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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 [1]. 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 [1]. 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.
References
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
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), p...
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.
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...
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.
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 si...
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.
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...
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.
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 i...
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.
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)
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.
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
meth...
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.
How soon after completion of the exercise regime were the cognitive measures taken, and what was the average length of the followup?
Dear Editor,
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 [1]. 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...
Show MoreDear 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), p...
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...
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
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 si...
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...
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 i...
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 c...
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 meth...
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