~  by Dr. Neville Wilson. 



AHA Issues ‘Presidential Advisory’ on Harms of Saturated Fat.

 On 13 June 2017 the American Heart Association (AHA) issued a new “Presidential Advisory” on dietary fats and cardiovascular disease, to “set the record straight” by warning of the harms that can be caused by consuming saturated fats. (1)

The newly published ‘Presidential Advisory’  is endorsed by its lead author, Frank Sacks, MD, of the Harvard T.H.Chan School of Public Healthy, Massachusetts, and is critical of any research that challenges the conventional view, claiming that public statements about the benefits of saturated fats “were not scientifically based”.

In this ‘Presidential Advisory’ the AHA has not budged from its long-standing adherence to the “diet-heart hypothesis”, and publically reasserts its position on saturated fats, claiming that the relationship between dietary saturated fats and cardiovascular mortality is causal.


Ask at own risk



Saturated fats are solid fats at room temperature, and are saturated with hydrogen atoms, and, having no double bonds, are chemically stable, and unlikely to be chemically reactive, or oxidized, as is the case with polyunsaturated fats.

Not all saturated fats are the same, with chain lengths varying from 3 to 12 carbons.

Short chain fatty acids are propanoic acid (3C), butyric acid ( 4C), and caproic acid (6C), medium chain fatty acids are found in several different foods, and long chain fatty acids (14C-24C) , with palmitic acid and stearic acid being the most saturated fats in food.

Butter contains butyric acid, and has fewer calories than margarine per pound, and coconut oil, one of the most saturated of natural fats, has 100 kilocalories less than a pound of soybean oil, the latter being an omega -6 polyunsaturated fatty acid, which has been promoted by the PRESIDENTIAL ADVISORY as a preferential dietary alternative to saturated fats.

Saturated fats have an important role in support of  human energy and body structures (lung surfactant), and many saturated fats raise cardio-protective HDL-C.  (thereby they may raise total cholesterol levels, but maintain a healthy total cholesterol/ HDL ratio).

The very long chain saturated fatty acids (20C-24C) are membrane fatty acids and essential for brain membrane integrity.

One example is  lung surfactant, which is a phospholipid with two molecules of palmitic acid linked to a phosphate and choline group.

Lauric acid (12C) is a medium – chain saturated fatty acid found in coconut and palm kernel, and has potent anti-microbial properties against lipid coated RNA and DNA viruses, numerous pathogenic gram positive bacteria, some pathogenic  gram negative bacteria, and various pathogenic protozoa. (2)

Lauric acid, derived from Coconut oil, is present in maternal milk, and plays a critical role in infant nutrition and protection against early life infections.

Coconut oil has also been shown to decrease pro-inflammatory cytokines (TNF-a, IL-1B, IL-6) relative to omega-6 polyunsaturated oils, and has, as a consequence, been used in therapies for acute and chronic inflammatory diseases. (Sadeghi et al 1999)

The Presidential Advisory has denounced the merits of coconut oil as a ”current fad”, thereby ignoring and dismissing its powerful anti-microbial properties against  human pathogens, and its powerful anti-inflammatory properties relative to omega-6 polyunsaturated fats.

Foods that contain saturated fats include the fat in meat, poultry, fish, butter, coconut oil, avocado, cheese and dairy cream.

The PRESIDENTIAL  ADVISORY recommends that these foods should be avoided in preference for the omega – 6 polyunsaturated fatty acids, which while having an essential role in human metabolism, tend to have inflammatory properties, which in excess can overcome the anti-inflammatory effects of dietary omega-3 fatty acids, as found in oily fish, some animal fats, and in egg yolks.


This way sign



In a 29 page document, with 139 clinical references, the  Advisory claims that “the rationale for decreasing saturated fats in the diet has been and remains on well established effects of saturated fat to raise low-density lipoprotein cholesterol (LDL-C), a leading cause of atherosclerosis”.

The second thrust of the Advisory statement is the recommendation to replace dietary saturated fat with polyunsaturated fats. “ Reducing saturated fat and replacing it with polyunsaturated fat in randomized controlled trials has reduced the incidence of CVD”, it claims.

Both of the above statements represent a long-standing commitment to the “diet-heart hypothesis”, as reflected in previous dietary recommendations and guidelines, and are dismissive of the large body of evidence, available from observational and population studies over several decades, that contradict the “diet-heart hypothesis”, and finds little support for the view that saturated fats are “harmful”, or causal, in cardiovascular disease, as stated in the current Presidential Advisory.

While a large body of contradictory studies do not provide evidence of support for the Presidential Advisory, evidence from selective studies has been presented to support the view that dietary saturated fat increases the risk for heart disease, and that dietary polyunsaturated fats decrease such risk.



The Advisory paper claims that evidence from controlled trials will show that “the reduction in serum cholesterol caused by substituting polyunsaturated fats for saturated fats prevented cardiovascular disease (CVD)”.

The paper then identifies 4 “core trials” and 5 “non-core” trials in support of its recommendations.

The 4 Core Trials are (a) The Dayton Trial (b) Oslo-Diet Heart Study (c) British Medical Research Council (d)  Finnish Mental Hospital Study.

(a)  The Dayton Trial compared the outcome of a control group eating a standard American diet rich in saturated fat to that of an experimental group who had replaced dietary saturated fat with omega – 6 rich polyunsaturated fats, derived from soybean oil. (3)

The experimental group reduced their serum cholesterol by 13% with fewer primary events, such as sudden death or myocardial infarction (heart attack), but the differences were not statistically significant, as the paper correctly acknowledges.

However, there were more deaths from cancer in the group eating the soybean polyunsaturated diet.

Despite the lower cholesterol levels in the soybean group, there was no difference between the degree of atherosclerosis in the 2 groups.

(b)  British Medical Research Council Trial was a London based Soybean study involving 393 men with a history of heart disease, and who were divided into 2 groups, an experimental group that replaced saturated fats with soybean oil, and a control group that ate a saturated fat diet.

The soybean group had a 22% reduction in serum cholesterol, and 62 of the 199 in the group had a recurrent coronary event, compared to 74 of the 194 who ate a saturated diet, so the small difference was not statistically significant.

However, there were 25 deaths from heart disease in each group, so no cardiac benefits were evident in the group that replaced saturated fats with polyunsaturated omega – 6 soybean oil. (4)

The authors of this study conceded, that “the results of this trial alone lend little support…to the suggestion that a diet of  this kind should be recommended in the treatment of patients who have suffered a myocardial infarction”.

And yet, this is the diet recommended in the Presidential Advisory !

(c)   Oslo Diet Heart Study was another soybean experiment in which a control group had a diet high in saturated fats, while an experimental group had a low saturated fat and high polyunsaturated fat intake.

Again, serum cholesterol was reduced by 14% in the experimental group, but sudden death occurred at the same rate in each group. (5)

However, there were some cardiovascular benefits for the experimental group that were given a low saturated /  high polyunsaturated diet, with a 29% reduction in recurrent heart attack and angina pectoris, inspite of sudden death being at the same rate in each group.

A cursory view of these numbers may lead to the assumption that the polyunsaturated group was the dietary preference responsible for the recorded benefits, but taking into account other confounding factors, this may not have been the case.

The control group that was given the high saturated fat / low polyunsaturated fat also had more men over the age of sixty, were of greater weight at the start of the trial,  and had an equal number of smokers as the diet group.

The diet group, given the polyunsaturated diet, were also given large quantities of sardines canned in cod liver oil, thereby increasing their omega 3 intake, known to have cardiovascular benefits. The increased omega – 3 intake would have served to offset the inflammatory effects of the omega – 6 polyunsaturated fats in their diet, thereby reducing the risk for cardiovascular events in the diet group.

The Presidential Advisory uses this study as one of its 4 “core trials” to prove the health benefits of a high polyunsaturated omega – 6 diet, but the study does not provide such evidence, given the confounding factors present.

(d)  The Finnish Mental Hospital Study again compared the outcomes from 2 different diets, one high in soybean polyunsaturated fats, and the other high in saturated fats, each given for 6 years, with a cross over of diets for a further 6 years. (6)

The cross-over design used in this study was complicated by an uneven distribution of risk factors in both groups, rendering it impossible to conclude whether any health benefits were due to the current diet, or the diet during the previous 6 years.

Furthermore, results were taken from patients who had been in hospital for only one month, as well as those who had been there longer.

This was a badly designed and poorly conducted study, which does not answer the questions about any possible health benefits for a polyunsaturated diet.

In addition to these “4 core studies” the Advisory makes mention of “other non-core trials”, listing the following : Stars, Dart, Rose, Minnesota and Sydney Diet-Heart Study, and discounting the value of their outcomes on the basis of not fully representing a polyunsaturated diet.

In the Sydney Diet-Heart Study, the outcomes of an experimental polyunsaturated diet, with restricted saturated fat to 10% of calories, and cholesterol intake to 300 milligrams or less,  was compared to outcomes from a control group, having  an unrestricted diet, and who were invited to eat as much as they liked.

After 5 years death rates were higher in the experiment group than in the control group (17.6% vs 11.6%)  despite  5% lower cholesterol levels in the experimental group.

The Advisory chose not to recognize the outcome of this trial, claiming that the polyunsaturated fat group had also consumed transfats, which are a recognized risk factor for poor health, and may have confounded the results.


While a large body of contradictory studies do not provide evidence of support for the Presidential Advisory, evidence from selective studies has been presented to support the notion that dietary saturated fat increases the risk for heart disease, and that dietary polyunsaturated omega 6 fats decrease such risk.

The above quoted 4 “core studies” do not provide the alleged evidence of protection against heart disease by replacing saturated fats with a polyunsaturated diet.

Reports from recent reviews of the literature, likewise, fail to provide supportive evidence for the Presidential Advisor, that saturated fats are detrimental to health, and polyunsaturated fats are protective and supportive of cardiovascular health.

In a recent (2014) review of 32 studies, involving 530,525 participants, with follow up ranging from 5 to 23 years, R Chowdhury, and others, reported 13 studies of high quality, and the rest of medium quality, without any of these trials supporting the AHA recommendations to substitute polyunsaturated fats for saturated fats (7)

In a 2010 meta analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, Drs Patty Sri-Tarino and Frank Hu identified 21 studies, involving 347,747 subjects, during a 5-23 year follow up, and reported that “ there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD”. (8)

The Presidential Advisory paper makes a passing reference to these 2 very large studies, and dismisses them on the grounds that they “did not take into consideration the replacement macronutrients “ and have therefore ”mistakenly concluded that there was no significant effect of saturated fat intake on cardiovascular (CVD) risk”.

The Presidential Advisory chooses to ignore important data that contradicts its dietary recommendations, and comes to its own conclusion, by stating “ taking into consideration the totality of evidence, LDL-Cholesterol links saturated fat and its replacement macronutrients to CVD by very strong scientific evidence that satisfies rigorous criteria for causality”

Clearly, any scientific “evidence” which purports to support the Presidential Advisory Policy will be shown to be based on selective data, rather than on the totality of data.




A classic example of  data selection to support a hypothesis was the 1956 Six Country Study, in which Ancel Keys demonstrated  a correlation between heart mortality and total fat available for consumption in six countries, while ignoring the available data from 22 countries which contradicted his hypothesis. (9)

In his 1958 Seven Countries Study the proposed link between fat, cholesterol and heart disease was demonstrated by hand picking 7 Countries for comparison.

However, this association was not present within the countries chosen, demonstrating that environmental, cultural, economic and other factors may have a confounding influence on dietary statistics.

Despite the flaws in his theory, Keys, through his powerful associations with the AHA,  succeeded in having his theories incorporated into the AHA dietary Guidelines in 1961. (10)

The Seven Countries Study prompted an explosion of epidemiological and clinical research into the role of dietary fat in cardiovascular disease, and while several studies have shown associations between cardiovascular risk factors and the dietary intake of saturated fats, such associations do not represent a proven cause.

Since a causal relationship between dietary saturated fats and heart disease has not been demonstrated in the totality of experimental evidence available to date, acceptance of the Presidential Advisory as an evidence – based nutritional directive remains questionable, necessitating a reappraisal of nutritional guidelines on fatty acids and cardiovascular disease.

National dietary bodies should therefore view the Presidential Advisory with caution before any consideration is made to include, and implement, such recommendations in National Dietary Guidelines.

The questionable role of saturated fats in cardiovascular disease had already been raised in 1998 by Dr. Uffe Ravnskov, (11) and to date, several critical  reviews of the literature have contradicted the  basis for the current Presidential Advisory.

The earlier correlations between saturated fat and cardiovascular disease, as reported by Ancel Keys, is  absent from these recent studies, and in a 1957 paper, J Yerushalmy exposed the weakness of such correlations, and the danger of choosing selective data to support a hypothesis. (12)

Despite critical objections, from several quarters, to the prevailing hypothesis, the AHA published its first dietary Guidelines in 1961, aimed at the American public,  advocating dietary polyunsaturated fats as a replacement for dietary saturated fats to reduce the risk of cardiovascular disease.

A  1961 Report by the Central Committee for Medical and Community Programmes declared “the reduction or control of fat consumption under medical supervision with reasonable substitution of polyunsaturated fats for saturated fats is recommended as a possible means of preventing atherosclerosis and decreasing the risk of heart attacks and strokes”.

The statement concluded that “there is as yet no final proof that heart attacks and strokes will be prevented by such measures” (13)

Up to 1961 there was no evidence for the AHA proposals, and since then studies have failed to support such proposals.

Several recent studies, likewise, show no evidence for the recurring AHA dietary warnings, that saturated fat intake is a risk factor for CVD. ((14) (15) (16) (17) (18) (19) (20) (21) (22)

In a 2015 Review and Meta-analysis of Observational Study,  reported in the BMJ, researchers concluded that “saturated fats are not associated with all cause mortality, CVD, CHD, Ischaemic stroke or type 2 Diabetes”.  (23)




In 1973 Raymond Reiser conducted a critical examination of the literature, exposing methodological and interpretational flaws in 40 trials, including the Keys study.

He showed how many authors had used vegetable oils saturated by hydrogenation, instead of natural saturated fats, and that the reported elevations of blood cholesterol in some trials may have been due to artificial rather than natural fats. (24)

Keys was later reported as acknowledging that “there is no connection whatsoever between cholesterol in food and cholesterol in blood. And we have known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit””.

Keys had also been reported as having stated that hydrogenated vegetable oils (polyunsaturated fats) might be the “underlying cause of the current epidemic of heart disease”.  (25)

This observation was neither acknowledged, nor implemented, by the AHA in its official recommendations to substitute dietary saturated fat with polyunsaturated vegetable oils.

A 20 year follow up study of women in the Nurses Health Study, by the Department of Nutrition at Harvard Public School of Health, reported “diets lower in carbohydrates and higher in protein and fat are not associated with increased risk of coronary heart disease in women”, but also added that “when vegetable sources of fat and protein are chosen, these diets may moderately reduce the risk of coronary heart disease”. (26)

In a 1998 paper Dr. Uffe Ravnskov PhD examined the relationship between dietary saturated fats and atherosclerotic disease, with reference to Observational studies, Population studies, Cohort studies and Experimental studies , and concluded from the available study outcomes that “there is little evidence that saturated fatty acids as a group are harmful, or that polyunsaturated fatty acids as a group are beneficial”  (27)


The AHA Consensus Report 2001:


In 2001 the Nutrition Committee of the American Heart Association produced a consensus report claiming support for their cornerstone policy that saturated fat had an atherogenic effect on arteries through its adverse effect on blood lipids.

The single supporting evidence offered for that consensus report was the 1997 paper by Drs Hu and Stampfer, who examined dietary fat intake and the risk of coronary heart disease in women, while ignoring the vast number of contradictory trials.

Regardless of the limited evidence in the Consensus Report, the joint WHO/FAO Expert Consultation in 2003 concluded, “ the relationship between dietary fats and cardiovascular disease (CVD), especially coronary heart disease, has been extensively investigated, with strong and consistent associations emerging from a wide body of evidence”.

It is clearly evident that no such “wide body of evidence” had been available to support the claimed association between saturated fats and cardiovascular disease.

In a later 2009 publication by a joint FAO/WHO Expert Consultation, the conclusions are markedly different to those of the 2003 report, acknowledging that the evidence is “unsatisfactory and unreliable” to judge about the influence of saturated fat on the risk of CHD (28) or diabetes and obesity. (29)


The National Cholesterol Education Programme (NCEP):


In November 1984 The National Heart, Lung and Blood Institute of America (NHLBI) launched their National Cholesterol Education Programme (NCEP) with the goal of reducing death from coronary heart disease in the USA, by lowering cholesterol and the reduction of dietary saturated fat.

Hundreds of millions of dollars had already been spent in trying to prove the validity of the diet-heart hypothesis.

The first 4 trials between 1980-1984 (Framingham, Honolulu, Puerto Rico and Chicago Study) failed to show a benefit for a fat restricted diet.

The MRFIT study, likewise, failed to support the hypothesis. (30)

By 1998 a total of 27 studies had already been published, including 34 cohorts of more than 150,000 individuals, with no strong evidence for the prevailing hypothesis that saturated fats were causal in cardiovascular disease.

In a recent systematic review and meta-analysis of 40 papers covering 11 trials, researcher Zoe Harcombe found that randomized controlled trials  do show that dietary modifications may reduce serum cholesterol to a marginally greater extent in intervention groups, compared with controls.

However, these reductions in serum cholesterol, they suggest, “do not appear to translate into an improved survival from all cause or coronary heart disease”.

Their conclusion, after reviewing these papers, is that “the available randomized controlled trials evidence does not support the current dietary fat guidelines”. (31)


The AHA Presidential Advisory :


The AHA ‘Presidential Advisory’ recommends that saturated fats be replaced by polyunsaturated vegetable oils, monounsaturated fats and carbohydrates, and promotes the notion of “good carbs” and “bad carbs”, (which is new to the vocabulary of the AHA !) and concedes that there are “simple” carbs that are “bad”, but there are also  “complex” carbs that are “good”, and that it is the “good carbs”  that should replace saturated fats in order to reduce the risk of cardiovascular disease.

Dr. Sacks, author of the Presidential Advisory, is critical of the rapidly growing support amongst consumers and scholars for a low carb / high fat (LCHF) preference, claiming that such recommendations were “not scientifically based”.

He further states, “ There has been a growing trend of media articles focusing on small studies suggesting some saturated fats are good for you”, and that “people advocating that eating butter and full-fat milk is beneficial. And coconut oil is a fad right now – but it is actually a saturated fat, which raises your LDL, so the AHA wanted to look at the issue again”. (32)

According to the Medscape report, Dr. David Jenkins, MD, Department of Nutritional Sciences and Medicine, University of Toronto, Ontario, Canada, agrees with the AHA statement, adding,   “…the AHA has always taken the stance that saturated fat is bad and that we should be eating more plant oils, and this view is endorsed by the vast majority of nutritionists who are scientifically qualified”.

Dr. David Katz, MD, director of the Yale University Prevention Research Center, likewise supports the AHA position, stating  “the conclusion is perfectly clear and entirely decisive. Saturated fat from the usual dietary sources increases the risk of heart disease, and its replacement with the wholesome foods and unsaturated fats reduces that risk”.

In a 2016 paper by Wang D D et al, the authors, likewise, defend the current dietary recommendations to replace saturated fat and trans-fat with omega 6-polyunsaturated fats.  (33)

They do so by their examination of the associations between specific dietary fats and total and cause specific mortality in 2 large cohort studies, (a) the Nurses Health Study (83,349 women)

(b) the Health Professionals Follow-up Study (42,884 men)

In a comparison of extreme quintiles, in these studies, they report greater associations of mortality with saturated fats (HR 1.08),than either polyunsaturated fats (HR 0.81), or monounsaturated fats (HR 0.89), and trans fats (HR 1.13).

Ravnskov et al, in a Dec 2016 letter to the Editor, questioned the methods used by Wang et al in their assessment of the associations they report, stating that the use of Food Frequency Questionaires, as used by Wang et al, are not an accurate, or reliable, method for obtaining dietary information from study participants.

Ravnskov et al also criticize the Wang paper for failing to take account of the recent findings, by Chowdhury 2014 (34)  and Siri-Tarino 2010 (35)    who report no  demonstrated associations between the intake of saturated fats and mortality in 46 observational and 21 cohort studies they conducted.


The LDL- Cholesterol Argument :


The Presidential Advisory also maintains that LDL-Cholesterol is a risk for cardiovascular disease, and that because dietary saturated fats increases LDL-C,  they should be replaced by polyunsaturated fats to reduce risk.

They also state that polyunsaturated fats are preferential, because they lower serum LDL-C, thereby reducing the risk for CVD.

The significance of serum low density lipoprotein (LDL) as a likely risk factor for coronary heart disease has once again emerged as a topic of intense debate, with traditional supporters of the “diet-heart” hypothesis making a strong defence of their long held view that saturated fat and LDL-C (the so called “bad cholesterol”) are the cause of atherosclerosis, and the major contributory factor for an increased risk for cardiac morbidity and mortality.

The perception that LDL is causal in arterial damage, and therefore a powerful risk factor for cardiovascular disease, has long been a fundamental premise in the AHA approach to risk reduction strategy, leading to policy statements about maximum reduction of blood LDL levels.

This view is reflected in the policy statements of the NCEP and its target proposals over several decades. (36), leading to recommendations to titrate lipid therapy to achieve LDL-C levels of less than 1.81 mmol/L.

Where the LDL trials fail to account for the distinction between harmless buoyant LDL  particles (Pattern A- non-atherogenic) and the small dense LDL (Pattern B –pro-atherogenic ) particles, their measurements of LDL-C do not amount to a measure of cardiovascular risk, and therefore have limited predictive value. (37)

Total serum cholesterol measurements, routinely quoted in trial studies, likewise, have poor predictive value, since they are influenced by HDL levels, which may be elevated by dietary saturated fats,  and may  consist of small dense (HDL3) particles that have anti-atherogenic properties, including potent efflux capacity and antioxidative and antipoptotic activities.




Lack of evidence for these target proposals was cited by Hayward RA and others in a 2006 paper. (38)

Furthermore, a lack of association between LDL-C in the elderly and mortality,  was been shown by Ravnskov and others, in their review of the literature, raising the vital question, that if LDL-C is not a risk factor for the elderly, why should it be risk factor in the young and middle-aged ?, and why should it be a target in the dietary guidelines ?

The inverse association between LDL-C is also evident from the literature, showing that low LDL-C  (not high LDL-C) is a risk for fatal diseases, since LDL can bind to a large range of microorganisms thereby inactivating them and their toxic products. (39)

In a meta-analysis of 19 cohort studies performed by the NHLB&I, including 68,406 deaths, total cholesterol was inversely associated with mortality from respiratory and gastrointestinal diseases, supporting evidence for the antimicrobial benefit of LDL-C. (40)

Studies including more than 140,000 individuals, followed for 10-30 years, show an inverse association between cancer and total cholesterol, (41) supporting an observation by Newman and Hully in 1996, that linked cancer to lipid lowering in rodent experiments. (42)

On the basis of such findings, there is little evidence for LDL-C lowering as a health benefit.

The PROVE-IT trial did nothing to “prove” that LDL-C lowering would improve mortality.

Since the 30% reduction in CHD mortality and 28% reduction in overall mortality in this randomized trial was likely to have been the result of the anti-inflammatory (pleiotropic) effects of 2 lipid lowering agents used.     (43)

The results from this trial prompted immediate revision of the official guidelines by the NCEP in 2004 to more aggressive LDL lowering, to achieve targets of 70 mg/dl in very high risk patients

In the subsequent A to Z trial LDL lowering was achieved with low dose and high dose statin (simvastatin) but the differences in cardiovascular death between the 2 groups was not statistically significant.

The TNT study followed in 2005, and was a further attempt to prove the benefits of LDL lowering, by comparing the effects of a high dose statin (Lipitor 80mg) with a low dose statin (Lipitor 10 mg).

While significant LDL lowering was achieved by both statins (77 mg/dl and 101mg/dl), there were no differences in overall mortality between the 2 groups (5.7 % vs 5.6%), with cancer deaths 13% higher in the 80mg dose of Lipitor, and greater adverse side effects in the higher dose statin. (8.1% vs 5.8%) (44)

Despite no mortality benefits from the trial, the lead researcher stated, “we need to make the assumption that mortality has been proven, that LDL lowering does in fact lower total mortality rates”.

The trial failed to prove that LDL lowering confers mortality benefits. Since the measure of inflammatory markers (CRP) in this study were never reported, the anti -inflammatory effects of the statins used could not be determined.

Mortality benefits in this study were assumed, and not proven.

In a later study which measured the effects of statins on CRP, the researchers reported “ atherosclerosis regressed in patients with the greatest reduction in CRP levels, but not in those with the greatest reduction in LDL-C”, thereby acknowledging that LDL-C was an unlikely cause of atherosclerosis, a contradiction of the ADVISORY statement.  (45)

In 2006 a Meta-analysis of Randomized controlled Trials was reported in the Archives of Internal Medicine. (46) in which the effects of intensive statin treatment were compared to those of usual care, no statins or low dose statins, in a group of hospitalized patients with cardiovascular disease.

While a 19% reduction in further  cardiovascular events   was reported, the authors concluded, “There is no significant evidence that reduction in LDL-C level explains these beneficial effects”

In a later study that year, researchers reviewed all controlled trials and cohort studies to date, to examine the independent relationship between LDL-C and cardiovascular events in patients who had LDL-C levels below the NCEP recommendations of less than 130 mg.dl

Their conclusion was “no clinical trial subgroup analysis or valid cohort or case-controlled analysis suggesting that the degree to which LDL-C responds to a statin independently predicts the degree of cardiovascular risk reduction” (47)

These and other findings contradict the Presidential Advisory that LDL-C is a causal factor in cardiovascular disease, and that reductions in LDL-C and dietary saturated fat will confer proven cardiovascular benefits to consumers.

In a 2013 editorial of Circulation, Dr. M B Rothberg challenged the traditional mantra that saturated fat “clogged coronary arteries” thereby increasing the risk of cardiovascular disease.

In another editorial that year, the British Medical Journal featured an opinion by UK Cardiologist Dr Aseem Malhotra, stating that the long-standing anti-fat mantra of the AHA,  has “paradoxically increased our cardiovascular risks”, and in an editorial in the April 25, 2017 edition of the British Journal of Sports Medicine, Dr Mulhotra and Dr Rita Redberg (Univ of California) highlight several studies in support of their view that LDL-C is not associated with CVD, and is inversely associated with all-cause mortality in the elderly.

They refer also to the evaluation of recovered data from the Minnesota Coronary Experiment (1968-1973) that showed an increased risk of death from a replacement of saturated fats with vegetable oils rich in linoleic acid (omega – 6), despite significant reductions in LDL and total cholesterol. (48)




In the more recent Fourier Trial  a new cholesterol lowering drug, called Evolocumab, was tested in 27,564 patients with atherosclerotic heart disease, who were divided into a control group and a placebo group, with the control group being given the drug by injection.(49)

The drug, known as a PCSK9-inhibitor, can lower LDL levels by as much as 60%.

Given as a twice monthly subcutaneous injection, in addition to statin therapy, the LDL levels in the treated group were lowered  by 59%, from 2.4mmol/L to 0.78 mmol/L.

At 26 months of trial the reduction in risk for the cardiovascular endpoints (cardiovascular death, heart attack, stroke or unstable angina) in treated patients was 11.3% compared to 9.8% in untreated patients, a mere benefit of 1.5%.

The trial, planned for 4 years, was terminated at 26 months, after 444 had died in the drug treatment group and 426 in the untreated group.

There were 18 more deaths in the drug treatment group.

Had the trial continued for its planned duration of 4 years, these figures might have been much worse, with the probability of a greater number of deaths from the LDL lowering treatment.

In this trial, the intensive lowering of LDL, by a very expensive drug, in a group of patients with heart disease did not confer any significant mortalty benefit compared with untreated patients,

At a cost of $14,500  per patient per year, the cost benefit of a drug that that failed to prevent death in 444 patients must be seriously reviewed.




It is worth noting that in 2013 the AHA and  ACC, in conjunction with the National Heart, Lung and Blood Institute (NHLBI), formally abandoned the traditional LDL targets, recommended for treating patients at risk of developing cardiovascular disease, on the basis that no evidence existed for treating to a target level of LDL. (50)

Although the 2013 Guidelines called for a shift away from LDL-cholesterol treatment targets, on the basis of “no evidence”, they did focus on risk management, and defined 4 groups of individuals who were considered to be likely candidates for statin treatment, on the basis of a risk score, determined by their age, blood pressure, smoking status, cardiovascular history and their level of LDL elevation.

So, acknowledging that no clinical evidence existed for treating LDL to the targets  as prescribed in previous guidelines, the ACC and AHA maintained their objective to reduce LDL levels, in patients regarded as high risk, using statin therapy.




In contrast to the AHA guidelines of 2013, the American Association of Clinical Endocrinologists (AACE) recently proposed a renewal of the target proposals for LDL, suggesting goals of <55 mg/dl, <70 MG/dl, <100 mg/dl, and <130 mg/dl for individuals at extreme, very high, high/moderate, and low risk for cardiovascular events, respectively. (51)

While the PRESIDENTIAL ADVISORY does not recommend targets, it continues to promote the policy of LDL-C reduction as a strategy to reduce cardiovascular events.

The debate as to whether such recommendations have strong experimental support continues, but remains questionable.

The recommendation to replace dietary saturated fats with omega 6 rich polyunsaturated fats. Likewise, remains questionable, given the evidence above.

A positive word from the PRESIDENTIAL ADVISORY is that a focus on whole food rather than on single nutrients, is a prerequisite for overall health, and that the Mediterranean style of eating exemplifies a healthy whole food approach to diet.




In the 2014 PREDIMED STUDY, a Mediterranean- style diet, high in fat from virgin oil and nuts reduced the risk of CVD by 30% in high risk patients, compared to those following a low fat diet, and appears to be a safe and health supporting dietary option.

Predimed provides evidence that a combination of  dietary saturated fats, monounsaturated fats, and omega-3 polyunsaturated fats can provide essential nutrition with proven cardiovascular benefits.



Dr. Neville Wilson,

30 June 2017.




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