Re: Harcombe et al. Evidence from randomised controlled trials did
not support the introduction of dietary fat guidelines in 1977 and 1983:
The claim made by the authors of this paper that guidelines on
dietary fat introduced in the 1970s and 1980s were not based on good
scientific evidence is misguided and potentially dangerous. Whilst it is
important to ensure an ongoing interrogation of the evidence linking d...
Re: Harcombe et al. Evidence from randomised controlled trials did
not support the introduction of dietary fat guidelines in 1977 and 1983:
The claim made by the authors of this paper that guidelines on
dietary fat introduced in the 1970s and 1980s were not based on good
scientific evidence is misguided and potentially dangerous. Whilst it is
important to ensure an ongoing interrogation of the evidence linking diet
and heart disease, this must be through an holistic assessment of the
evidence base and recognition of the clear improvements in population
cholesterol levels and heart health that have taken place over the past 40
years.
In their assessment of the meta-analysis of randomised controlled
trial (RCT) data for saturated fat intake and heart disease mortality,
Harcombe et al.1 have taken a classical pharmaceutical approach to the
evidence, with the assumption that as with drugs, RCTs provide the gold
standard for formulating public health guidelines on diet. The assumption
that RCTs represent the pinnacle of the evidential hierarchy against which
other types of study compare unfavourably has been repeatedly shown to be
unproven for diet. In fact such an approach would be inappropriate for
most population based recommendations (as was also argued in the
accompanying editorial by Bahl 2).
Most dietary guidelines have been developed using an approach to risk
assessment which is based on assessing the degree of consistency and
quality of the data from a number of different types of studies;
convergence of the evidence represents the gold standard for risk
assessment in the study of diet-disease relationships. This approach uses
RCT data where it is available and with due caution for the extrapolation
of the findings to healthy populations, since many are conducted in high
risk individuals or those with existing disease. At the time of the
introduction of the UK and US guidelines, consistent evidence for
cholesterol raising effects of saturated fats was available from animal
studies, cross country comparisons, retrospective case control and
prospective cohort studies. The RCT studies discussed by Harcombe et al 1
were available to the expert committees at the time the guidelines were
drawn up. These findings were in part responsible for the decisions not to
recommend complete replacement of dietary saturated fats with
polyunsaturated fats, due to possible adverse effects of higher intakes of
these fats. At the time the recommendations were made evidence was also
available from trials conducted in metabolic ward and semi-free-living
settings in volunteer subjects. These showed effects of saturated fats on
circulating cholesterol to be so consistent that investigators were able
to develop predictive algorithms which would estimate the cholesterol
outcome based on the fat composition of the diet being fed.3
The discovery of the LDL receptor in the 1970s 4 paved the way to a
molecular based understanding of the mechanisms by which different dietary
fatty acids influence the hepatic uptake and excretion of circulating LDL
and thereby circulating LDL cholesterol concentrations. So a feasible
molecular mechanism was beginning to emerge which subsequently powerfully
supported the epidemiological and experimental studies.
In support of their own findings Harcombe et al.1 highlight the
recent meta-analyses of the cohort data 5, 6 which has argued that more
recent cohort studies have shown lower relative risk ratios for saturated
fat than earlier studies. Within these analyses it is astonishing to note
the limited attention given to the changes that have taken place in
population diets over the past 40 years, since this is a potentially
powerful confounding factor in long term cohort studies. Since the 1960s,
dietary fat intake in the UK has fallen by 50% -from around 125g/d to less
than 83g/d today. Saturated fat intakes have fallen even more dramatically
- from around 55g/d to around 30g/d today, with most of this change
occurring between 1975 and 1995.7,8 For the cohorts which were initiated
in the 1960s and 1970s the baseline diet measured at the outset of the
study bears little resemblance to the diet the subjects would have been
eating during the subsequent follow up periods. Those few cohort studies
which have undertaken repeat diet assessments have confirmed that the risk
ratio has reduced as population diet has changed, thereby providing real
life evidence of the benefits of the recommended diet. Exactly similar
changes are seen for trans fats; where repeat dietary assessment data are
available within cohort studies the risk ratio for the population study
group has fallen as levels of trans fats in the background diet has
reduced. In the Nurses Health Study after an 8 year follow up the odds
ratio fell from 1.67 reported in 1993 9 to 1.53 in 1997 10 and to 1.33 in
2005 11. It is intriguing to note the concerns regarding recommendations
for saturated fats have not been raised for trans fatty acids despite
exactly similar 'limitations' concerning the types and quality of evidence
available. There are no RCTs of coronary mortality available for trans
fatty acids, with lipoprotein biomarker outcomes used to support reduction
in intakes of these fats.
As far as more recent studies are concerned, those established since
1995 demonstrate a much narrower range of saturated fat intakes than was
the case in the 1960s and 1970s. The lower risk ratios reflect the fact
that significant proportion of the study cohorts are now eating levels of
saturated fats that do not elevate LDL cholesterol and lead to risk of
heart disease. It should be expected that outcomes from studies conducted
since 1995 will be less likely to observe significant effects of either
trans or saturated fat on heart disease, precisely because the recommended
diets have been beneficial to population heart health. Given the
improvements in both levels of cholesterol and rates of heart disease
world-wide in those countries which have introduced measures to reduce
intakes of saturated fats, it would seem that an RCT, with corresponding
ethical approval for its conduct, would surely be required to reverse
existing recommendations?
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:e000196.
2. Bahl R. The evidence base for fat guidelines: a balanced diet.
Open Heart 2015;2:e000229.
3. Keys A, Parlin RW. Serum-cholesterol response to changes in
dietary lipids. Am J Clin Nutr 1966; 19: 175- 181.
4. Goldstein JL, Brown MS. Familial hypercholesterolemia:
identification of a defect in the regulation of 3-hydroxy-3-methylglutaryl
coenzyme A reductase activity associated with overproduction of
cholesterol .PNAS 1973; 70: 2804-2808.
5. DiNicolantonio J. The cardiometabolic consequences of replacing
saturated fats with carbohydrates or ?-6 polyunsaturated fats: Do the
dietary guidelines have it wrong? Open Heart 2014;1:e000032.
6. 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. Ann Intern Med 2014; 160:398-406.
7. Diet, Physical Activity and Obesity Statistics 2006. British
Heart Foundation Statistics Database.
8. National Diet and Nutrition Survey. Results from Years 1-4
(combined) of the Rolling Programme (2008/2009 - 2011/12). Public Health
England and the Food Standards Agency.
9. Willett WC, Stampfer MJ, Manson JE, et al. Intake of trans fatty
acids and risk of heart disease in women. Lancet 1993; 341: 581-585.
10. Hu FB , Stampfer MJ, Mason JE. et al. Dietary fat intake and risk
of coronary heart disease in women. N Engl J Med 1997; 337:1491-1499
11. Oh K, Hu FB, Manson JE. et al. Dietary Fat Intake and Risk of
Coronary Heart Disease in Women: 20 Years of Follow-up of the Nurses'
Health Study Am. J. Epidemiol 2005; 161: 672-679
We would like to thank you for your interesting and helpful comments.
We are currently finalising the follow-up paper, which is to consider
all RCT evidence for current dietary guidelines before and since their
introduction, to see if they have been supported in hindsight. We will
review the risk of bias assessment tool, as suggested.
We do accept the role that cohort studies can play but wanted to
focu...
We would like to thank you for your interesting and helpful comments.
We are currently finalising the follow-up paper, which is to consider
all RCT evidence for current dietary guidelines before and since their
introduction, to see if they have been supported in hindsight. We will
review the risk of bias assessment tool, as suggested.
We do accept the role that cohort studies can play but wanted to
focus on RCTs to ask if this evidence alone supported the introduced
dietary guidelines. One of the authors, ZH, is undertaking a PhD on the
topic of the evidence base for dietary fat guidelines and is reviewing RCT
and cohort evidence before and after the recommendations were introduced.
The Sydney heart study was excluded for sensitivity analysis and the
results remained non-significant. The process was repeated with the
exclusion of each study individually and no combination of remaining RCTs
could establish a significant result.
We commented on the weight data in the discussion: "Studies of the
time report weight, not body mass. Weight changes were not recorded in two
studies[1 2]. Two studies noted no significant weight change in
intervention or control groups[3 4]. The Research Committee study[5]
reported mean weight loss as 7.5% in the intervention group and 4.8% in
the control group. Woodhill et al[6] reported a mean weight loss of 6.5%
and 6.0% in the intervention and control groups respectively." The weight
information available did not serve as an explanation for differences in
cholesterol levels.
We stand by our conclusion that, having reviewed evidence available
to the committees, the guidelines should not have been introduced.
1. Rose GA, Thomson WB, Williams RT. Corn Oil in Treatment of
Ischaemic Heart Disease. BMJ 1965;1(5449):1531-33 doi:
10.1136/bmj.1.5449.1531[published Online First: Epub Date]|.
2. Leren P. The Oslo Diet-Heart Study. Circulation 1970;42: 935-42
doi: 10.1161/?01.CIR.42.5.935 [published Online First: Epub Date]|.
3. Dayton S, Pearce ML, Hashomoto S, Dixon WJ, Tomiyasu U. A
Controlled Clinical Trial of a Diet High in Unsaturated Fat in Preventing
Complications of Atherosclerosis. Circulation 1969;40(1S2):II-1-II-63 doi:
10.1161/01.cir.40.1s2.ii-1[published Online First: Epub Date]|.
4. Medical Research Council. Controlled trial of soya-bean oil in
myocardial infarction: Report of a research committee to the Medical
Research Council. The Lancet 1968;292(7570):693-700 doi:
http://dx.doi.org/10.1016/S0140-6736(68)90746-0[published Online First:
Epub Date]|.
5. Research Committee. Low-fat diet in myocardial infarction: A
controlled trial. The Lancet 1965;2(7411):501-4
6. Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket
RB. Low fat, low cholesterol diet in secondary prevention of coronary
heart disease. Advances in experimental medicine and biology 1978;109:317-
30
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
Re: Harcombe et al. Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983:
The claim made by the authors of this paper that guidelines on dietary fat introduced in the 1970s and 1980s were not based on good scientific evidence is misguided and potentially dangerous. Whilst it is important to ensure an ongoing interrogation of the evidence linking d...
We would like to thank you for your interesting and helpful comments.
We are currently finalising the follow-up paper, which is to consider all RCT evidence for current dietary guidelines before and since their introduction, to see if they have been supported in hindsight. We will review the risk of bias assessment tool, as suggested.
We do accept the role that cohort studies can play but wanted to focu...
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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