With great interest we read the meta-analysis of Harcombe and co-
workers titled "Evidence from randomized controlled trials did not support
the introduction of dietary fat guidelines in 1977 and 1983: a systematic
review and meta-analysis" published in volume 2 of the Open Heart Journal
[1]. In their article, the authors systematically reviewed randomized
controlled trials investigating the associations between dietary fa...
With great interest we read the meta-analysis of Harcombe and co-
workers titled "Evidence from randomized controlled trials did not support
the introduction of dietary fat guidelines in 1977 and 1983: a systematic
review and meta-analysis" published in volume 2 of the Open Heart Journal
[1]. In their article, the authors systematically reviewed randomized
controlled trials investigating the associations between dietary fat,
serum cholesterol and the development of all-cause mortality and CHD
mortality. Harcombe and colleagues concluded that dietary recommendations
were introduced for 220 million US and 56 million UK citizens by 1983, in
the absence of supporting evidence from RCTs. Indeed, there has been a lot
of debate regarding the potential role of dietary fat in the pathogenesis
of CHD, with an intensive debate of the validity of the results [2-4].
In a recently published meta-analysis on dietary fatty acid in the
secondary prevention of coronary heart disease, we included overall 12
trials with 7150 patients (with five out of six RCTs similar to the ones
included by Harcombe and colleagues) [5]. After performing pairwise meta-
analyses as well as uni- and multivariate meta-regression we did not
observe any evidence for beneficial effects of reduced/modified fat diets
in the secondary prevention of coronary heart disease. Therefore, we
concluded that recommending higher intakes of polyunsaturated fatty acids
in replacement of saturated fatty acids was not associated with risk
reduction.
However, we think that some statements in the meta-analysis by Harcombe
and colleagues should be interpreted with caution and would like to
comment one some basic as well as some methodological issues. The authors
state that "RCTs provide the best evidence". RCTs in nutrition research
are often prone to inherent methodological constraints. E.g., they
sometimes cannot be controlled with "true" placebos, but rather by a
limitation of certain aspects of nutrient compositions, food groups or
dietary patterns. Other limitations include lack of double blinding, poor
compliance and adherence, crossover bias and drop-out. Thus, in the field
of nutritional epidemiology, well-designed prospective cohort studies will
provide important evidence as well [5 6]. Quality scales such as the PEDro
scale used by Harcombe et al. should be avoided. Instead, the Risk of bias
assessment tool should be given preference [7]. In addition, "double
counts" of the participants in the control group (as done with the study
by Rose et al., 1965) should be avoided. The authors neglect to comment on
the fact that in the Sydney Diet Heart Study a commercial margarine
probably high in trans fatty acids was used to deliver PUFA to the
intervention group [8]. A sensitivity analysis excluding this trial would
be highly appropriate. Moreover, the reductions in total cholesterol
observed in the low-fat group warrants further attention, since it is well
known that weight change might represent a potential confounder in the
interpretation of blood lipid levels [9].
Although systematic reviews and meta-analyses may help to merge and
ultimately enhance evidence based nutritional guidelines, some concerns
were expressed regarding the validity and application to nutrition and
nutritional sciences [10 11]. Although there are some limitations to
incorporate systematic reviews into nutrition research, there are strong
reasons to apply them as evidence based approaches for dietary guidelines.
First, scientific findings about 'what one should eat' is almost always
echoed by media coverage and therefore potentially models public opinion
about nutrition. Media coverage makes use of a reductionist and
sentimental approach to bring their story to the readers, which may
sometimes obscure actual findings of the study. Nutrition research has
been criticized on numerous occasions [12]. Systematic reviews and meta-
analysis can help to improve nutrition based dietary guidelines by
incorporating more homogenous dietary recommendations. However, one has to
keep in mind that systematic reviews are only as good as the studies they
pool together. Instead of creating some kind of "dietary fat-gate"
involving Senator George McGovern (again), Harcombe and co-workers should
be more conservative in their conclusions with regard to the limitations
of their own meta-analysis as well as the studies included in it.
References
1. Harcombe Z, Baker JS, Cooper SM, et al. Evidence from randomised
controlled trials did not support the introduction of dietary fat
guidelines in 1977 and 1983: a systematic review and meta-analysis. Open
Heart 2015;2(1) doi: 10.1136/openhrt-2014-000196[published Online First:
Epub Date]|.
2. Chowdhury R, Warnakula S, Kunutsor S, et al. Association of
dietary, circulating, and supplement fatty acids with coronary risk: a
systematic review and meta-analysis. Annals of internal medicine
2014;160(6):398-406 doi: 10.7326/M13-1788[published Online First: Epub
Date]|.
3. Willett WC, Stampfer MJ, Sacks FM. Association of dietary,
circulating, and supplement fatty acids with coronary risk. Annals of
internal medicine 2014;161(6):453 doi: 10.7326/L14-5018[published Online
First: Epub Date]|.
4. Schwingshackl L, Hoffmann G. Association of dietary, circulating,
and supplement fatty acids with coronary risk. Annals of internal medicine
2014;161(6):455-6 doi: 10.7326/L14-5018-6[published Online First: Epub
Date]|.
5. Schwingshackl L, Hoffmann G. Dietary fatty acids in the secondary
prevention of coronary heart disease: a systematic review, meta-analysis
and meta-regression. BMJ open 2014;4(4):e004487 doi: 10.1136/bmjopen-2013-
004487[published Online First: Epub Date]|.
6. Satija A, Yu E, Willett WC, et al. Understanding nutritional
epidemiology and its role in policy. Advances in nutrition 2015;6(1):5-18
doi: 10.3945/an.114.007492[published Online First: Epub Date]|.
7. Higgins JP, Green S. Cochrane Handbook of systematic reviews,
Version 5.1.0 http://handbook.cochrane.org/. updated March 2011
8. Ramsden CE, Zamora D, Leelarthaepin B, et al. Use of dietary
linoleic acid for secondary prevention of coronary heart disease and
death: evaluation of recovered data from the Sydney Diet Heart Study and
updated meta-analysis. BMJ 2013;346:e8707 doi: 10.1136/bmj.e8707[published
Online First: Epub Date]|.
9. Dattilo AM, Kris-Etherton PM. Effects of weight reduction on blood
lipids and lipoproteins: a meta-analysis. The American journal of clinical
nutrition 1992;56(2):320-8
10. Blumberg J, Heaney RP, Huncharek M, et al. Evidence-based
criteria in the nutritional context. Nutrition reviews 2010;68(8):478-84
doi: 10.1111/j.1753-4887.2010.00307.x[published Online First: Epub Date]|.
11. Mann JI. Evidence-based nutrition: Does it differ from evidence-
based medicine? Annals of medicine 2010;42(7):475-86 doi:
10.3109/07853890.2010.506449[published Online First: Epub Date]|.
12. Ioannidis JP. Implausible results in human nutrition research.
BMJ 2013;347:f6698 doi: 10.1136/bmj.f6698[published Online First: Epub
Date]|.
At last I know how these damaging and pernicious guidelines came
about. They introduced a dark age of medicine and dogma that continues to
effect my practice.
How I struggle to get patients to accept eggs and butter as part of a
healthy diet . It's my belief that sugar and other carbohydrates are the
real problem.
I have seen great results for 70 patients in my practice with the
metabolic syndrome usi...
At last I know how these damaging and pernicious guidelines came
about. They introduced a dark age of medicine and dogma that continues to
effect my practice.
How I struggle to get patients to accept eggs and butter as part of a
healthy diet . It's my belief that sugar and other carbohydrates are the
real problem.
I have seen great results for 70 patients in my practice with the
metabolic syndrome using the low carbohydrate, higher fat diet for an
average of 13 months. Despite the eggs and butter their cholesterol levels
improved along with significant weight loss and improvements in diabetic
control.
When will the guidelines be re written to properly reflect what we
know about fats. All we seem to have at present is confusion
Hopefully the meta-analysis by Harcombe et al. (1) may inspire the
authorities to correct their dietary recommendations, because other
studies have shown that the intake of saturated fatty acids (SFA) does not
increase the risk of cardiovascular disease.
Not only did the authors of the dietary guideline from 1977 and 1983
ignore the dietary trials; they also ignored several unsupportive cohort
studies. Before 1...
Hopefully the meta-analysis by Harcombe et al. (1) may inspire the
authorities to correct their dietary recommendations, because other
studies have shown that the intake of saturated fatty acids (SFA) does not
increase the risk of cardiovascular disease.
Not only did the authors of the dietary guideline from 1977 and 1983
ignore the dietary trials; they also ignored several unsupportive cohort
studies. Before 1977 three prospective population studies had shown no
significant difference of SFA intake between CHD patients and people free
of CHD, and in 1983 five more had been published and with the same result.
Together these studies included 1920 patients with CHD and 45615 without
(2).
Furthermore, numerous studies published since then have acquitted SFA
in various ways. Let me mention only a few of the most important ones.
Today more than 30 population studies have shown the same result as
mentioned above, and in seven of ten prospective cohort studies patients
with stroke had eaten less SFA than those without; in the other three, no
difference was seen (2). Dietary information is of course inaccurate. A
more reliable method is to analyse the short fatty acids 12:0-15:0 in the
fat cells, because their contents reflect the intake of SFA during the
preceding weeks or months. In three case-control studies of patients with
CHD and healthy controls no difference was found as regards the content of
these fatty acids; in two studies it was even significantly lower in the
patients. These studies concerned only patients with first myocardial
infarction or patients who were not on a diet, and a diet bias is
therefore unlikely (3).
1. Harcombe Z, Baker JS, Cooper SM, et al. Open Heart 2015;2:e000196.
doi:10.1136/openhrt-2014-000196
2. Ravnskov U. The questionable role of saturated and polyunsaturated
fatty acids in cardiovascular disease. J Clin Epidemiol 1998;51:443-60.
3. Ravnskov U. Is saturated fat bad? In: Modern Dietary fat intakes in
disease promotion. Nutr Health 2010, part 2, p 109-9
The data is accumulating to show the adverse outcomes in critically
sick patients with persistently elevated troponins. An elegant study by
Amman et al (1) in 58 critically ill patients without acute coronary
syndromes concluded "Positive troponin levels were associated with higher
mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006).
Troponin-positive patients had significantly high...
The data is accumulating to show the adverse outcomes in critically
sick patients with persistently elevated troponins. An elegant study by
Amman et al (1) in 58 critically ill patients without acute coronary
syndromes concluded "Positive troponin levels were associated with higher
mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006).
Troponin-positive patients had significantly higher median levels of tumor
necrosis factor (TNF)-alpha, its soluble receptor, and interleukin (IL)-6.
A subgroup of 10 aplastic patients was troponin-negative at study entry.
Three became troponin-positive during leukocyte recovery and subsequently
died, whereas all the others stayed troponin-negative and survived. Flow-
limiting coronary artery disease was not demonstrable at autopsy or stress
echocardiography in 72% of troponin-positive patients".
The results of the present study ( 2), if reproduced in larger
studies in patients with acute exacerbation of chronic obstructive
pulmonary disease; the future guidelines will include estimation and
trajectory of troponin for such patients to assess prognosis. Presently,
there is no way to influence the poor natural history of such patients
.However the future is to explore possible interventions to favourably
influence the natural history. The authors deserve congratulations for
their thought-provoking work.
References:
1.Amman P ,Maggiorini M, Bertel O, et al.Troponin as a risk factor
for mortality in critically ill patients without acute coronary
syndromes.J Am Coll Cardiol .2003;41:2004-2009.
2.Arne Didrik Hoiseth, Anke Neukamm, Tor-Arne Hagve, Torbjorn Omland,
Pol H Brekke, and Vidar Soyseth.
The clinical value of serial measurement of high-sensitivity cardiac
troponin T in acute exacerbations of chronic obstructive pulmonary
disease. Open Heart 2014 1:e000001; doi:10.1136/openhrt-2013-000001
The current dietary guidelines are strongly associated (at least
temporally) with an exponential growth in obesity and Type 2 diabetes.
These unintended consequences may have arisen due to increased consumption
of carbohydrate in order to reduce fat in the diet.
If the guidelines cannot rely on a solid basis of science then they
should be withdrawn and re-written. There is a precedent - we no longer
have limits...
The current dietary guidelines are strongly associated (at least
temporally) with an exponential growth in obesity and Type 2 diabetes.
These unintended consequences may have arisen due to increased consumption
of carbohydrate in order to reduce fat in the diet.
If the guidelines cannot rely on a solid basis of science then they
should be withdrawn and re-written. There is a precedent - we no longer
have limits on dietary cholesterol.
As a layman I feel I have been deceived by "lipophobic cardiologists"
and my food supply has been altered on the basis of false or missing
evidence. I am confronted by red traffic light labels on foods we have
eaten for centuries and I feel the establishment has lost the plot on this
one.
As Professor David Haslam said, it's time for the demonisation of
saturated fat to stop - https://www.youtube.com/watch?v=kf8m04Gu4X0
I beg to differ from the authors about the etiology of CVD and
hypertension related to sugar and salt. Both high carbohydrate diets
(sugar) and salt (1-5) activates the sympathetic nervous system as well
stress, ageing, air pollution, salt, smoke, hypertension, diabetes,
etc...;
The sympathetic activation may represent the true cause of coronary artery
disease according our acidity theory of atherosclerosis developed in...
I beg to differ from the authors about the etiology of CVD and
hypertension related to sugar and salt. Both high carbohydrate diets
(sugar) and salt (1-5) activates the sympathetic nervous system as well
stress, ageing, air pollution, salt, smoke, hypertension, diabetes,
etc...;
The sympathetic activation may represent the true cause of coronary artery
disease according our acidity theory of atherosclerosis developed in 2006.
For more information please see the Powerpoint slides (6) presented by us
in November 2012 at the Fourth International Conference of Advanced
Cardiac Sciences - "The King of Organs Conference, 2012", held in Saudi
Arabia Kingdom.
I'm the author of the book "Acidity Theory of Atherosclerosis - New
Evidences", 2012 available at Amazon.com and other bookstores.
1. 'Volume-expanded' hypertension: the effect of fluid overload and the
role of the sympathetic nervous system in salt-dependent
hypertension,Journal of Hypertension, V30; N1: January 2012
doi:10.1097/HJH.0b013e32834f6de1
2. de Champlain J, Farley L, Cousineau D, van Ameringen MR. Circulating
catecholamine levels in human and experimental hypertension. Circ Res
1976; 38:109-114.
3. 6. Louis WJ, Doyle AE, Anavekar S. Plasma norepinephrine levels in
essential hypertension. N Engl J Med 1973; 288:599-601.
4. Sever PS, Osikowska B, Birch M, Tunbridge RD. Plasma noradrenaline in
essential hypertension. Lancet 1977; 1:1078-1081.
5. Lake CR, Kopin IJ, Ziegler MG, Coleman MD. Plasma catecholamines and
neurogenic hypertension. N Engl J Med 1977; 297:53-54.
6. Powerpoint presentation at
http://www.infarctcombat.org/AcidityTheory.pptx
With great interest we read the meta-analysis of Harcombe and co- workers titled "Evidence from randomized controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis" published in volume 2 of the Open Heart Journal [1]. In their article, the authors systematically reviewed randomized controlled trials investigating the associations between dietary fa...
At last I know how these damaging and pernicious guidelines came about. They introduced a dark age of medicine and dogma that continues to effect my practice.
How I struggle to get patients to accept eggs and butter as part of a healthy diet . It's my belief that sugar and other carbohydrates are the real problem.
I have seen great results for 70 patients in my practice with the metabolic syndrome usi...
Hopefully the meta-analysis by Harcombe et al. (1) may inspire the authorities to correct their dietary recommendations, because other studies have shown that the intake of saturated fatty acids (SFA) does not increase the risk of cardiovascular disease.
Not only did the authors of the dietary guideline from 1977 and 1983 ignore the dietary trials; they also ignored several unsupportive cohort studies. Before 1...
Dear Sir:
The data is accumulating to show the adverse outcomes in critically sick patients with persistently elevated troponins. An elegant study by Amman et al (1) in 58 critically ill patients without acute coronary syndromes concluded "Positive troponin levels were associated with higher mortality (22.4% vs. 5.2%, p < 0.018) and a lower LVEF (p = 0.0006). Troponin-positive patients had significantly high...
The current dietary guidelines are strongly associated (at least temporally) with an exponential growth in obesity and Type 2 diabetes. These unintended consequences may have arisen due to increased consumption of carbohydrate in order to reduce fat in the diet.
If the guidelines cannot rely on a solid basis of science then they should be withdrawn and re-written. There is a precedent - we no longer have limits...
I beg to differ from the authors about the etiology of CVD and hypertension related to sugar and salt. Both high carbohydrate diets (sugar) and salt (1-5) activates the sympathetic nervous system as well stress, ageing, air pollution, salt, smoke, hypertension, diabetes, etc...; The sympathetic activation may represent the true cause of coronary artery disease according our acidity theory of atherosclerosis developed in...
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