In 1933 Nikolai Anitschkov  produced his thesis that  a high dietary intake of cholesterol led to increased levels of blood cholesterol, resulting in infiltration and accumulation  on the inner walls of the arteries, thus causing vessel blockage, and ultimately  ischaemic death of the heart muscles being fed by these arteries.

His conclusions were based on feeding experiments involving rabbits who were force-fed high levels of dietary cholesterol, resulting in excessively high levels of blood cholesterol and organ tissue saturated with cholesterol.

In the same year Rudolph Schoenheimer conducted experiments with mice, feeding them large amounts of cholesterol,  then measuring their circulating levels of plasma cholesterol.

It is worth noting the outcomes of these early experiments within the context of prevailing notions regarding dietary and plasma cholesterol. Current perceptions that dietary cholesterol is harmful to cardiovascular health are based on the belief that such diets cause elevations of blood  cholesterol levels, thereby initiating the atherosclerotic process which leads to cardiovascular disease. (CVD).

Consequently, targets for blood cholesterol lowering have been incorporated into conventional therapeutic protocols.

Anitschkow’s rabbits demonstrated an accumulation of cholesterol that was markedly evident in their blood vessels, body tissues and skin. These rabbits died shortly afterwards.

We now know that because rabbits are herbivorous animals, they were unable to digest and metabolise the cholesterol-rich fodder given to them, and not having the mechanisms for storage, metabolism or excretion, they finally died, not from cholesterol blocked arteries, or from plaque rupture, as in humans, or from any form of heart disease, but ultimately from starvation !

Similar experiments with carnivorous animals have failed to produce these unnatural effects.

Furthermore, post-mortem studies, conducted by Lande and Sperry in 1936, showed no correlation between atherosclerosis and blood levels of cholesterol (1), and Mathur et al, in 1961, confirmed these conclusions after performing 200 human autopsies. (2).)

Schoenheimer’s mice, on the other hand, synthesised small amounts of cholesterol in response to large dietary intake, and conversely, synthesised large amounts when fed small amounts of cholesterol, thereby demonstrating the presence of  a  bio-feedback system, whereby  the end product of a synthetic pathway interrupts  the regular mechanics of that pathway in an inhibitory fashion.

The intricate  mechanisms of the bio-feedback system  were described by Gordon Gould in 1950, following his demonstration of decreased cholesterol synthesis by the liver in response to an increased intake of dietary cholesterol, and increased biosynthesis in response to a decreased intake. We now know that most of plasma cholesterol is synthesised in the liver, and that only about 15% is derived from absorption through the gut, and that a healthy liver maintains homeostatic cholesterol levels through its bio-feedback system, for essential biochemical functions.

It is also worth noting that the discoveries of Schoenheim and Gould are not well known, whereas the hypothesis of Anitschkow  is well known, despite its flawed methodology and invalid conclusions.

Also noteworthy, is the observation that 3 years later Ancel Keys produced his 6 Country Study, purporting to link coronary heart disease to a  high cholesterol diet. (3).

This exercise was doomed to failure  by  Keys’ clear disregard for available data from 22 countries which contradicted his hypothesis.  ( 4 ).

Keys embarked on another study ( 1958-1964) to promote his earlier hypothesis, and produced the well known 7 Countries Study in which he attempted to link dietary fat and coronary heart disease by analysing data from 16 selected populations in 7 Countries.

Again, Keys ignored data which contradicted his hypothesis, by selectively excluding populations within these countries where the incidence of coronary heart disease (CHD) did not correlate with dietary patterns  of fat intake.

Prof. Yudkin, from theUniversityofLondon, conducted a similar study to distinguish hypothesis from fact, and concluded that the proponents of the lipid hypothesis were quoting only those data “which supported their view” (5).

His data contradicted the conclusions of Keys, showing vast differences in Coronary Heart Disease (CHD) mortality between countries despite similarities in total fat intake.

The value of Yadkin’s analysis lies in the revelation that total calorie intake, from various sources, rather than from dietary fat alone, was linked to CHD.

Another factor contributing to the weakness of this study was the fact that in 1960 transfats and n-3 polyunsaturated fats (PUFAS) could not be identified, a fact attested to by Henry Blackburn, a project officer in the study at that time, who acknowledged the selection bias by stating that it was based on “convenience”.

(The study was limited to information about saturated fats (SFA), monounsaturated fats (MUFA), and polyunsaturated fats (PUFAS) raising questions about its accuracy in respect of types of fat being studied.)


Data from the WHO MONICA PROJECT (Monitering Trends in Cardiovascular Disease)  reflects recorded blood cholesterol levels in population groups from 27 different countries, and found none of the correlations between such levels and coronary heart disease, clearly contradicting the hypothesis of Keys.

His hypothesis, while severely criticised by some of his colleagues, nevertheless flourished, by virtue of his powerful position within the American Heart Association (AHA).

Despite the failure of these 2 studies, the AHA Nutrition Advisory Committee promoted the underlying hypothesis, enabling its acceptance into official policy, and its incorporation into the dietary guidelines of the AHA in 1961. (7).

The AHA continues to propagate the hypothesis that dietary saturated fat and cholesterol are the major culprits in the incidence of CHD, and their guidelines consistently call for dietary reductions of cholesterol containing foods, ostensibly, to reduce the risk of cardiovascular disease, a major cause of mortality in the western world.

Contrary to the recommendations from prevailing guidelines, numerous lines of research have shown no correlation between levels of serum cholesterol and dietary intake of saturated fats, even where 20%-50% of calories were derived from saturated fats.

It is an unfortunate fact of history that many bio-medical models, worldwide, ignore the findings of MONICA PROJECT, and choose to propagate these unfounded dietary perceptions, thereby perpetuating a hypothesis that was not rooted in scientific evidence, and   doomed at its outset.


The diet heart idea is based on the propositions that :

(i)                 The amount and type of fat we eat determines the level of cholesterol in our blood. This refers to dietary cholesterol and saturated fats, primarily from animal products, such as butter, meat, milk and eggs, and also products derived from palm and coconut oils.

(ii)               That high levels of blood cholesterol are dangerous in that they cause atherosclerosis, and should thus be avoided through dietary restriction, or by reduction and substitution with unsaturated fats, or reduction  by drug intervention with cholesterol-lowering agents.

(iii)             Atherosclerosis causes coronary heart disease (CHD) by the blockage of coronary arteries, as a consequence of consuming dietary cholesterol and saturated fats.

Not only do these presuppositions remain unproven, but they have also been proved to be false. They nevertheless form the basis of guidelines that were propagated by the American Heart Association (AHA), and continue to influence  bio-medical models  on a world-wide scale by shaping national health directives and public health recommendations to reduce dietary saturated fats in order to maintain “heart health” .



The AHA continues to promote the perception that dietary fat intake and obesity and heart disease are causally linked, and that “low fat” and “fat free” are synonymous with “heart health”.

Policy statements by the AHA have been unquestioningly incorporated into the collective wisdom of health authorities, globally and nationally, finding expression in public health warnings about the dangers of fat and cholesterol.

(Several health bodies inIreland have authoritatively echoed these sentiments in their official literature . By so doing they ignore the critical evidence that contradicts these statements, while  promoting dietary principles that have questionable value.)

The official website of the AHA contains fearsome dietary warnings that clearly bolster the “anti-fat “ campaign. It says, “ Eating food that contain saturated fats raises the level of cholesterol in your blood. High levels of blood cholesterol increase your risk of heart disease or stroke. Be aware too, that many foods high in saturated fat are high in cholesterol which raises your blood cholesterol even higher “.

The website then recommends preferable substitutes for saturated fat, such as vegetable oils and vegetable replacements for traditional meat and dairy products. It also recommends the avoidance of tropical oils in favour of vegetable oils. (8).

The AHA and the Heart and Lung and  Blood Institute (HLBI) recommend reductions in dietary fat intake to treat or prevent coronary artery disease (CAD), calling for intakes of 30% (a reduction from 40% in the 1960s) of total calorie energy, and the American Cancer Society has called for a 50% reduction in fat intake, from 40% to 20 %, for the prevention of colon and breast cancer. (9).

Their agreed policy is for a reduction of saturated fat from 11% to 6% or 8% of energy intake, along with a reduction in dietary cholesterol. They further recommend an elimination of saturated  fat from the diet and replacement by carbohydrates from grains, vegetables, legumes and fruit.




Recommendations by the AHA to replace tropical oils with vegetable oils are linked to historical events in which political and economic forces served to entrench and support the vegetable oil industry at the expense of the tropical oil industry. (10)

This gave rise to the “Dietary Goals for the United States”, which in the absence of supportive scientific evidence, was published by the Senate Select Committee on Nutrition and Human Needs in 1977, in which it was reported that, “saturated fat causes heart disease”.

In 1984 the results of the Lipid Research Clinics Coronary Prevention Trial (LRC-CPPT) were published,  prompting the National Institute of Health (NIH) and the National Cholesterol Education Programme (NCEP), and the AHA to launch an aggressive low fat campaign to the American public based on a clinical trial which showed only a 0.04% absolute reduction of heart disease for the cholesterol lowering effect of cholestyramine, despite the exaggerated claims of a 24% risk reduction, which was relative (RRR),  rather than absolute (ARR) .

The wisdom of the policy has been questioned repeatedly by various researchers, and the strength of the purported evidence, not only challenged, but clearly weakened by contradictions within the evidence itself.


A plethora of studies, at great cost and over many years, have been conducted for purposes of justifying the diet-heart idea.

Strong positive correlations between saturated,  animal , dairy and total fat intake and CHD were shown in several large ecological studies, but, as in the 7 Countries Study, selective bias invariably influenced their interpretations, and the wide variations in lifestyle, geneticicity and ethnicity within these communities rendered their data invalid as evidence for a causal relationship between SFA intake and CHD.

Schaeffer comments that, unfortunately, this type of data is still being used to support the lipid hypothesis of CHD. (11).


Attempts to overcome the inherent weaknesses of ecological and case control studies were sought by conducting prospective (cohort ) studies, hopefully reducing bias, and assessing dietary patterns prior to diagnoses of disease being made, and comparing controls with intervention groups from the same cohort.

A review of  reports from 24 cohort studies investigating the association between SFA and the risk of CHD showed positive associations in only 4, these being the Honolulu Heart Study , theIreland– Boston Study , A Canadian Study,  and a U.K Study, thereby raising questions about the purported role of saturated fatty acids and polyunsaturated fats in cardiovascular disease.( 12).

Better known amongst the cohort studies are the 3 largest, namely, The Nurses Health Study (13), Health Professionals Study ( 14), and the Alpha Tocopheral, Beta Carotene Cancer Prevention Study ( 15 ).

In neither of these major studies was a positive association shown between SFA intake and

CHD risk.

Hu et al have likewise concluded that the number of cohort studies that have directly addressed associations between dietary intake and risk of CHD is “ surprisingly small and the results are not consistent”.

Could such a recognition eventually bring about a paradigm shift ?


 In a 20 year follow-up on women in the Nurses Health Study researchers from the Department of Nutrition, Harvard Public School of Health reported that “ diets lower in carbohydrates and higher in protein and fat are not associated with increased risk of CHD in women. When vegetable sources of fat and protein are chosen, these diets may moderately reduce the risk of CHD”  (16).

The Harvard Public School of Health, nevertheless, continues to promote the mantra that “saturated fat and cholesterol appear to increase the risk of coronary heart disease as predicted by their effects on blood lipids”. (17).

In a search for Optimal Diets for Prevention of Coronary Heart Disease, Hu and Willett, at HarvardPublic School, reported reviews from 147 selected studies claiming “compelling evidence from metabolic studies, prospective cohort studies, and clinical trials in the past several decades to support substituting unsaturated fats for saturated fats as a strategy in preventing CHD.”  (18).

It is clear from the studies quoted above that no such “compelling evidence” existed, a fact attested to later by Frank Hu in his call for a “paradigm shift” in respect of the low fat campaign. (2007).

The HarvardPublic SchoolHeartbeat Newsletter (27 Oct., 2009) continues to promote PUFAS on the grounds that they lower LDL at the expense of saturated fats (SFA). The School, in fact, prioritises  LDL lowering,  while  failing to emphasise the important role that SFA play in raising anti-atherogenic HDL. Their Health message advises “to lower your LDL by cutting back on saturated fat, substituting extra-lean ground beef for regular, low fat or skim milk for whole milk, vegetable oil margarine for butter…”

Furthermore, they continue to vilify saturated fats by wrongly including them amongst the harmful trans fats, stating, “transfats boost LDL as much as saturated fats do” .

This statement ignores the distinctive differences between these types of fats in respect of their physiological properties and biological functions, ignoring the potential health benefits of SFA.

It is refreshing, and timely, to note the reversal of opinion in an editorial comment by Frank Hu  (Harvard Public School of Health) stating the “NEED FOR A PARADIGM SHIFT” in respect of the “ the low fat campaign…to reduce saturated fat intake”. He acknowledges that “this hypothesis has since played a major role in shaping national dietary guidelines”  which resulted in the “incrimination of all fats, despite clear evidence that this view was not supported scientifically”. ( 19).

In defense of the diet – heart hypothesis Daniel Steinberg  refers to the “skeptics vs the preponderence of evidence”. But the “preponderence of evidence” is clearly absent, as suggested by the capitulation and revised opinion of Dr. Frank Hu, of Harvard.

There has,  in fact,  never been scientific support for the Diet-Heart idea. The absence of compelling evidence from epidemiological studies to show a positive association between SFA and CHD risk, and likewise, a protective effect for CVD by substituting polyunsaturated fatty acids (PUFAs) was clear , and this  fact created the need for randomised controlled trials (RCT) to be conducted.


A search for evidence for a causal link between dietary SFA and CHD prompted the following trials:

(a). The London Hospital Trial involving 80 patients in which the groups eating a fat-restricted diet had a higher mortality rate than the control group.

(b)  Medical Research Council involving 252 males following a first myocardial infarction in which an intervention group ate a low fat diet compared to a control group eating a normal diet. Serum cholesterol levels were lower in the intervention group, but there was no significant difference in mortality between the 2 groups.

(c ).  The Oslo Diet Heart Study involved 412 males and compared a control group with a dietary intervention group consuming SFA (8.5%), PUFA (20.7%) and MUFA (10.2%). As a secondary prevention trial there were fewer relapses in the intervention group, and lower CV and total mortality, but not of statistical significance.

(d).  Soybean Oil Study , involving 393 males following a first myocardial infarction and randomised to 2 groups comparing their  normal diet and a 80g low-saturated fat meal daily.

Although serum cholesterol was lowered by an average of 22 % in the intervention group there was no difference in fatal CHD after 7 years.

(e). The Los Angeles Veteran Study compared the outcome of 2 groups of veterans, some with and others without, a history of CVD. The control group included 40% of energy from animal fats in their normal diet and the intervention group had 2/3 of animal fat replaced by vegetable oils. Although there was no statistical difference for myocardial infarction or sudden death between the groups, overall total mortality was greater in the intervention group. (lower fat intake).

(f). The Sydney Diet- Heart Study: compared the outcome of  2 groups of  males following a first myocardial infarction. The control group obtained 13.5% of energy from SFA, including butter, and 9.5% of energy from PUFA , while the intervention group substituted margarine (PUFA) for butter, obtaining 9.8% energy from SFA and 15.1% from PUFA. After 5 years more subjects in the PUFA group (16.7%) had died than in the SAFA group (11.8%).

(g). The Finnish Mental Hospitals Study : compared the diets in 2 hospitals over a 12 year period, swopping diets after the first 6 years. A comparison was made between a low cholesterol diet including PUFA margarine and soybean milk, and a cholesterol diet including butter and whole milk. No mortality benefits were evident from the intervention diets, despite  a 15% lowering of cholesterol. The weakness of the trial was its hospital based diets, rather than  a study of the individual diets of the inpatient participants, many of whom smoked or were on medication. No allowances were made for these distinctive lifestyle differences in the patients.

(h).  The Minnesota Coronary Survey:  A primary prevention study involving 9057 institutionalised males and females in which there was no difference in CV events, or death or total mortality, between  2 groups with 39% vs 38% energy from fat, with the  control group ingesting 18% from SFA  and 5% from PUFA and the intervention group ingesting 9% from SFA and 15% from PUFA. Both groups had a similar intake of MUFA (16% vs 14%).


Several well-known studies have tested the benefits for cardiovascular health of multiple dietary and lifestyle interventions. These studies were not consistent in their design and significant variations in respect of their diets, drugs and lifestyle changes rendered them unsuitable to gauge the role of SFA in cholesterol levels or CHD events.

Collectively, their results did not show a benefit for total mortality, apart from the Indian Diet Heart Study in which the group ingesting fruit, vegetables and nuts reflected a lower mortality rate than the control group which was on a low fat diet, and the Lyon Diet Heart Study which compared outcome from a “prudent “ diet and a “Mediterranean “ diet, and in which fewer events and deaths were recorded in the  intervention group, despite no differences in total cholesterol, LDL-C or HDL-C between the 2 groups.


(a)       The Tecumseh Study :  In a 24 hour dietary recall of 957 men and 1082 women

preceeding venipuncture for lipid determination, serum cholesterol and triglyceride

levels were unrelated to quality, quantity, or proportions of fat, carbohydrate, or protein

consumed in the 24 hour recall period. (20 ).

(b)      A review by Ahrens E.H. in 1979 concludes that a reduction in dietary fat is considered

to be “unwise, impractical, and unlikely to lead to a reduced incidence of

arteriosclerotic disease” ( 21 ).

(c )   In an assessment of dietary prevention of coronary heart disease Conor W.E. showed

that increases in dietary cholesterol between 500mg and 600mg per day resulted in little

additional change in plasma cholesterol. ( 22 ).

(d )   The effects of fat modified diets were shown in a survey by Vessby et al to be a

reduction in HDL-C, which were not reversed on a polyunsaturated fatty acid (PUFA)

diet. (23).

(Note: The AHA recommends a PUFA diet in place of SFA diets.)

(e )  A commentary by Reiser R. on the Rationale of the Diet-Heart Statement of the

American Heart Association (AHA) examined the original publications on which the

recommendations of the AHA were based, and found them to be “obsolete or

misquoted”. The Rationale also reported that “all dietary intervention trials were flawed

in one  or another aspect of experimental design”. ( 24. )


(f)      A descriptive overview of 16 published controlled trials was conducted by Ramsay et al to evaluate the long term efficacy of diets in lowering serum cholesterol concentration. Their conclusions stated that the response to the step 1 diets of the NECP were too small to have any value in the clinical management of adults with serum cholesterol concentrations above 6.5 mmol/L. (25).

(g)     Dr. Uffe Ravnskov examined the quotation bias in reviews of the diet-heart idea enabling him to dispute the argument that ““consensus committees have settled the issue unanimously”. He examines 3 recent authoritative reviews which defend the diet-heart idea and reveals their inherent  flaws. (26 ).

(h)     A systematic overview of 19 randomised controlled trials (RCT) by OxfordUniversityresearchers  concluded that individualised dietary advice for reducing cholesterol is modestly effective in free-living subjects. (27).

(i)       A prospective cohort study of 80082 women in the Nurses’Health Study  examined the effects of dietary saturated fatty acids on blood lipids, and concluded that intakes of short to medium-chain saturated fatty acids were not significantly associated with the risk of CHD. ( 28).

(j)       The impact of egg limitations on coronary heart disease risk was assessed by McNamara at the Egg Nutrition Centre. A review of 167 cholesterol- feeding studies indicates that dietary cholesterol increases both LDL and HDL cholesterol, with little change in the LDL: HDL ratio. These data help explain the epidemiological studies showing that dietary cholesterol is not related to coronary heart disease incidence or mortality across or within populations. (29).

(k)     The relationship between dietary cholesterol, plasma cholesterol and atherosclerosis is reviewed by McNamara  with reference to animal feeding studies, epidemiological surveys and clinical trials. The review concludes that there is a null relationship between dietary cholesterol and coronary heart disease morbidity and mortality, and that dietary cholesterol has little effect on the plasma LDL: HDL ratio. (30 ).

(l)       The differences in risk factors for coronary heart disease among the three main ethnic groups in Singapore were investigated in a cross sectional study. Dietary factors , while correlating with serum cholesterol at a group level, did not explain the differences in serum cholesterol levels between ethnic groups independently of age, obesity, occupation and other lifestyle risk factors. (31).

(m)   The Dietary Effects on cardiovascular disease risk  factors are reviewed by Nicolosi et al in a summary of dietary intervention outcomes.  Dietary reductions of saturated fats were shown to  not only decrease LDL, but also HDL, thus harming the lipid profile. Dietary interventions which do not alter the lipoprotein fractions are also considered in this review. ( 32 ).

(n)     Ravnskov describes the diet-heart idea as an hypothesis out of date, and is maintained only because allegedly supportive , but insignificant findings, are inflated, and because most contradictory results are misinterpreted, misquoted or ignored. (33) .

(o)     The Diet-heart hypothesis: a critique by S.L Weinberg, MD. “This diet (low fat-high carbohydrate ) can no longer be defended by appeal to the authority of prestigious medical organizations  or by rejecting clinical experience and a growing medical literature suggesting that the much-maligned low carbohydrate-high protein diet may have a salutary effect on the epidemics in question”. ( 34) .

(p)     Effects of dietary saturated fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids  and apolipoproteins: A meta-analysis by Mensink et al of 60 controlled trials evaluating the effects of the amount and type of fat on total:HDL – cholesterol and on other lipids showed that Lauric acid decreased the ratio the most, with little effect by Myristic  and Palmitic acids, and slight effects by Stearic acid. (35).

(q)     In the Medical Research Council National Survey of Health and Development (UK) results from a cohort of  British adults in 1989 and 1999 found that consumption of red or processed meat assessed separately was not related to the major risk factors for CHD. (36).

(r)       A reappraisal of the impact of dairy foods and milk fat on cardiovascular disease risk was conducted by a conference of scientists for purposes of considering the scientific basis for the current recommendations to reduce the intake of saturated fats. The conclusion of the conference was that “ there is no clear evidence that dairy food consumption is consistently associated with a higher risk of CVD”  and “recommendations to reduce dairy food consumption irrespective of the nature of the dairy product should be made with caution”. (37).

(s)      Challenging the Role of Dietary Cholesterol:  A panel of International Experts in genetics, nutrition, fatty acid, cholesterol metabolism and coronary heart disease reviewed the evolutionary aspects of human diets, and in a recent publication postulated the role of an imbalance between omega –6 and omega- 3 PUFA in the incidence of CHD. (38) .


Evidence for a causal relationship between dietary cholesterol and saturated fats has never been demonstrated, and the mortality benefits derived from higher levels of  SFA compared with low fat diets suggest property mechanisms that are inherent within specific SFA.

During 1969 – 1971 the measurement of VLDL, LDL and HDL were added to testing protocols for CVD risk assessment,  and HDL was defined as a protective factor against CAD.  However, supportive arguments for the Diet-Heart idea, and the restricting of dietary SFA, are generally based on the perceived dangers of raised total cholesterol and LDL levels.

TheInstituteofMedicine, in 2002, several years later, recommended calls for a saturated fat intake “as low as possible” since these fats “boost the level of harmful low density cholesterol (LDL-C) in the bloodstream”.

The earlier recognition that dietary SFA raised total cholesterol by virtue of HDL-C increases did not modify the recommendations to limit SFA intake, and these recommendations continue to dominate current dietary guidelines.

The role of SFA in favourably modifying lipoproteins has become an area of intense enquiry in recent years, with added implications for protection against cardiovascular disease and consumer dietary choices.


Not all SFA are identical in hypercholesterolaemic potential (raising cholesterol levels), and their capacity for modifying lipoproteins depends on chain length, and sole, or combined presence in food sources.

The shorter chain SFA (C4,C6,C8,C10) do not raise serum cholesterol since they are transported directly to the liver after absorption, via the portal system, and not incorporated into chylomicrons.

Medium chain SFA  appear to have variable cholesterol raising effects, the accuracy of which is not easily determined, but these changes are due to increases in HDL, which is more marked with Lauric acid, and less so with Myristic, Palmitic and Stearic acids. (39).

Increases in HDL improve the (total cholesterol) TC: HDL ratio, which is a more specific marker than either LDL or total serum cholesterol, ( 40 ),   and while all fatty acids elevate HDL when substituted for carbohydrates, the effect is diminished with increasing unsaturation of the fat. (41).

In other words, the more saturated the fats, the better the TC : HDL ratio with greater potential for cardiovascular protection.(42).

Kraus et al confirmed these findings in a 2006 study, by showing that a diet rich in SFA resulted in a steady state concentration of total and LDL cholesterol and an increase in the HDL concentration regardless of reduced dietary energy. (43 ).

Mozaffarian et al demonstrated a reduced progression of coronary atherosclerosis in post menopausal women with a greater saturated fat intake. ( 44).

Conversely, reductions in dietary saturated fats were shown by Bergland et al to adversely affect HDL- sub-populations by decreasing the larger HDL2-cholesterol concentrations.

HDL2 particles are less dense than HDL3 particles and have greater anti-atherogenic potential.

A high HDL2 : HDL3 ratio is thus favourable as an anti-atherogenic marker, as demonstrated by Tholstrup in 1994. ( 45).

A higher SFA diet improved HDL2 levels and the anti-atherogenic potential in  patients with documented atherosclerotic cardiovascular disease. (46).

Recommendations ( according to the AHA)  to limit the intake of SFA may lead to their replacement with carbohydrates, which may give rise to unwanted elevations of triglycerides, and a decrease in the protective HDL sub-populations. (47).


The underlying metabolic cause of CAD in many patients is not elevated serum cholesterol.

In fact, the Framingham Study reported that 80% of individuals who go on to have a CAD have the same total blood cholesterol values as those who do not suffer a similar event.

The most common metabolic contributor to CAD is the atherogenic lipoprotein profile, characterised by an abundance of highly atherogenic small, dense low density lipoprotein particles (SD-LDL), and a deficiency of high density lipoprotein HDL2b subtypes, most commonly associated with CAD protection. This trait is present in 50% of men with CAD, and is not reflected by total or LDL values. ( 48).


Recent lines of study have expanded our understanding of metabolic issues that contribute to CAD, by identifying the small dense LDL trait, an inherited disorder linked to a position on chromosome 19 reflected by a predominance of small dense LDL particles and which is present in 50 % of men with CAD, and which is independent of LDL concentrations. (49).


The predominance of these small dense LDL particles is called the atherogenic lipoprotein particle (ALP), since it is linked to several pro-atherogenic influences, such as greater susceptibility to oxidative damage, and reduction in high density lipoprotein 2b (HDL2b) which plays a predominant role in reverse cholesterol transport.


4 major studies (Boston Area Health Study, Physicians Health Survey, The Standard Five City Project, and The Quebec Canadian Study ) (50) all confirmed the presence of small dense LDL particles as providing a 3-fold increase in risk for cardiovascular events.


This risk factor is not identified by measurement of total cholesterol or LDL and is a likely explanation for the high incidence of CAD in the majority of patients who do not have raised levels of cholesterol.


Reductions of small dense LDL are evident after carbohydrate restricted diets and exercise ( 51),  and increases are also associated with low SFA and low cholesterol intakes.(52).


Dreon et al found that dietary SFA were associated with increases in larger LDL particles, and decreases in the atherogenic small dense LDL particles. (53).


Krause et al, in 2006, confirmed that a high SFA diet decreases these small dense LDL particles. (54).


The high carbohydrate – low fat diet, currently being recommended by national health authorities as a preventative measure for CHD, may reduce serum LDL, but they are also likely to  reduce beneficial HDL, and increase atherogenic small dense LDL particles.


Whereas the large, buoyant  LDL particles are protective against CVD they have been shown, in men, to undergo change in response to a low fat – high carbohydrate diet, with a phenotype shift characterised by a preponderance of small dense LDL particles.


Dreon, A J. showed that a low fat diet is not associated with improved lipoprotein profiles in these subjects. (55).




Specific apolipoproteins are attached to each of the known lipoproteins and are likewise subjected to similar, but not identical, dietary influences that affect lipoproteins.ApoA is attached to HDL and apo B is attached to LDL, and also to IDL, VLDL and Lp(a).


ApoC-iii is also an independent risk factor for CHD and impairs the clearance of  Apo B from the circulation through inhibition of lipoprotein lipase activity.


Apolipoproteins play a key role in both the structure and function of plasma lipoproteins. Genetically controlled variations of apolipoprotein can affect lipoprotein structure, composition and metabolism. For example, polymorphic forms of apolipoprotein E (apo E) interact with dietary fats to influence plasma lipoprotein concentrations. Thus assessments of apo E  phenotypes is useful in the diagnosis of familial dyslipoproteinaemia.


The effect of dietary SFA on LDL size is influenced by apoE genotype in healthy subjects.


In aCosta Ricastudy a high SFA diet elicited a greater LDL response in carriers of the apo E2 (17%) and apoE4 (14%) compared to non-carriers (6%).

Variability in susceptibility to CHD in the presence of dietary fats is likely due to the presence or absence of these genetic variations. (56).


A small study by Smith D.R et al compared the effects of lean beef enriched in oleic acid, on ten hypercholesterolaemic men and found that apo A-1, but not HDL or LDL were sensitive to the dietary beef. ( 57).


In another small study of Puma Indian subjects, by Abbott et al, a high fat/high carbohydrate diet contributed to a decrease in LDL in all the subjects. This was not a purely SFA diet, however. ( 58 ).


A Dutch study by Sundram K, et al, involving 38 males, demonstrated that Palm oil, as maximised in a Dutch-type diet significantly increased levels of apoA-1, while reducing apoB. Palm oil has a polyunsaturated/ saturated fat (P:S)   ratio of 0.2.

HDL2 was increased and the apoB: apo A ratio was significantly decreased, thereby conferring an anti-atherogenic benefit. There were no significant effects on total cholesterol levels.

In a similar study in 1984, Heine R.J. et al tested the effects on serum lipoproteins in rhesus monkeys following a high polyunsaturated / saturated fat (P:S =2.2) and a low polyunsaturated / saturated fat diet (P:S = 0.3) and found the high P:S diet decreased LDL, but also decreased HDL by 23%  and apoA-1 BY 13 %. , thereby showing greater benefit for the high saturated fat diet compared to the high PUFA diet.  ( 59).


In the AMORIS study by Walldius G. et al the apo A : apo B ratio was  found to be highly predictive of risk for fatal myocardial infarction (MI), even in the case of normal or low concentrations of LDL- C.  The INTERHEART study confirmed these findings in a study based on 30,000 individuals from 52 countries. ( 60).


In the  MONICA/KORA   (AUGSBURG) study 1414 men and 1436 women were investigated and their high apo B levels showed a strong relationship to increased risk of MI, which also correlated with apo B : apo A-1 ratios. (61).


Since dietary SFA raise HDL levels they  are more likely to improve the apo A: apo B ratio, and thereby confer a health benefit rather than risk for CHD.




Lipoprotein (a) is a lipoprotein particle in which the protein ( apolipoprotein B-100) is chemically linked to another protein, its levels being genetically (KIV-2) determined.

Increased blood levels of Lp(a) are associated with a 2-3 times increased risk for cardiovascular disease, according to a recent Danish study reported in the Journal of the American Medical Association. (62).


Lowering  Lp(a) levels is thus likely to reduce the risk of CHD, and since statins, which reduce blood LDL levels, do not lower Lp(a),  novel and alternative therapeutic agents for this purpose have been called for by Dr. Borge Nordestgaard, a lead researcher in the Danish study.


However, it has long been known, but not widely recognised, that dietary SFA reduce Lp(a) levels, thereby imparting cardiovascular benefits.


In a comparison of risk factors for premature CHD in men, Genest et al, in 1992, graded in decreasing order of significance the following factors : smoking > hypertension > decreased apo A-1 > increased apo B > increased Lp(a).


In 1995 Almendinger et al demonstrated the cardio-protective properties of butterfat over partially hydrogenated soybean and partially hydrogenated fish oil by virtue of butterfat causing a comparative decrease in Lp(a) levels.


Ginsberg , in 1998, demonstrated similar effects, with increases in Lp(a) levels when SFA levels were reduced, while maintaining constant levels of MUFAS, PUFAS and cholesterol. ( 63).


In 2004 Silaste et al demonstrated that serial reductions in levels of SFA , from 28 > 20 > 19 resulted in corresponding increases in Lp(a), and when levels of PUFA increased 11> 13 > 19 levels of Lp(a) increased correspondingly, indicating a cardio-protective property of SFA, not demonstrated with PUFAS. ( The AHA and national health bodies recommend a substitution of SFA by PUFAS !). ( 64).


More recently, Shin et al demonstrated increased plasma concentrations of Lp(a) during a low fat diet, high carbohydrate diet , which were also positively linked to increased plasma concentrations of apolipoprotein C-iii bound to apolipoprotein B containing lipoproteins. ( 65) .




.           Emerging lines of evidence strongly support the observations that dietary SFA improve plasma anti-atherogenic lipoproteins, which in turn improve the ratios of apo A : apo B. These improved ratios have been shown to have  a prognostic value for reduced risk of CHD and MI.


Since  these values can be measured directly and are not dependent on the calculations using the Friedewald formula, and are also independent of total cholesterol or LDL levels, the rationale for their incorporation into clinical guidelines  appears to be well founded.   (66).


The medium- chain SFA ,through their  anti-atherogenic properties, confer cardiovascular benefits, rather than risks, when compared to low fat/ high carbohydrate diets, and should be encouraged as part of a healthy diet for cardiovascular protection.


Recommendations to substitute PUFAS or carbohydrates for SFA, as propagated by the AHA, are ill advised since they  are not supported by scientific data, and do not confer demonstrable health benefits.


The consumer public, seeking to minimise the risks for cardio-vascular disease, should be advised  to avoid  dietary selections which include a preponderance of trans-fats, as found in commercially prepared foods,  or excessive intakes of  omega-6 PUFAS,  and to selectively improve their intake of healthy saturated fats, such as whole milk (unskimmed), eggs, butter and animal fats, and to replace polyunsaturated fats and vegetable oils with health giving tropical oils rich in saturated fat.


National Guidelines that warn of the dangers of saturated fats and call for their dietary restriction or substitution on the basis of their hypercholesterolaemic (“high cholesterol”) properties are not supported by the larger body of experimental evidence.



Dr. Neville Wilson.

LeinsterClinic – Medical Suite.

10 January. 2010.





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