Dietary fat intake and prevention of cardiovascular disease: systematic review
BMJ 2001; 322 doi: https://doi.org/10.1136/bmj.322.7289.757 (Published 31 March 2001) Cite this as: BMJ 2001;322:757All rapid responses
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Thank you to all who have taken the trouble to comment on our
recently published systematic review1. We are interested in the
contrasting interpretations of the findings: Drs Ravenskov, Livingstone,
Segall and Sichiery feel that the results point to lack of efficacy of
dietary fat modification, whilst Drs Collins, Mann and Relimpo emphasise
its effectiveness.
We agree with Drs Collins, Relimpo and JA Consumer that the important
factor in interpretation of the results is time. As pointed out,
lifestyles take time to harm. We don’t expect to see excess deaths a
couple of years after a young person starts smoking, but we know that, in
a cohort, effects on survival will be evident by retirement age. In the
meantime we expect to see an increase in smoking related morbidity, minor
at first (coughs, chest infections) with more serious illness gradually
appearing. It seems likely that this is the type of pattern (but
healthful rather than harmful) we are seeing when we look for effects of a
fat modified diet. Up to about two years we see very little outward
effect, although clearly many trialists were hoping to find effects in
shorter periods of time than this. From two to five years we see an
improvement in cardiovascular events in the modified fat group (but no
effects on death). It may be that in ten years or so there is a clear and
strong effect on cardiovascular deaths and even total mortality, but we do
not know this as there are no trials long enough to confirm or refute
this. Meta-regression strengthens this possibility, showing a greater
difference between cardiovascular events in modified fat and control
groups over longer times. This was the reason for our tentative
conclusion that there is ‘a small but potentially important reduction in
cardiovascular risk with reduction or modification of dietary fat intake’.
To address some of the criticisms of the methodology:
Professor Hu and colleagues are concerned over our inclusion of both
fat lowering and fat modifying interventions in the review. Both types of
diet reduce serum LDL cholesterol. It is interesting to note that almost
all of the event data come from fat modification trials: of 40
intervention arms included, 2/15 that aimed to lower total fat intake had
80 CV events and 46 deaths; 10/14 that aimed to modify the type of fat
eaten had 663 CV events and 1003 deaths recorded, other arms with events
aimed to make both changes.
We share Dr Ravenskov’s concern that very few of the included trials
were double blinded. Blinding participants to their own dietary intake is
costly and complicated, and may not even be feasible. The most important
type of blinding is that of the physician or assessor who decides whether
or not a cardiovascular (CV) event has taken place. Counting combined CV
events in trials with adequate physician blinding we find 423 events/8521
person years in the control group and 365/9205 in the intervention groups
(relative risk ~0.80). This compares with 220/2442 and 208/2469 (relative
risk ~0.93) from trials where physician blinding is unclear or inadequate.
Lack of physician blinding does not appear to be exagerating the effect of
dietary fat on cardiovascular events, rather the reverse.
Rules for inclusion of studies into the review were decided before we
were aware that some studies would aim to modify fat intake, while
increasing overall fat intake. It is inappropriate to change inclusion
criteria in response to unwelcome results of the studies found. The two
trials that resulted in increased fat intake (London corn/olive2 and MRC
soya3) almost certainly did result in dramatic changes in type of fat
ingested, and in serum total cholesterol levels (people in the fat
modification arm of MRC soya had mean falls in serum cholesterol of 0.64
mmol/L more than those in the control arm at 4 years, in the corn oil arm
of London corn/olive cholesterol fell by 0.58 mmol/L more than the control
at 12 to 18 months, however cholesterol rose in the olive oil arm,
including only 26 participants, by 0.3 mmol/L more than control). Figure
1 illustrates the relationship between mortality rate ratio and the
observed change in % energy taken as fat achieved in the intervention
group (compared with the control group). When the diet increased total
fat intake, the treatment effect tended to favour the control group. This
result did not reach statistical significance.
Figure 1. Meta-regression of total mortality versus percentage energy from
total fat
Professor Mann is right in his comments that some trials included
were small and of short duration. When we began the review we did not
know whether there might be short term effects of dietary fat on CV events
or mortality (via thrombotic mechanisms for example) that might be visible
early after dietary modification. Results from the review in trials of 6
to 24 months duration make this unlikely, which is useful to know. In
meta-analysis small trials have an important role to play in augmenting
larger trial data, despite their not having sufficient power individually
to provide useful data on death or events. However, there are too few
small trials to provide much help here. Again, this was not known when we
began the review.
As stroke and peripheral vascular events were (sadly) poorly
recorded, the numbers of cardiovascular events were little different from
coronary heart disease events (25 peripheral vascular events and 32
strokes, 57 events, in the control group, and 27 and 18 respectively, 45
events, in the intervention group - as there are fewer peripheral vascular
and stroke events in the intervention group adding these to the coronary
events will tend to enhance the apparent effect of
fat intervention compared to control, not reduce it).
Compliance is always an issue in lifestyle trials, and for this
reason we expected to see a differential effect of subgrouping trials
according to food provided or dietary advice given. However, if anything
diet advice trials seem to have a slightly better effect on cardiovascular
events (original paper, fig 5). Despite trials not achieving their stated
dietary goals, the mean fall in serum total cholesterol was 0.64 mmol/L
(11.1% of the intitial mean 5.8 mmol/L) in the experimental compared to
control groups.
We did, of course, try to separate out the effects of reducing fat
intake, from those of modifying type of fats consumed, through meta-
regression (using dietary fat intakes actually achieved, as in figure 1).
Unfortunately there is insufficient information from adequately documented
trials to generate robust estimates of the effects of total fat, saturated
fat, poly-unsaturated fat or even change in serum cholesterol on CV events
(original paper, table 2). However, despite some epidemiological
observations not supporting a benefit of low fat diets on coronary heart
disease4, all of the meta-regressions using trial data suggest that less
total fat, or less of any fat fraction, is protective of cardiovascular
events. That the association for mono-unsaturated fats is the most robust
(so that the greater the reduction achieved in mono-unsaturated fats in
the intervention group compared to the control group, the greater the
reduction in cardiovascular events) should make us pause in our
interpretation of the observational data.
We feel that it is important to realise that half a century on from
the genesis of the diet-heart hypothesis there have been so few people
enrolled in dietary fat trials, and for such very short periods (in marked
contrast to the numbers of people and years in the statin trials). Over 50
years, dietary fat trials have amassed only 30,000 person years of
observation in trials over 6 months long, and only 8,300 person years of
observation in trials longer than two years for which useable data on
mortality are available. Much more data is available already for statins
- the 4S trial5 alone amassed over 19,000 person-years of observation, a
mean of over 4 years for each person.
We feel that some of the comments on our systematic review are
actually justifications as to why a larger effect was not seen. Given the
paucity of the data available, we feel it is remarkable that an effect was
seen at all. We are criticised for including studies that provided
interventions other ‘than would today be considered desirable’. However,
what is clear to us following the review is that, whatever views may be
fashionable, due to a lack of good long term trial data we still do not
know what types of dietary fat changes (fat lowering or fat modification)
are protective against cardiovascular events or death. Data from cohort
studies (that may conflict with trial data due to higher levels of
inherent bias) and trials with intermediate outcomes (such as serum
cholesterol) do not give us the whole picture.
Lee Hooper, Carolyn Summerbell, Nigel Capps, Rudolph Riemersma,
Rachel Thompson, Shah Ebrahim and George Davey Smith.
Reference List
1. Hooper L, Summerbell CD, Higgins JPT, Thompson RL, Capps N, Davey
Smith G et al. Dietary fat intake and prevention of cardiovascular
disease: systematic review. BMJ 2001;322:757-63.
2. Rose GA, Thomson WB, Williams RT. Corn oil in treatment of
ischaemic heart disease. British medical Journal 1965;1:1531-3.
3. MRC. Controlled trial of soya-bean oil in myocardial infarction.
Lancet 1968;2:693-9.
4. Hu FB, Stampfer MJ, Manson JE, Rimm EB, Colditz GA, Rosner BA et
al. Dietary fat intake and the risk of coronary heart disease in women.
N.Engl.J.Med. 1997;337:1491-9.
5. Randomised trial of cholesterol lowering in 4444 patients with
coronary heart disease: the Scandinavian Simvastatin Survival Study (4S).
Lancet 1994;344:1383-9.
Competing interests: No competing interests
Hooper and colleagues may be interested to note that their paper
"Dietary fat intake and prevention of cardiovascular disease: systematic
review" (BMJ 2001:322:757-63) has been cited in "Medicine Weekly - the
voice of Irish medicine", in support of the argument that the link between
dietary fat and heart disease is largely "spurious and confounded".
I
assume that this spin on their systematic review can be traced in part to
the "This Week in the BMJ" headline "Reducing dietary fat has little
effect on cardiovascular disease". Clearly for many readers of the BMJ
this headline conveys the essential message of the paper. Few will have
read the paper in its entirety and even fewer will have taken the trouble
to download and peruse the unweildly table giving details of the studies
included in the meta analysis. The references to "40 intervention arms" in
the "This Week in the BMJ" summary and to 27 studies in the abstract of
the paper are frankly misleading. The reader should be alerted to the fact
that the conclusions on cardiovascular disease events are based on 16
studies of which only 5 had a mean follow-up of greater than 2 years. The
mortality data are even more sparse, based on 11 studies with
interventions of variable intensity. The protective effect of reduction or
modification of dietary fat on CVD events observed in the 5 studies with
at least 2 years follow-up is the major finding from this review and
should have been highlighted by the BMJ. Both the authors of the paper and
the journal have a responsibility not to add to the confusion on the role
of dietary fat in the causation of cardiovascular disease.
Competing interests: No competing interests
In the published article, Prof GD Smith was abundantly clear about
the goals of his meta-analysis, but now he obfuscates! The objective was
stated in the title: "Cholesterol lowering and mortality: the importance
of considering initial level of risk", and all the figures and tables
concerned this relationship. The central finding was an equation that
predicted odds ratio in the treated compared to placebo group as a
function of the inverse of the initial CHD risk. Stated plainly, the
higher the initial risk, the greater the relative risk reduction in
mortality. The authors used this equation to predict the results of
cholesterol lowering treatment, and even to give clinical guidelines. This
equation yields increases in mortality when the rates in the statin trials
are used. Moreover, the premise of the equation, that odds ratio is a
function of risk, has not generally proven true in the statin trials where
relative risk reduction for mortality and other endpoints has been largely
independent of level of risk.
Competing interests: No competing interests
EDITOR: The paper by Hooper at al. (BMJ 2001;322: 757-63) on dietary
fat
intake and prevention of cardiovascular disease is timely and well
conducted. Reduction of dietary fat is one of the main points included on
the dietary recommendations of many countries, however research has not
proved that eating a low fat diet increase the life expectancy.
Therefore,
and based on the results of the systematic review conducted by the
authors,
I consider that their conclusions are misleading. The authors concluded, "
alteration of dietary fat intake had small effects on total mortality" in
the abstract-results. However, the overall relative risk and the relative
risks of the detailed analysis conducted are highly consistent with lack
of
association between fat intake and mortality (rate ratio 0.98; CI
0.86-1.12).
There is also a lack of association for cardiovascular
mortality (rate ratio 0.91; CI 0.77-1.07). The only association found was
with cardiovascular events, however this association was vanished when the
authors excluded a trail that supplemented with fish oil. The total
mortality with 1430 events allows a powerful message of lack of
association
for a very hard outcome, but the authors concluded, " we are left with a
suggestion that less total fat or less of any individual fatty acid
fraction in the diet is beneficial". How the authors were left with this
suggestion is not easily grasp from the data.
Rosely Sichieri
Assistant professor
Depto Epidemiology,
State University of Rio de Janeiro
E-mail: rsichier@hsph.harvard.edu
Competing interests: No competing interests
The predictive value of meta analysis
Hu et al criticise our meta-analysis of fat lowering trials on the
basis that a meta-analysis I was involved with of cholesterol lowering
trials (1) 'would predict that statin drugs would increase mortality in
the 4S WOSCOPS, LIPID, and CARE trials, whereas the opposite in fact
occurred'. This is not the case. Our meta-analysis was a meta-regression
which demonstrated that the greater the cholesterol reduction, the greater
the reduction in coronary heart disease (CHD) mortality. Trials up until
the time of our meta-analysis (1993) had generally only produced small
cholesterol reductions (e.g. 9% in the WHO clofibrate study and the Lipid
Research Clinics cholestyramine study), the exception being the partial
ileal bypass surgery trial which produced a 23% reduction (2). The meta-
regression analysis relating percent cholesterol reduction to CHD
mortality would have predicted an odds ratio of 0.51 for CHD deaths on
treatment with simvastatin in the 4S trial, which produced a 25% net
reduction in cholesterol level; the observed result was 0.58. This would
clearly have produced a benefit in terms of all-cause mortality. At the
time our analysis was carried out there was insufficient direct data to be
certain about whether statins would result in any adverse influence on
other causes of death. We showed that in trials up to that date a small
increase in non-CHD mortality was observed. This was only seen in drug
trials (not in diet or surgical studies) and the increase in non-CHD
mortality was not related to the degree of cholesterol reduction,
demonstrating that it was not the fall in cholesterol which produced this
effect, but it was a side-effect of the drug therapies used (with fibrate
drugs being the class contributing most data to the meta-analysis). The
question of whether the statin agents would have such side effects was an
open question in 1993; since then large-scale trials have ruled out any
major effect in this regard. The purpose of meta-analysis and meta-
regression is to provide a quantitative overview of current trial findings
and highlight areas of uncertainty. The power of trials and meta-analyses
of such trials over observational data, which Hu et al seem to value more
highly in their response (with respect to trans fatty acids in relation to
CHD events, for example) is highlighted by the work of this group on
vitamin E supplement use and CHD, where (probably due to uncontrolled
confounding) highly misleading suggestions of major benefits were claimed
(3), which failed to be confirmed by large-scale RCTs (4).
(1) Davey Smith G, Song F, Sheldon TA. Cholesterol lowering and
mortality: the importance of considering initial level of risk. BMJ
1993;306:1367-1373.
(2) Ebrahim S, Davey Smith G, McCabe C, Payne N, Pickin M et al.
What role for statins? A review and economic model. Health Technology
Assessment 1999;3(19):1-91.
(3) Stamfer MJ et al. Vitamin E consumption and the risk of CHD in
women. NEJM 1993;328:1444-9
(4) Hooper L, Ness A, Davey Smith G. Vitamin E and CHD. Lancet, in
press.
Competing interests: No competing interests
Dear Sir,
Despite its popular use in combining findings from multiple studies,
meta-analysis has many well-known pitfalls (1). These include lack of
homogeneity of the studies, failure to consider important covariates,
inadequate understanding of the scientific subject in question, failure to
consider quality of the studies, and biases in including or excluding
certain studies. Some of these pitfalls are exemplified in the paper by
Hooper et al. (BMJ 2001;322:757-63), who reviewed 27 intervention trials
of fat reduction or modification. There are several problems with this
meta-analysis. First, it mixed conceptually different dietary
intervention approaches, i.e., total fat reduction vs. using unsaturated
fats to replace saturated fat. Neither epidemiology nor clinical trials
support a benefit of low-fat diets on either serum cholesterol or risk of
coronary heart disease (CHD). Substitution of vegetable oils rich in
unsaturated fats for saturated or trans fats, on the other hands, lowers
LDL and reduces cardiovascular endpoints, as indicated by several previous
systematic reviews of this topic. A second problem is that the meta-
analysis mixed studies specifically on cardiovascular disease with those
designed for other purposes (such as cancer prevention, weight loss, and
so on). It is questionable whether cardiovascular endpoints are
adequately ascertained in studies designed for other purposes.
Another problem of the meta-analysis is that it did not adequately
consider compliance of the subjects. Poor compliance to a low-fat diet is
a well-known problem in dietary trials. For example, the DART study (2)
was unable to achieve anywhere close to the goal set for total fat. This
and other trials showed minimal reduction in serum cholesterol with the
dietary intervention, demonstrating poor adherence. In two earlier trials
which showed cardiovascular benefits of unsaturated fats (3, 4), adipose
tissue fatty acid levels were used to monitor compliance. Although the
Finnish Mental Hospital Study (4) was not included in the meta-analysis as
it did not meet the subjective criteria, it did provide important evidence
for an effect of fat modification.
This meta-analysis highlights potential perils in combining “oranges”
and “apples” in aggregating dietary studies. The included trials are a
veritable hodge-podge of aims, methodologies, populations, and quality –
This same kind of approach was applied by one of the authors to
cholesterol lowering drug trials (5). The results from that meta-analysis
would predict that statin drugs would increase mortality in the 4S,
WOSCOPS, LIPID, and CARE trials, whereas the opposite in fact occurred.
Thus, similar degree of caution is needed to interpret results from either
a meta-analysis or an individual study.
Frank B. Hu, MD PhD
Frank Sacks, MD
Walter C. Willett, MD, DrPh
Dept. of Nutrition,
Harvard School of Public Health,
Boston, MA 02115
Reference:
1. Bailar JC, 3rd. Passive smoking, coronary heart disease, and meta-
analysis. N Engl J Med 1999;340(12):958-9.
2. Burr ML, Fehily AM, Gilbert JF, Rogers S, Holliday RM, Sweetnam PM, et
al. Effects of changes in fat, fish, and fibre intakes on death and
myocardial reinfarction: diet and reinfarction trial (DART). Lancet
1989;2:757-761.
3. Dayton S, Pearce ML, Hashimoto S, Dixon WJ, Tomiyasu U. A controlled
clinical trial of a diet high in unsaturated fat in preventing
complications of atherosclerosis. Circulation 1969;40:(Suppl II):1-63.
4. Turpeinen O, Karvonen MJ, Pekkarinen M, Miettinen M, Elosuo R,
Paavilainen E. Dietary prevention of coronary heart disease: The Finnish
Mental Hospital Study. Int J Epidemiol 1979;8:99-118.
5. Smith GD, Song F, Sheldon TA. Cholesterol lowering and mortality: the
importance of considering initial level of risk. Bmj 1993;306(6889):1367-
73.
Competing interests: No competing interests
I think that data presented by Hooper et al in the BMJ are not
analyzed properly. Taking into account the prolonged time that it takes to
make an atherosclerotic cardiovascular tree, it is not fair to demand a
dietary intervention to prove clear-cut statistically significant benefits
in a so short period. For this reason, I think that only studies with long
follow-up should be considered at this regard. If one makes so (even
though such a period remains considerably short), a significant degree of
protection is obtained. In addition, if one compares that very degree of
protection with that achieved by well-established protecting practices
like low-dose aspirin, blood pressure lowering or lipid lowering therapy,
one could find that dietary intervention to lower fat is not much less
effective and considerably cheaper.
Taking into account that we deal with healthy people (primary
prevention), offering a protective RR of 0.76 in only two years is not
only a relevant result, but an encouraging one. Just compare that with RRs
obtained from other well-documented risk-lowering interventions in the
primary prevention setting.
Given the current epidemic of metabolic and cardiovascular disease,
the message that authors give to the scientific community is openly
misleading. I would strongly favour a correction of data interpretation.
Competing interests: No competing interests
The BMJ website of the week (31 March) makes a claim which has
already reached this part of the world, and will no doubt trouble those
involved with health promotion worldwide: "So it’s official: low fat diets
don’t do much to improve cardiovascular morbidity and mortality." This
statement is derived from the paper in the same issue by Hooper et al
(pages 757-763), the title of which declares it to be a systematic review
relating to "Dietary fat intake and prevention of cardiovascular disease".
The opening sentence of the website review is unfortunate since it does
not accurately represent the conclusions of the article. The article
itself is disappointing since while it might fulfil the Cochrane review
criteria for a metaanalysis of clinical trials, it certainly does not
provide a systematic review of the topic.
It is surely important to consider the overall appropriateness of
each trial before its inclusion in a metaanalysis. Several of the trials
included are small or of short duration. It is difficult to imagine how
the risk of coronary heart disease which has accrued over a prolonged
period, perhaps a lifetime, may be reversed by dietary modification in
less than two years. The DART trial (fat modification arm) contributed
the greatest number of cardiovascular endpoints, yet there are at least
two reasons why this trial was most unlikely to be able to show a
beneficial effect. Limited dietary instruction was given and not
surprisingly there was no appreciable reduction in cholesterol. Since
modification of fat quality results in a predictable average change in
cholesterol level, there was clearly limited compliance with the dietary
advice. Furthermore the study was of too short a duration (2 years) to
have expected a reduction in clinical events and mortality. The Veteran’s
Administration Study which contributed the second largest number of deaths
fulfilled all the criteria for a good randomised, controlled, double-blind
clinical trial. Yet the experimental diet involved a ratio of
polyunsaturated to saturated fatty acids of 1.5, far greater than would
today be considered desirable. Such a diet would be expected to reduce
cholesterol and coronary heart disease morbidity and mortality – as indeed
it did, but perhaps not total mortality, as was also the case. Is it
appropriate to compare such a dietary intervention with that used in the
Oslo Study where saturated fats were replaced by a range of whole grain
cereals, vegetables, fruit and some unsaturated fatty acids and in which
study cardiovascular events and total mortality were reduced. Meta-
regression analyses were employed to disentangle these issues but one
might question whether the statistical power was sufficient to achieve
this. One might also question why the authors chose to examine total
cardiovascular rather than coronary artery endpoints since there has never
been any serious understanding that changing dietary fat does much to
prevent strokes. The link is with coronary heart disease.
Finally one might expect that in a systematic review it would be
appropriate to interpret the results of the clinical trials in the context
of the enormous body of descriptive epidemiology which supports the
dietary fat–cholesterol–coronary heart disease link. While evidence based
medicine now relies almost exclusively on clinical trials as far as drug
treatments are concerned, when considering evidence based nutrition with
nutrient-disease links accumulating over a lifetime it is imperative to
consider epidemiological and experimental evidence in conjunction with
trials.
Having described a litany of shortcomings of the published
metaanalysis, it is nevertheless important to note the tentative
conclusions offered by the authors of the paper : "There is a small but
potentially important reduction in cardiovascular risk with reduction or
modification of dietary fat intake, seen particularly in trials of
longer duration." The conclusion appears to have been largely ignored in
the website annotation and to be underplayed in the "This week in the BMJ"
paragraph referring to this paper.
It is most disappointing to find that a Journal as distinguished and
influential as the BMJ has utilised a rather sensational and inaccurate
approach.
Jim Mann, Professor in Human Nutrition and Medicine, University of
Otago, P O Box 56, Dunedin, New Zealand
Murray Skeaff, Senior Lecturer in Human Nutrition, University of
Otago, P O Box 56, Dunedin, New Zealand
Stewart Truswell, Professor of Human Nutrition, University of Sydney,
New South Wales, Australia
Competing interests: No competing interests
My complements on the meta-analysis, but I am amazed at the the
conclusion. Your headlines state that low fat diets are not much help, but
mortality is decreased by 9% and events by 16%. If you are in the 9%
group, it is 100% death. To say that this is only "marginal" is sending
the wrong message to America. We have observed in the Ornish Program that
survival is even more pronounced at the five year mark. It takes months to
remodel the coronaries and to stablize plaque. Progression of coronary
heart disease does not occur over night. The strongest case occurs in
societies that have a lifetime of fat restriction, events and survival are
significantly better in comparison to countries with high fat diets.
No need to change the study, just the headlines. Low fat diets eventually
create long term benefits! Just give the diet time!
In addition, one must remember that studies have shown that the most
beneficial effect is the change in the protein base from animal to plant
coupled with a low fat diet.
Richard E. Collins, MD
Competing interests: No competing interests
Re: Meta-analysis of dietary trials: Potential perils of combining "oranges" and "apples"
The Hu, Sacks and Willett rapid response in eBMJ to the Hooper et al
meta-analysis regarding the lack of conclusive evidence of cardiovascular
benefit by dietary fat changes suggests that the Finnish Mental Hospital
Study (1) gives important evidence of benefit of unsaturates.
This Finnish study would have been rightfully excluded as no fish oil
or other omega-3 directed studies were included like, for example, the
Lyon Diet Heart Study. The referred to male-subject part of the Finnish
study demonstrates the effects of simultaneous increases in omega-6
linoleic and in omega-3 alpha-linolenic fatty acids in hospital diets.
While the abstract and the paper itself stress the benefits of
polyunsaturated over saturated (dairy) fats via an observed 16% serum
cholesterol reduction, there was no consideration by the authors of the
fact that the soybean oil used was both high in omega-3 and in omega-6
polyunsaturates.
The Finnish study could be considered the world's first large omega-3
trial as the benefits found would be in line with the Lyon study (and
possibly in spite an excessively high omega-6 supply). It is now well
accepted that linoleic and alpha-linolenic acids have fundamentally
different -and naturally opposing- roles in health ... with high omega-3
but low omega-6 fats (fish, canola and flax) demonstrating benefits in
cardiovascular diseases and in arrhythmia prevention.
For those not current with this Finnish cross-over design trial, the
linolenic intake was 5.6 g/d, vs. 1.9 g/d in the control group (before
processing losses) while similarly linoleic was 34 g/d vs. 11 g/d
[coronary heart disease death or major ECG change: 4.2 vs. 12.7 / 1000 man
-years; RR=0.33; P=0.001].
To put these amounts of polyunsaturates in perspective, the
International Society for the Study of Fatty Acids and Lipids in their
1999 Adult Adequate Intake recommendations
(http://www.issfal.org.uk/adequateintakes.htm) suggests that this
linolenic intake would be just below "adequate" in the control group and
became "adequate" in the treatment group. On the other hand, linoleic was
about twice the "upper limit" in the control and was boosted to 5 times
the ISSFAL recommended upper limit in the treatment group.
With these confounding and possibly opposing effects in health, it is
no wonder that the past 5 decades of fat-changes studies (apart from omega
-3 studies) have not come up with clear answers and as long as
polyunsaturate studies and statin drug studies, continue to be presented
as being "cholesterol lowering studies" without considering their multiple
positive and negative effects, confusion will reign. Hooper et al
provided an important contribution by pointing out some of the weaknesses
in the studies and in the popular fat recommendations.
(1) Turpeinen O, Karvonen MJ, Pekkarinen M, Miettinen M, Elosuo R,
Paavilainen E. Dietary prevention of coronary heart disease: The Finnish
Mental Hospital Study. Int J Epidemiol 1979 Jun;8(2):99-118.
Eddie Vos
Sutton Qc Canada J0E 2K0
vos@health-heart.org
Competing interests: No competing interests