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Displaying 1-10 letters out of 301 published

  1. The type of fat matters

    Dear Editor,

    I read with interest the narrative review by Timothy David Noakes and Johann Windt

    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 (LFHC) diets.

    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 size.(9, 10)

    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 Mediterranean Diet.(11)

    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 beneficial.

    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 is beneficial.(17,18)

    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 greater benefits.

    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)

    References

    (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. 2002;43:1363-1379

    (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 Organization, 2016.

    (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. 2002;132(4):715-8.

    (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. 2008;359(3):229-41.

    (12) Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in saturated fat intake for cardiovascular disease. Cochrane Database Syst Rev. 2015;6:CD011737.

    (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 medicine 2010;7(3):e1000252.

    (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- 1290.

    Conflict of Interest:

    None declared

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  2. Associations and causality

    Dear Editor,

    The article identifies "associations" between various sports and longevity. Associations do not deal with the issue of causality. Yet articles like this seem to imply that there is a causal relationship. I'm sure the authors would acknowledge that "correlation does not imply causation". Yet articles like this seem to imply that "yes, we know we haven't proved causality, but (nudge nudge, wink wink) we all know that really it is a causal relationship".

    There is far too much of this pseudo science about these days aided by the availability of large data stores and the tools to extract associations.

    Conflict of Interest:

    None declared

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  3. Greg Mirt

    Dear Editor,

    As for Fifa standards this is very lovely explained as well. The benefit of activity is in common interest of health professionals and the state.

    Conflict of Interest:

    Physiotherapy

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  4. Response to: "Does sports participation (including level of performance and previous injury) increase risk of osteoarthritis? A systematic review and meta-analysis"

    Dear Editor,

    We read with interest the systematic review by Tran and colleagues recently published online(1). The findings build on our own observations in a systematic review of running and knee osteoarthritis (OA)(2). Although the focus of our review was narrower than that of Tran et al, which investigated evidence relating to OA of all joints across a variety of sports, we would like to comment on some of the similarities and differences to our own observations.

    The findings of both reviews revealed the inconsistent design and often poor quality of studies in this area of research. Even focussing on one sport, as we did with running, we found that studies had used heterogeneous populations and methods, as well as differing criteria to define OA. Similarly, Tran et al identified this heterogeneity and rated the quality of the evidence as very low, echoing our own conclusions. This makes it especially difficult to interpret the evidence, not to mention the challenges that arise through using a broad range of exposure variables (different sports) and outcomes (different criteria for OA diagnosis in multiple joints). In contrast to Tran et al, we chose not to combine prospective studies in a meta-analysis: as well as having fewer eligible studies in our review (we included only knee OA), we felt the heterogeneity of the included studies did not allow meaningful combination of the results in a pooled estimate.

    Despite this divergence in methods, our narrative analysis of the evidence revealed similar results to that of Tran et al. We disagree, however, in the interpretation of these results. Tran et al conclude that the low-quality evidence supports a relationship between sport and OA in elite participants, but no association between running and OA. In contrast, we would interpret the results of both reviews as a lack of evidence of an association between running and OA, rather than evidence of no association. The poor quality of many of the studies, combined with a dearth of studies which control for important confounders (e.g. previous injury), does not fill us with confidence that the available literature is a reflection of the true relationship (if any) between running and OA.

    We should also like to mention some further interesting evidence from case-control studies that we included in our review. Our literature search found three case-control studies with knee replacement as an outcome(3-5), whereas Tran et al include only one of these(4) in their review. Interestingly, when combined in a meta-analysis, the pooled estimate of these studies suggested runners had almost 50% reduced odds of undergoing surgery due to knee OA. Although we hazard some possible explanations for this in our paper, we are mindful that any interpretation must be cautious, given the small number of retrospective and unadjusted studies. Furthermore, there was no cohort evidence to support this finding. Nevertheless, we feel this highlights the importance of taking into account the heterogeneity in study design and outcome definition. The apparent lack of association observed in prospective studies, none of which used surgery as a criterion for OA, may be masking a more complicated picture.

    We would like to thank the authors for their thorough review, contributing a broader picture of the evidence relating to sports and OA. Based on the conclusions of both reviews we would recommend the following. Firstly, we would like to endorse the authors' plea for further evidence from well-designed, prospective investigations, which appropriately consider the potential for confounding arising from sport type, intensity, and injury. Only then will we be able to evaluate whether there is in fact no association between sports (including running) and OA, as opposed to no evidence of an association. Secondly, there is a need for effective translation of knowledge from research (for example, in injury prevention) into clinical practice in order to support safe participation in sports at all levels and potentially reduce risk of disease onset. Finally, and perhaps most importantly, we recommend that, in the absence of strong evidence to the contrary, clinicians continue to promote sporting participation to the public, given the other well-established and varied benefits to health.

    References

    1. Tran G, Smith TO, Grice A, Kingsbury SR, McCrory P, Conaghan PG. (2016) Does sports participation (including level of performance and previous injury) increase risk of osteoarthritis? A systematic review and meta-analysis. BJSM. Retrieved from doi:10.1136/bjsports-2016-096142. Accessed Dec 9 2016.

    2. Timmins KA, Leech RD, Batt ME, Edwards KL. (2016) Running and knee osteoarthritis: a systematic review and meta-analysis. Am J Sports Med. Retrieved from doi:10.1177/0363546516657531. Accessed Dec 9 2016.

    3. Kohatsu N, Schurman D. (1990) Risk factors for the development of osteoarthritis of the knee. Clin Orthop Relat Res, 261:242-6.

    4. Sandmark H, Vingard E. (1999) Sports and risk for sever osteoarthritis of the knee. Scan J Med Sci Sports, 9:279-84.

    5. Manninen P, Riihimaki H, Heliovaara M, Suomalainen O. (2001) Physical exercise and risk of severe knee osteoarthritis requiring arthroplasty. Rheumatology, 40(4):432-7.

    Conflict of Interest:

    None declared

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  5. Oral Health Screening in Pre-Participation Medicals

    For over 40 years oral health screening is part of all pre- participation medical examinatios at the Portuguese Sports Medicine Centers in The National Institute of Sports. Preparticipation medicals are compulsory for all athletes who wish to play competitive sports and none gets full clearance without a full treatment of any oral/dental pathology. We are aware that oral health is fundamental to maintain sports performance and general health and this theme is part of the syllabus of our post-graduate Sports Medine courses.

    Conflict of Interest:

    None declared

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  6. This editorial is misleading

    Dear Editor,

    This editorial is misleading. Claiming that the Eatwell Guide is not evidence based is factually wrong. The Guide is based on comprehensive expert reviews of the evidence undertaken by the independent Scientific Advisory Committee on Nutrition (SACN) which advises government, and its predecessor, the Committee on Medical Aspects of Food Policy.

    The latest revisions to the Eatwell Guide were informed by SACN's 2015 evidence review on carbohydrates and health which included 600 recent research papers. The report halved the maximum sugar levels we should be consuming. It also recommended that we should eat more fibre from fruits, vegetables and pulses. Moreover, the Eatwell Guide's proposals are in line with the international evidence-base and recommendations of organisations such as the World Health Organization.

    Harcome blames the Eatwell Guide and its predecessors for the dramatic increases in obesity and diabetes which have occurred since the 1970s, based on highly tenuous correlations. She naively assumes that we as a population are meeting the current guidelines, when in fact survey data of nutrition intakes show the opposite to be true. For example, 87% of UK adults are eating too much sugar, 74% are failing to consume 5 portions of fruit and vegetables a day, 68% are eating too much salt and 66% are eating too much saturated fat.1

    The reason why levels of some diet-related diseases are on the rise is not because the guidelines are wrong. It is because our food environment is not supportive of healthy eating.

    This article is unhelpful because it will generate public and professional confusion, and undermine confidence in the government's evidence-based Eatwell Guide to healthy eating.

    References

    1. NatCen Social Research, MRC Human Nutrition Research & University College London Medical School, 2015a. National Diet and Nutrition Survey Years 1-4, 2008/09-2011/12. [data collection]. 7th Edition. UK

    Conflict of Interest:

    No financial or industry funding links to declare. Dr Mwatsama is a Registered Nutritionist (Public Health), and was a member of the Expert Reference Group which oversaw the review of Public Health England's Eatwell guidelines for healthy eating.

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  7. Two forward, one back in concussion

    Dear Editor,

    I commend Raftery et al in their recent editorial on concussion assessment in sport, in particular rugby's response on this matter (1). Undoubtedly one of the major issues facing sport is the lack of clarity and consistency in identifying concussions on the field; a symptom of the deficiencies in the last output from the Concussion in Sport Group (the 'Zurich Consensus')(2)

    However, while a commendable effort, on reading the article I am anxious about contradictions in the detail provided on World Rugby's protocol, which I believe are an oversight by the authors.

    Specifically, while clearly defining much needed indications for immediate and permanent removal from play ('Criteria Set 1'), the authors then suggest that these criteria confirm concussion 'unless proven otherwise'.

    The inclusion of the get out clause, 'unless proven otherwise', without qualification or expansion is, I believe, an error and does not reflect my understanding of rugby's HIA process. As it is written, Raftery et al are proposing that a player can sustain a blow to the head, be knocked unconscious or suffer a seizure or display tonic posturing or display any of the other Criteria 1 signs, but later might be 'cleared' of having sustained a brain injury via subjective post-match testing.

    The natural conclusion from this being a player can be KO'd on Saturday after a knee to the head, but apparently 'proven' not concussed in subsequent, after match and fallible tests and be back in training or play 2 days later.

    To my knowledge there are no tests that can unequivocally and confidently 'prove' a player is not concussed, as suggested. I would expect the authors are aware of that, and did not intend the draft to suggest a protocol that allows players with elements in Criteria Set 1 to be later cleared of brain injury in this way.

    Unfortunately, unless this is clarified, then there is a danger of promoting the false belief that a robust and infallible test is in current practice that can 'prove' a player has not sustained a brain injury despite being knocked unconscious after a blow to the head. The alternative is the current working definition of 'concussion' needs revisited.

    References

    1. Raftery et al. It is time to give concussion an operational definition: a 3-step process to diagnose (or rule out) concussion within 48 h of injury: World Rugby guideline. Br J Sports Med 2016;doi:10.1136/bjsports- 2016-095959

    2. McCrory P, Meeuwisse WH, Aubry M, et al. Consensus statement on concussion in sport: the 4th International Conference on Concussion in Sport held in Zurich, November 2012. Br J Sports Med 2013;47:250-8.

    Conflict of Interest:

    None declared

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  8. Efficacy versus effectiveness

    Dear Editor,

    As a rural and purely clinical sports medicine practitioner, I fully agree with the premise of this article. Whilst applauding the wonderful data being produced from around the world, so little of it has any relevance in my practice. There appears to be much back slapping happening in the research centres, though so little work on effectiveness of exercise regimes. I agree that the focus on rigorous methods excludes much community based research, and this limits the production of useful research in the real world. I have often been met with blank looks from researchers when asking them how an exercise intervention can be implemented in real world, and especially isolated, or socially disadvantaged settings. This article is one of the few I have read that endeavors to understand and explain the dichotomy.

    Conflict of Interest:

    None declared

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  9. Quantitative Assessment of Cognitive Molecules Supplementary to Doping Test

    Dear Editor,

    We have read the respective article, and we agreed to all stated observations and recommendations. This is a very useful article for many researchers and especially for the scientists working with addiction sciences.

    We would just like to emphasise on the use of quantitative assays for the cognitive molecules (Lee et al., 2009) beside doping test. Mental performance is the attribute of three different interconnected domains; namely, Memory, attention and creativity. Many of the neuro-circuits and different specific molecules, involved in such pathways have been reported in this modern era of technology. Millions of smart drugs or nootropic drugs have been reported targeting these specific molecules.

    We believe even though the doping test as per its principle is a general test available but at the same time, there is a need of looking at the molecular mechanisms which may vary from one individual to other and yes, if there is no effect on the cognitive molecules, then as per stated in the title, depending on the use of specific smart drug for targeting either memory or attention or creativity must have raised the said molecule and such molecules are needed to be quantified in the executives inclusive of the coaches in the team for a better understudying of the specific fraction of mental performance Vs doping test.

    Conflict of Interest:

    None declared

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  10. Time loss injuries compromise team success in Elite Rugby Union

    Dear Editor,

    Injury data from the RWC 2011, 89.1 per 1000 player-hours2011 and the earlier tournament of 2007, 83.9 per 1000 player-hours may have had an effect on all teams.

    But success could only be accorded to the winner in the final match. The All Blacks had a long history of not even making the semi-finals. However the RWC 2011 success was not due to the negative effect of injury on the team but rather on the individual team members,for instance the goal kicker. Other reasons may be due to the organisational arrangements by the coach and support of its management and the infrastructure of the national rugby. At the RWC 2015 success was clearly a cognitive achievement by all teams when they compare themselves with earlier RWC tournaments but did injury have an effect? Or was success due to organisational arrangements?

    References

    Fuller C.W et al.(2008) IRB Rugby World Cup 2007

    Fuller C.W et al.(2012) IRB Rugby World Cup 2011

    Conflict of Interest:

    None declared

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