outcome could be quite different, unless subjects were match on many physiological and anatomical similarities. This would also make random control trials almost impossible.
There are other ways by which foot orthoses can be implied to change tissue kinetics. Changes in muscle activity in the presence of foot orthoses would imply that tissue kinetics has changed. Such evidence exists if not strongly (19), although evidence exists of rocker shoes altering muscle activity (20.21). As stated before orthoses and shoes work on the same interface.
Foot orthoses may also be able to initiate a neuro-mechanical effect. Something touching the body will create a reaction, possibly just in reaction to avoid the object as occurs when we feel a small stone in our shoe. What ever induces changes in muscle activity is likely to change kinematics, energetics as well as internal and external kinetics.
Again it must be understood that a so-called ‘sham orthosis’ has the potential to alter biomechanics and energetics. This single fact seriously questions whether random control trials using a so-called ‘sham orthosis’ are suitable for testing so called ‘real foot orthosis’ efficiency.
Another consideration is that poor biomechanics is primarily more than just forces being applied to the body in the wrong direction. Joint and muscle dysfunction are intrinsically linked. As a consequence, outside of the research world, foot orthoses are rarely used in isolation. If exercises, mobilisation, manipulation, shoe selection and foot orthoses all produce statistically arguable benefit when studied individually, there might yet be a significant effect when each are combined appropriately together. There is a challenge for research to look at treatment protocols rather than one treatment at a time!
Where the possibility of merely a placebo effect achieved by foot orthoses can firmly be challenged is in papers like Halstead et al (22), which looks at changes in pathology over time with foot orthoses on MRI and is the kind of randomised control trial that is more suitable for foot orthoses. More of these studies on diagnostic image changes produced by foot orthoses are required if we are ever going to learn more specifically which prescription variances are required to reduce stress and therefore strain on specific musculoskeletal tissues and their pathologies. Whether the outcome is good or bad, will still give us a far greater insight into the orthoses ability to change tissue stresses.
The reason good foot orthoses research is limited is more a result of most studies not knowing what effects they wished achieve to resolve particular pathologies. Especially so in studies where symptoms, rather than pathology is chosen. These ‘chosen’ pathologies need to be very specific, for in just the case of Achilles tendinopathy the mechanical causes are multiple, and specific areas within the tendon function differently (23.24.25).
To compare effects of a foot orthosis prescription in a manner similar to a random control trial of a pharmaceutical would need a large scale study performed on subjects of similar mass, strength, tissue age, morphology, and limb segment lengths. Subjects would need to have the same pathology and mechanism of injury with the same level of tissue damage. I would also suggest that treatment orthoses were tested for effects on energetics too to test comparable effects on mechanical efficiency. Any other type of random control study risk being like testing a drug for its effect on abdominal pain, regardless of the cause. Sadly most foot orthoses studies published at present make establishing truth within them extremely difficult and the construction of coherent random control reviews almost impossible.
1. Landorf K, Keenan AM, Herbert R. Effectiveness of foot orthoses to treat plantar fasciitis: a randomized trial. Arch Intern Med. 2006. 166:1305-10. doi: https://doi.org/10.1001/archinte.166.12.1305
2. Davis I, Zifchock R, Deleo A. A comparison of rearfoot motion control and comfort between custom and semicustom foot orthotic devices. J Am Podiatr Med Assoc. 2008. 98(5):394-403. PMID:18820043
3. Redmond A, Landorf K, Keenan AM. Contoured, prefabricated foot orthoses demonstrate comparable mechanical properties to contoured, customised foot orthoses: a plantar pressure study. J Foot Ankle Res 2009. 2:20. doi: https://doi.org/10.1186/1757-1146-2-20
4. Short L, Chockalingam N. Kinematic comparison of functional foot orthoses produced to three different manufacturing protocols: An exploratory study. OA Musculoskeletal Medicine 2015 10;2(2):14.
5. Trotter, L, Pierrynowski, M. The short-term effectiveness of full-contact custom-made foot orthoses and prefabricated shoe insets on lower-extremity musculoskeletal pain. J Am Podiatr Med Assoc. 2008. 98(5): 357-363. PMID:18820037
6. Trotter, L.C., Pierrynowski, M.R. (c). Changes in gait economy between full-contact custom-made foot orthoses and prefabricated inserts in patients with musculoskeletal pain. J Am Podiatr Med Assoc. 2008. 98(6): 429-435. PMID:19017850
7. McPoil TG, Cornwall MW. The effect of foot orthoses on transverse tibial rotation during walking. J Am Podiatr Med Assoc. 2000. 90(1): 2-11. doi: https://doi.org/10.7547/87507315-90-1-2
8. Reed L, Bennett P. Changes in foot function with the use of Root and Blake Orthoses. J Am Podiatr Med Assoc. 2001 91(4):184-193. PMID:11319248
9. Branthwaite HR, Payton CJ, Chockalingam N. The effect of simple insoles on three-dimensional foot motion during normal walking. Clin Biomech. 2004. 19(9):972-977. doi: https://doi.org/10.1016/j.clinbiomech.2004.06.009
10. Eslami M, Begon M, Hinse S, et al. Effect of foot orthoses on magnitude and timing of rearfoot and tibial motions, ground reaction force and knee moments during running. J Scien Med Sport. 2009. 12(6): 679-684. doi: https://doi.org/10.1016/j.jsams.2008.05.001
11. Levinger P, Menz H, Marrow A, et al. Relationship between foot function and medial knee joint loading in people with medial compartment knee osteoarthritis. J Foot Ankle Res. 2013. 6:33 http://www.jfootanleres.com/content/6/1/33
12. Rodrigues P, Chang, R, TenBroek T, et al. Medially posted insoles consistently influence foot pronation in runners with and without anterior knee pain. Gait Posture. 37(4):526-531. https://doi.org/10.1016/j.gaitpost.2012.09.027
13. Divert C, Mornieux G, Baur H, et al. Mechanical comparison of barefoot and shod running. Int J Sports Med 2005. 26(7): 593-598. doi
14. Eslami M, Begon M, Farahpour, et al. Forefoot-rearfoot coupling patterns and tibial internal rotation during stance phase of barefoot versus shod running. Clin Biomech 2007. 22(1): 74-80. doi: https://doi.org/10.1016/j.clinbiomech.2006.08.002
15. Nakajima K, Kakihana W, Nakagawa T, Mitomi H, et al. Addition of an arch support improves the biomechanical effect of a laterally wedged insole. Gait Posture. 2009. 29(2): 208-213. doi: https://doi.org/10.1016/j.gaitpost.2008.08.007
16. Zhang X, Li B, Hu K, et al. Adding an arch support to a heel lift improves stability and comfort during gait. Gait Posture. 2017 58(1): 94-97. doi: https://doi.org/10.1016/j.gaitpost.2017.07.110
17. Ferber R, Davis IM, Williams DS. Effect of foot orthotics on rearfoot and tibial coupling patterns and variability. J Biomech. 38(3): 477-483.
18. Nigg B, Baltich J, Hoerzer S, et al. Running shoes and running injuries: mythbusting and a proposal for two new paradigms:’preferred movement path’ and ‘comfort filter’. Br J Sports Med. 2015 49(20): 1290-1294. doi: https://doi.org/10.1136/bjsports-2015-095054
19. Murley G, Landorf K, Menz H et al. Effect of foot posture, foot orthoses and footwear on lower limb muscle activity during walking and running: A systematic review. Gait Posture 2009. 29(2): 172-187. doi: https://doi.org/10.1016/j.gaitpost.2008.08.015
20. Stöggl T, Müller E. Magnitude and ariation in muscle activity and kinematics during walking before and after a 10-week adaption period using unstable (MBT) shoes. Footwear Scienc. 2012: 4(2): 131-143.
21. Maffiuletti N. Increased lower limb muscle activity induced by wearing MBT shoes: physiological benefits and potential concerns. Footwear Scienc. 2012: 4(2): 123-129.
22. Halstead J, Chapman G, Gray J et al. Foot orthoses in the treatment of symptomatic midfoot osteoarthritis using clinical and biomechanical outcomes: a randomised feasibility study. Clin Rheumatol. 2016. 35(4): 987-996. doi: https://doi.org/10.1007/s10067-015-2946-6
23. Zifchock, R, Piazza, S. Investigation of the validity of modelling the Achilles tendon as having a single insertion site. Clin Biomech. 2004. 19 (3): 303-307. doi: https://doi.org/10.1016/j.clinbiomech.2003.11.010
24. Lee, S, Piazza, S. Inversion-eversion moment arms of gastrocnemius and tibialis anterior measures in vivo. J Biomech. 2008. 41(16): 3366-3370. doi: https://doi.org/10.1016/j.jbiomech.2008.09.029
25. Franz J, Slane L, Rasske K, et al. Non-uniform in vivo deformations of the human Achilles tendon during walking. Gait Posture. 2015. 41(2):192-197. doi: https://doi.org/10.1016/j.gaitpost.2014.10.001
Response to: We need to talk about manels: the problem of implicit gender bias in sport and exercise medicine
A recent editorial in the British Journal of Sports Medicine asserted that the presence of implicit bias in Sport and Exercise Medicine (SEM) is negatively affecting women in the field.1 We are concerned with the editorial’s lack of scientific approach, poor standard of evidence, and exclusion of important facts.
The editorial argued implicit bias results in pronounced real-world effects in the form of gendered differences in SEM and society as a whole. However, no substantial scientific evidence of the magnitude of implicit bias’s real-world consequences on gender differences was presented. Instead, circular reasoning was utilized as implicit bias was assumed to manifest the gendered differences present in the SEM field and society.
Implicit bias has been criticised within its field of psychology. A recent meta-analysis found little evidence that measurements of implicit bias are associated with any real-world manifestations of explicit bias or behaviour.2 Indeed, Patrick Forscher, one of the study’s authors implied in an interview that implicit bias’ use in policy making could be wasteful and even harmful.3
Research suggests gender has an influence on personality, career preferences, and priorities.4 Indeed, where more freedom is allowed, the greater the disparity in traditionally gendered sectors.5 Extrapolation of thes...
Research suggests gender has an influence on personality, career preferences, and priorities.4 Indeed, where more freedom is allowed, the greater the disparity in traditionally gendered sectors.5 Extrapolation of these basic biological and social facts indicate the potential for gendered differences in roles (e.g. serving on a panel) to be a result of situations arising from free choice. These are very important points to consider when discussing discrepancies between genders, yet were not mentioned in the editorial.
The argument above is of course not for absolute biological determinism, nor that sexism does not exist. Recognizing the fact that there are differences between women and men does not mean equity between genders cannot exist. However, valid evidence should take precedence over ideological narratives. Any statements on this topic should be made with caution as to avoid promoting unnecessary interventions.
The authors of the editorial are free to critically examine the evidence presented opposing their conclusions. However, the editorial demonstrated a low standard of evidence. For this conversation to move forward a higher standard of evidence should be sought and adhered to.
In conclusion, the authors of the editorial failed to meet the necessary burden of proof to claim that implicit bias is a primary cause for the complex phenomenon of gender discrepancies in SEM or society. As such, the likelihood is high that the interventions cited within the editorial are unwarranted and unhelpful.
1. Bekker, S. et al. We need to talk about manels: the problem of implicit gender bias in sport and exercise medicine. British Journal of Sports Medicine bjsports–2018–099084–4 (2018). doi:10.1136/bjsports-2018-099084
2. Forscher, P. S. et al. A meta-analysis of change in implicit bias. PsyArXiv 1–68 (2017). doi:10.17605/OSF.IO/DV8TU
3. Goldhill, O. The world is relying on a flawed psychological test to fight racism. Quartz (2017). Available at: https://qz.com/1144504/the-world-is-relying-on-a-flawed-psychological-te.... (Accessed: 9 April 2018)
4. Su, R., Rounds, J. & Armstrong, P. I. Men and things, women and people: A meta-analysis of sex differences in interests. Psychological Bulletin 135, 859–884 (2009).
5. Stoet, G. & Geary, D. C. The gender-equality paradox in science, technology, engineering, and mathematics education. Psychol Sci 095679761774171–20 (2018). doi:10.1177/0956797617741719
Table 3: First supplement "Beta Alanine". This should read "Caffeine" as described in the text.
First, I'd like to thank you for your precious work, as I'm doing a research about kitesurfing injuries statistics.
As kitesurfing instructor, I'd like to tell that in picture n°2, I think the guy is intentionally doing a trick. The kite is flying high, pulling him up. As far as the kite pulls the rider above the center of gravity, put the upper body below that point (as in the picture) requires strength, control and intentionality.
In really dangerous situation (those that need the rider to use quick release safety system), you usually can see the kite low in the air in front of the rider (power zone) pulling hard and the rider's legs behind.
I don't want to say that the situation described in the picture couldn't be dangerous at all, but in this case it depends on factors you can't see in the picture (obstacles, beach, other people, maximum height of the jump...).
Again, thanks for your research work and thanks to people working on safety on the beaches and in kitesurfing.
Whilst plantar heel pain be a more appropriate term than plantar fasciitis the later is more diagnostic than plantar heel pain which is more symptomatic. It is suggested that the attachments to the os calcis ought to be termed plantar enthesopathy for instance plantar enthesitis
I thank Dr. Batacan et al. for their excellent meta-analysis “Effects of high-intensity interval training on cardiometabolic health” in the March 2017 issue of the British Journal of Sports Medicine . Even if the effects of high-intensity interval training (HIIT) on inflammation are still unclear, research in the coming years will hopefully prove more positive benefits. For example, two recent studies showed effects through a long-term HIIT (12 weeks or more) in the inflammatory profile of overweight/obese adults, such as decreased interleukin (IL) 6, and increased IL-10 concentrations [2, 3].
But regardless of the various health effects of HIIT, I think the following fact is also worth mentioning for consumers. Health is a motivation to start with regular exercise, but mostly no motive to stay in the long term. On a permanent and regular basis, sport is only practiced when factors such as pleasure and enjoyment are added to the movement. Therefore, I am especially pleased that even overweight/obese teenagers and adults feel HIIT for an enjoyable and time-efficient form of exercise, as several recent studies demonstrate [4-8].
To Dr. Batacan and colleagues: Very well written, correct results, and appropriate references. Congratulations!
1. Batacan RB Jr, Duncan MJ, Dalbo VJ, Tucker PS, Fenning AS. Effects of high-intensity interval training on cardiometabolic health: a systematic review and meta-analysis of inte...
1. Batacan RB Jr, Duncan MJ, Dalbo VJ, Tucker PS, Fenning AS. Effects of high-intensity interval training on cardiometabolic health: a systematic review and meta-analysis of intervention studies. Br J Sports Med 2017;51(6):494-503.
2. Steckling FM, Farinha JB, Santos DL, Bresciani G, Mortari JA, Stefanello ST, et al. High intensity interval training reduces the levels of serum inflammatory cytokine on women with metabolic syndrome. Exp Clin Endocrinol Diabetes 2016;124(10):597-601.
3. Gerosa-Neto J, Antunes BM, Campos EZ, Rodrigues J, Ferrari GD, Rosa Neto JC, et al. Impact of long-term high-intensity interval and moderate-intensity continuous training on subclinical inflammation in overweight/obese adults. J Exerc Rehabil 2016;12(6):575-580.
4. Lee S, Spector J, Reilly S. High-intensity interval training programme for obese youth (HIP4YOUTH): a pilot feasibility study. J Sports Sci 2017;35(18):1794-98.
5. Smith-Ryan AE. Enjoyment of high-intensity interval training in an overweight/obese cohort: a short report. Clin Physiol Funct Imaging 2017;37(1):89-93.
6. Kong Z, Fan X, Sun S, Song L, Shi Q, Nie J. Comparison of high-intensity interval training and moderate-to-vigorous continuous training for cardiometabolic health and exercise enjoyment in obese young women: a randomized controlled trial. PLoS One 2016;11(7):e0158589.
7. Martinez N, Kilpatrick MW, Salomon K, Jung ME, Little JP. Affective and enjoyment responses to high-intensity interval training in overweight-to-obese and insufficiently active adults. J Sport Exerc Psychol 2015;37(2):138-49.
8. Heinrich KM, Patel PM, O'Neal JL, Heinrich BS. High-intensity compared to moderate-intensity training for exercise initiation, enjoyment, adherence, and intentions: an intervention study. BMC Public Health 2014;14:789.
How soon after completion of the exercise regime were the cognitive measures taken, and what was the average length of the followup?
Saturated fat is an essential element in our diet. Our body uses saturated far for energy, hormone production, facilitating vitamin absorption and most importantly, for coating and padding to protect our cellular membranes and organs. In the last two decades, saturated fat has been demonised as the main culprit leading to fatty deposits in the coronary artery and causing heart attacks (myocardio-infarction) when the deposits block up the artery. The truth is that myocardio-infarction is not directly caused by deposition of saturated fat called ‘plaque’ in our coronary arteries. The main cause of myocardio-infarction is the rupture of the plaque . The main cause of rupture is inflammation [2-4]. There are many factors which will trigger an inflammation response in our body. These include: infection, stress, allergy, and injury…etc. Other genetic factors and social and environment factors also play an important role. I salute the authors of this paper for their strong spirit of science, identifying new evidence which challenges previous views. “The important thing is not to stop questioning. Curiosity has its own reason for existing”. - Albert Einstein As an epidemiologist, public health practitioner and an educator, I concur with the author’s suggestion of the non-pharmaceutical approach to maintain good health. This simple approach involves an easy short daily walking exercise and eating a good balanced diet with...
Saturated fat is an essential element in our diet. Our body uses saturated far for energy, hormone production, facilitating vitamin absorption and most importantly, for coating and padding to protect our cellular membranes and organs. In the last two decades, saturated fat has been demonised as the main culprit leading to fatty deposits in the coronary artery and causing heart attacks (myocardio-infarction) when the deposits block up the artery. The truth is that myocardio-infarction is not directly caused by deposition of saturated fat called ‘plaque’ in our coronary arteries. The main cause of myocardio-infarction is the rupture of the plaque . The main cause of rupture is inflammation [2-4]. There are many factors which will trigger an inflammation response in our body. These include: infection, stress, allergy, and injury…etc. Other genetic factors and social and environment factors also play an important role. I salute the authors of this paper for their strong spirit of science, identifying new evidence which challenges previous views. “The important thing is not to stop questioning. Curiosity has its own reason for existing”. - Albert Einstein As an epidemiologist, public health practitioner and an educator, I concur with the author’s suggestion of the non-pharmaceutical approach to maintain good health. This simple approach involves an easy short daily walking exercise and eating a good balanced diet with everything consumed in moderation.
1. Hansson , G.K. Inflammation, Atherosclerosis, and Coronary Artery Disease. New England Journal of Medicine, 2005;352(16):1685-1695.
2. Kovanen, P.T., M. Kaartinen, and T. Paavonen. Infiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction. Circulation, 1995:92(5):1084-1088.
3. van der Wal, A.C., et al. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation, 1994;89(1):36-44.
4. Moreno, P.R., et al. Macrophage infiltration in acute coronary syndromes. Implications for plaque rupture. Circulation, 1994; 90(2): 775-8.
I read with interest the narrative review by Timothy David Noakes and
However, the very name of this diet, 'low-carb, high-fat' can be
misleading, because it does not tell us which type(s) of fat such a diet
is high in. To the extent that low-carb, high-fat (LCHF) diets are low in
carbohydrates and high in monounsaturated and polyunsaturated fats (MUFAs
and PUFAs, respectively), p...
However, the very name of this diet, 'low-carb, high-fat' can be
misleading, because it does not tell us which type(s) of fat such a diet
is high in. To the extent that low-carb, high-fat (LCHF) diets are low in
carbohydrates and high in monounsaturated and polyunsaturated fats (MUFAs
and PUFAs, respectively), particularly Omega-3 PUFAs, I would broadly
agree with the statements made in the review.
However, the authors also note that such diets are usually high in
animal proteins, such as steak and other unprocessed animal meats, as well
as coconut oil, all of which tend to be high in saturated fats (SFAs), and
concerns should be raised about this.
For example, a 2016 meta-analysis of randomized control trials found
that low-carb diets resulted in an increase in LDL-cholesterol, which is,
as the authors of the meta-analysis indicate, an "important"
cardiovascular risk factor.(1)
The authors of this narrative review do have some responses to this.
Firstly, they argue that this ignores a shift from small, dense LDL
particles to large and buoyant ones. Yet, according to Berneis and Krauss,
"large LDL particles also can be associated with increased coronary
disease risk, particularly in the setting of normal or low triglyceride
levels."(2)That said, I accept that large LDL particles may be less
damaging than small, dense LDL particles.
The authors of this review also note other positive changes in risk
factors on LCHF diets, particularly when compared to low-fat, high-carb
This, however, ignores the fact that we could potentially achieve
improvement in all of the main cardiovascular risk factors, from HDL to
triglycerides to ApoB to LDL-C (and its subfractions). We can do this with
a diet that is relatively low in carbohydrates and saturated fat, but is
relatively high in MUFAs and PUFAs, particularly Omega-3 PUFAs.
Indeed, replacing saturated fats with MUFAs and PUFAs has, in
general, been shown to improve the total:HDL cholesterol ratio, considered
by many to be the best marker of heart disease. This replacement has also
been shown to lower ApoB concentrations.(3)
Furthermore, replacing saturated fats with two key PUFAs, alpha-
linolenic acid (ALA) and linoleic acid (LA) has been shown to produce a
statistically significant improvement in the triglyceride to HDL ratio,
while replacement of saturated fat with MUFAs produced a non-significant
improvement.(4) EPA and DHA, two other polyunsaturated fats, are also
known to produce a substantial decrease in triglycerides and an increase
in HDL, relative to carbohydrates.(5)
Confirming this are RCTs which demonstrate that low-carb diets which
are high in MUFAs and PUFAs and relatively low in saturated fat result in
favourable changes in cardiovascular risk factors, including weight loss.
In addition to many of the improvements that LCHF diets produce mentioned
in this narrative review, a 2008 intervention study looking at a ketogenic
Mediterranean Diet found decreases in LDL-C resulting from the diet.(6)
The EcoAtkins trial also found that, relative to a high-carbohydrate
vegetarian diet, a low-carbohydrate vegan diet produced improvements in
LDL-C, the total: HDL ratio and ApoB concentrations.(7)
Similarly, a high-GI diet high in MUFAs reduces the total:HDL-C ratio
relative to a high-GI diet high in saturated fat.(8)
Studies have also found that diets higher in PUFAs and/or MUFAs and
correspondingly lower in saturated fats favourably affect LDL particle
While the authors of this narrative review cite one trial suggesting
that a low-carb diet may even do better than a Mediterranean Diet, it is
important to note that people on the low-carb diet "were counseled to
choose vegetarian sources of fat and protein". Indeed, their total fat
intake increased to a greater extent than their saturated fat intake, as a
percentage of energy, and the numbers indicate that unsaturated fat intake
was increased to a greater extent than their saturated fat intake.
Furthermore, total fat as a percentage of energy was only 33% on the Med
Diet in that trial, significantly lower than the ~40% common in a
The authors of this narrative review claim that the benefits of
replacing saturated fats with PUFAs are "unproven", yet at least two meta-
analyses of RCTs have found that replacing them with PUFAs is beneficial
(12,13), and a meta-analysis of prospective cohort studies has found that
higher intake of the Omega-6 PUFA, linoleic acid, is beneficial.(14)
While concerns have been raised about Omega-6 PUFAs, due to possible
confounding by Omega-3 PUFAs in RCTs and prospective cohort studies (alpha
-linolenic acid in particular in the latter)(15), all this would show is
that replacing saturated fats with sources of PUFAs, as long as plant
and/or marine sources of Omega-3 PUFAs are specifically increased too, is
When plant sources of MUFAs were predominantly consumed, as in the
PREDIMED trial, prospective analysis found that replacing saturated fats
with MUFAs reduced the risk of cardiovascular disease.(16) Similarly, two
recent cohort studies have found that replacing saturated fats with MUFAs
In line with the mechanistic, observational and clinical evidence
cited above, an analysis of two cohorts in 2010 concluded that vegetable-
based low-carbohydrate diets were associated with lower CVD and all-cause
mortality risk, whereas animal-based low-carb diets were associated with
higher all-cause mortality risk.(19)
All in all, the evidence suggests that a Mediterranean-style diet
naturally low in saturated fat, sugar and refined carbohydrate, and
perhaps lower in whole-grains and unrefined carbohydrates than a
traditional Mediterranean diet, can not only produce the "unique" benefits
of a LCHF diet cited in this narrative review, but can produce even
This would be a diet rich in fruits, vegetables, healthy plant
proteins such as legumes and beans, and MUFAs and Omega-3 PUFAs, one or
both of which can be found in some plant oils (olive, canola, flaxseed),
nuts, seeds and oily fish. We now have two well-conducted RCTs examining
events (not just risk factors) demonstrating the substantial benefits of
this dietary pattern.(20, 21)
(1) Mansoor N, et al. Effects of low-carbohydrate diets v. low-fat
diets on body weight and cardiovascular risk factors: a meta-analysis of
randomised controlled trials. Br J Nutr. 2016;115(3): 466-79.
(2) Berneis KK, Krauss RM. Metabolic origins and clinical
significance of LDL heterogeneity. The Journal of Lipid Research.
(3) Mensink RP, et al. Effects of dietary fatty acids and
carbohydrates on the ratio of serum total to HDL cholesterol and on serum
lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J
Clin Nutr. 2003;77(5):1146-1155.
(4) Mensink RP. Effects of saturated fatty acids on serum lipids and
lipoproteins: a systematic review and regression analysis. World Health
(5) Harris WS. n-3 fatty acids and serum lipoproteins: human studies.
Am J Cln Nutr. 1997;65(5 Suppl):1645S-1654S.
(6) Perez-Guisado J, et al. Spanish Ketogenic Mediterranean Diet: a
healthy cardiovascular diet for weight loss. Nutr J. 2008;7:30.
(7) Jenkins DJ, et al. The effect of a plant-based low-carbohydrate
("Eco-Atkins") diet on body weight and blood lipid concentrations in
hyperlipidemic subjects. Arch Intern Med. 2009;169(11):1046-54.
(8) Jebb SA, Lovegrove JA, Griffin BA, et al. Effect of changing the
amount and type of fat and carbohydrate on insulin sensitivity and
cardiovascular risk: the RISCK (Reading, Imperial, Surrey, Cambridge, and
Kings) trial. Am J Cln Nutr. 2010;92(4):748-58.
(9) Kratz M, Gulbahce E, von Eckardstein A, Cullen P, Cignarella A,
Assmann G, Wahrburg U. Dietary mono- and polyunsaturated fatty acids
similarly affect LDL size in healthy men and women. J Nutr.
(10) Egert S, Kratz M, Kannenberg F, et al. Effects of high-fat and
low-fat diets rich in monounsaturated fatty acids on serum lipids, LDL
size and indices of lipid peroxidation in healthy non-obese men and women
when consumed under controlled conditions. Eur J Nutr. 2011;50(1):71-79.
(11) Shai I, et al. Weight-loss with a Low-Carbohydrate,
Mediterranean or Low-Fat Diet. New England Journal of Medicine.
(12) Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in
saturated fat intake for cardiovascular disease. Cochrane Database Syst
(13) Mozaffarian D, Micha R, Wallace S. Effects on coronary heart
disease of increasing polyunsaturated fat in place of saturated fat: a
systematic review and meta-analysis of randomized controlled trials. PLoS
(14) Farvid MS, Ding M, Pan A, et al. Dietary linoleic acid and risk
of coronary heart disease:a systematic review and meta-analysis of
prospective cohort studies. Circulation 2014;130:1568-78.
(15) Ramsden CE, et al. All PUFAs Are Not Created Equal: Absence of
CHD Benefit Specific to Linoleic Acid in Randomized Control Trials and
Prospective Observational Cohorts. World Rev Nutr Diet. 2011;102:30-43.
(16) Guasch-Ferre M, et al. Dietary fat intake and risk of
cardiovascular disease and all-cause mortality in a population at high
risk of cardiovascular disease. Am J Cln Nutr. 2015;102(6):1563-73.
(17) Li Y, et al. Saturated Fats Compared with Unsaturated Fats and
Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease: A
Prospective Cohort Study. J Am Coll Cardiol, 2015;66(14):1538-48.
(18) Wang DD, et al. Association of Specific Dietary Fats with Total
and Cause-Specific Mortality. JAMA Intern Med. 2016;176(8):1134-45.
(19) Fung TT, van Dam RM, Hankinson SE, Stampfer M, Willett WC, Hu
FB. Low-carbohydrate diets and all-cause and cause-specific mortality: two
cohort studies. Ann Intern Med. 2010;153(5):289-98.
(20) de Lorgeril M, et al. Mediterranean Diet, Traditional Risk
Factors, and the Rate of Cardiovascular Complications After Myocardial
Infarction. Circulation. 1999;99:779-785.
(21) Estruch R, et al. Primary Prevention of Cardiovascular Disease
with a Mediterranean Diet. New England Journal of Medicine. 2013;368:1279-