1. Dietary recommendations were issued by the
U.S. Select Committee on Nutrition and Human
Needs and the UK National Advisory Committee on
Nutritional Education in 1977 and 1983, respectively.
In each case, the government focused heavily on
reducing consumption of dietary fat to combat coro-
nary heart disease. The official advice was, and re-
mains into 2015, to restrict overall fat intake to 30%
and saturated fat intake to 10% of total calories.
One might assume that the national guidelines
were based on a plethora of hard evidence. Not so,
according to obesity researcher Zoe Harcombe. Ear-
lier this year, her team published a review and meta-
analysis of randomized controlled trials accessible in
1983 to the U.S. and UK committee members. Their
conclusion? The “best evidence” then available “did
not support the contention that reducing dietary fat
intake would contribute to a reduction in coronary
heart disease or related mortality.”1
Harcombe et al. narrowed their collection of
professional literature down to six relevant studies
including a total of 740 deaths, 423 from coronary
heart disease, among 2,467 participants—all male.
Every trial but one had examined only secondary
prevention participants—in other words, those who
had already experienced myocardial infarction. The
remaining study was composed of 20% secondary
and 80% primary prevention subjects.
Somewhat interestingly, five of the six trials
never examined the effects of dietary interventions
set at levels matching the eventual recommenda-
tions. The one study that had examined the conse-
quences of a diet limited to 10% saturated fat,
according to Harcombe, actually “reported a higher
incidence of all-cause mortality and coronary heart
disease in the intervention group.”
In fact, Harcombe et al.’s overall analysis re-
vealed no statistically significant relationship be-
tween dietary intervention and either all-cause
mortality or heart deaths, despite the fact that re-
ductions in mean serum (blood) cholesterol levels
were significantly greater among the intervention
groups. This, they insist, “undermines the role of
serum cholesterol levels as an intermediary to the
development of coronary heart disease and contra-
venes the theory that reducing fat generally and sat-
urated fat particularly potentiates a reduction in
coronary heart disease.”
As such, Harcombe concludes, “it seems in-
comprehensible that dietary advice was introduced
for 220 million Americans and 56 million UK citi-
zens, given the contrary results from a small num-
ber of unhealthy men.” And because other reviews
of more recent evidence have also questioned the
same diet-heart hypothesis upon which these rec-
ommendations were based, her group contends, our
governments’ “dietary advice not merely needs re-
view; it should not have been introduced” in the
first place.
Harcombe’s position on the diet-heart hypothe-
sis is characteristic of an expanding and increas-
ingly popular minority view that saturated dietary
fats in particular have been wrongly demonized as
killers. In this article, I’ll briefly discuss the debate’s
history and many of the most important studies and
reviews published by nutrition researchers on each
side of the scientific rift. In some cases—to reveal
the debate’s curious ferocity on the one hand, and
notable lack of scientific confidence on the other—
I’ll also include certain experts’ personal opinions
and criticisms. Finally, I’ll attempt to expose what
the science really says, if anything, about the much-
disputed diet-heart hypothesis and the foods we re-
ally ought to eat.
From Proposal to Hypothesis
In the January 4, 1985 issue of Science, investigative
journalist Gina Kolata covered the 47th consensus
panel report from the National Institutes of Health,
published some three weeks earlier. Since 1961, the
American Heart Association had urged Americans
to consume less saturated fat and cholesterol, and
The Diet-Heart
Hypothesis
A Skeptical Analysis
BY KENNETH W. KRAUSE
ARTICLE
2 SKEPTIC MAGAZINE volume 20 number 2 2015

2. recommended its so-called “prudent diet” emphasizing
fruits, vegetables, and vegetable oils.
The NIH had been hesitant to take a firm position on
the controversial diet-heart hypothesis, according to Kolata,
because the scientific literature focusing on the connection
between dietary cholesterol and saturated fatty acids (SFA)
on the one hand, and heart disease on the other, did “not
show that lowering cholesterol makes a difference.”2
But the NIH’s hesitancy was finally overcome by the re-
sults of a then-new study conducted by the National Heart,
Lung and Blood Institute on the effects of a cholesterol-re-
ducing diet along with a drug, cholestyramine, on about
4,000 middle-aged men with elevated serum cholesterol lev-
els.3
On average, the intervention group’s cholesterol had
plunged by 13.4% since the investigation began in 1973, or
8.5% better than the average decrease found among placebo-
treated controls.
According to the NHLBI, its researchers had provided not
only “strong evidence” of a “causal role” for low-density
lipoprotein cholesterol, or LDL-C, in the pathogenesis of coro-
nary heart disease (CHD), but good reason as well to extend
its findings to “other age groups and women” along with “oth-
ers with more modest elevations of serum cholesterol.”
Others were less impressed. In an interview with Kolata,
University of Chicago and frequent NIH statistician, Paul
Meier, deemed the new study’s findings “weak,” referring to
the disappointing and statistically insignificant distinction be-
tween the intervention and control groups in terms of deaths
from all causes. And although incidences of angina, bypass
surgery, and abnormal exercise electrocardiograms all dropped
in the modified diet-drug group, Kolata judged that the new
study had “failed, as every other trial did, to prove that lower-
ing blood cholesterol saves lives.”
But perhaps most provocative was the panel’s recom-
mendation that all Americans from the age of two should re-
duce their consumption of SFA and cholesterol. Also
interviewed by Kolata, Thomas Chalmers of the Mt. Sinai
Medical School argued that the report “made an uncon-
scionable exaggeration of the data,” emphasizing that “there
is absolutely no evidence that it’s safe for children to be on a
cholesterol-lowering diet.”
In a subsequent letter to Science, Daniel Steinberg, who
had chaired the NIH consensus development conference, crit-
icized Kolata for devoting the lion’s share of her article to “no
more than a handful among some 600 conferees.”4
“The
panel’s recommendation,” he countered, “is sound when all of
the evidence is taken into account.” Such evidence also
quickly led to the National Cholesterol Education Program in
1985, a new NIH administration created to instruct physicians
how to identify and treat “at-risk” patients.
In fact, there was much agreement among the confer-
ees. But dissent in 1984 was both loud and determined, as it
remains at the dawn of 2015. The differences between the
debates then and now are as multifactorial as heart disease
itself. Journalists and popular authors publish infuriated or
one-sided narratives alleging conspiracies between re-
searchers, big food, and government agencies to intention-
ally mislead the public for personal gain. And while new
studies and reviews have lately called the very foundations of
the diet-heart hypothesis into question, some leading scien-
tists have entrenched themselves as well, separating into
mutually antagonistic nutritional camps.
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3. From Hypothesis to Policy
The classic diet-heart hypothesis (D-Hh) posits
simply enough that diets high in SFA and choles-
terol (and low in polyunsaturated fatty acids
[PUFA]) raise serum total and LDL cholesterol lev-
els and lead to the accumulation of atheromatous
plaques. These plaques gradually narrow coronary
arteries, reduce blood flow to the heart, and can
eventuate in myocardial infarction.
Early evidence linking heart disease to foods
rich in cholesterol (and SFA), including red meat,
eggs, and shellfish, derived from animal experi-
ments. In 1913, for example, a Russian pathologist
reported the ability to induce atherosclerotic-like
lesions in rabbits by feeding them copious amounts
of cholesterol.5
Others soon replicated these re-
sults, mainly with other herbivorous animals. Many
researchers objected, however, that such creatures
were naturally ill-suited to metabolize cholesterol.
And when similar experiments were carried out on
non-herbivorous (and more human-like) dogs, they
added, the animals appeared to tolerate the choles-
terol much better.
But the D-Hh wasn’t formally articulated until
University of Minnesota physiologist Ancel Keys
presented the concept in 1952 at Mt. Sinai hospital
in New York. Also published in a famous paper the
following year, Keys employed a simple yet power-
ful graph correlating in precise curvilinear fashion
total fat intake as a percentage of all calories with
death rates from heart disease among men in six
countries—Japan, Italy, England and Wales, Aus-
tralia, Canada, and the United States.6
Detractors claimed that Keys intentionally ig-
nored data from 22 other countries. And when re-
searchers scrutinized additional data from those
nations, they found not only that Keys’ correlation
was greatly diminished, but that no association
whatsoever existed between dietary fats and death
from all causes.7
Nevertheless, according to James
DiNicolantonio, a cardiovascular researcher at St.
Luke’s Mid America Heart Institute, Keys’ early
data “seemingly led us down the wrong ‘dietary-
road’ for decades to follow.”8
Nevertheless, the most convincing early evi-
dence for the D-Hh may have originated from Keys’
Seven Countries Study of 16 cohorts (12,763 rural
males age 40-59) in Greece, Italy, the former Yu-
goslavia, the Netherlands, Finland, the U.S., and
Japan. By this time, Keys had refined his initial pro-
posal to impugn primarily SFA and animal products
(dietary cholesterol not so much). Indeed, in this,
the first multi-country epidemiological undertaking
in history, coronary mortality and the five-year inci-
dence of CHD were positively correlated with SFA
but not with either total fat or PUFA intake.9
The cross-cultural results were striking. Upon a
25-year follow-up, inter-population death rates from
CHD had differed dramatically. In East Finland, for
example, 268 per 1000 lumberjacks and farmers liv-
ing on diets high in meat and dairy had died. By con-
trast, of the Greeks of Crete who in terms of dietary
fats subsisted on olive oil and very little meat, only
25 per 1000 had perished. Perhaps most notably,
however, SFA had accounted for 22% of the Finns’,
yet only 8% of the Cretans’, total calories.
But Keys was and continues to be criticized for
having “cherry-picked” his Seven Countries data.
Some argue that information from populations in
countries like France, Switzerland, Germany, Nor-
way, or Sweden, for example, might have chal-
lenged Keys’ hypothesis. Some, like journalist Nina
Teicholz, have recently gone so far as to charge that
he deliberately selected “only those nations…that
seemed likely to confirm it.”10
Indeed, Keys’ data was not chosen randomly.
But Henry Blackburn, Keys’ colleague in the Seven
Countries study, sees no reason why the popula-
tions should have been selected entirely by chance.
“Demonstrating a lack of understanding of how sci-
entists approach new questions,” he explains, the
critics ignore the fact that “any savvy scientist at an
early phase of questioning knows to look first not
randomly but across wide variations of the cause
under consideration, in this case diet.”11
Others observed of Keys’ results that CHD
mortality varied widely within certain countries.
“Despite similar risk factors and diet,” Danish inde-
pendent researcher Uffe Ravnskov found that “the
5-year incidence of fatal CHD in Crevalcore, Italy,
was more than twice that in Montegiorgio, while in
Karelia it was five times higher than in West Fin-
land; and on Corfu, 6-7 times higher than on
Crete.”12
Thus, for these and other dissenters, the
supposed correlation between diet and heart dis-
ease was little more than a well-staged illusion.
On May 28, 1980—only five years previous to
the NIH’s consensus report on the same subject—
the Food and Nutrition Board of the National Acad-
emy of Sciences issued a far more controversial
paper, Toward Healthful Diets, finding no clear evi-
dence that reducing serum cholesterol through di-
etary intervention could prevent CHD. Therein, the
15-member Board reproved those “who seek to
change the national diet” for assuming a nominal
risk in widespread dietary adjustment and for rely-
4 SKEPTIC MAGAZINE volume 20 number 2 2015

4. ing so heavily on epidemiological rather than exper-
imental evidence.
Critics of the Board accused its members of
maintaining inappropriately cozy relationships
with big food organizations like the American Egg
Board. In response to the report itself, Robert Levy,
director of the NHLBI, offered the following faint-
hearted guidance: “Existing information indicates
that Americans should hedge their bets and seek a
diet lower in saturated fats and cholesterol, at least
until more evidence is available.”13
At that point, only the Academy and the Ameri-
can Medical Association stood in defiance of the U.S.
government and at least 18 distinguished health or-
ganizations. For better or worse, America had offi-
cially become a low-fat, low-cholesterol nation.
The Modern Macronutrient Wars Begin
In her now-classic tome, Food Politics, Marion Nes-
tle—NYU professor of nutrition and former nutri-
tion science adviser to the DHHS, USDA, and
FDA—affirmed that “scientists consistently have
demonstrated the health benefits of diets rich in
fruits and vegetables [and] limited in foods and fats
of animal origin.”14
She continued:
Decades ago, researchers discovered that high levels
of cholesterol in the blood predispose individuals to
coronary heart disease and that saturated fat (most
prominent in meat and dairy products) raises blood
cholesterol more than monounsaturated fats (typi-
cal of olive oil). They also observed that polyunsatu-
rated fats (most prominent in vegetable seed oils)
reduce blood cholesterol levels.
In fact, by the time Food Politics was first pub-
lished in 2002, every major health organization, in-
cluding the National Academy of Sciences, had
agreed that saturated fatty acids (SFA) raise the risk
of cardiovascular disease (CVD), including coronary
heart disease (CHD), and that their replacement
with either monounsaturated fatty acids (MUFA) or
polyunsaturated fatty acids (PUFA)—including all
Omega 3 and Omega 6 fatty acids—reduces that risk.
But when I contacted Nestle in the summer of
2014 her position seemed less definite. For exam-
ple, when I inquired about the wisdom of current
governmental and non-governmental guidelines re-
lating to SFA intake, most if not all of which warn
the entire public against consumption greater than
10%—in some cases, more than 6%—of total calo-
ries, Nestle flatly replied, “I don’t think the jury is
in yet on this one.”
So what’s the problem? The “jury” seemed to
be “in” decades ago. Despite consistency among of-
ficial guidelines, the research community now
seems hopelessly—indeed, zealously—divided on
the topic. Meanwhile, average Americans grow in-
creasingly confused about dietary fats. Science is
relentlessly progressive by nature, but its nutri-
tional constituent appears paralyzed. Why?
Consider a recent wave of conflicting studies.
In 2009, researchers led by Danish epidemiologist
Marianne Jakobsen, pooled data from 11 cohort
studies to examine the effects of replacing SFA with
MUFA, PUFA, or carbohydrates (CHO) on CHD
risk.15
After 4-10 years of follow-up, along with
5,249 coronary events and 2,155 coronary deaths
among 344,696 participants, Jakobsen et al. con-
cluded that MUFA were unassociated, CHO were
modestly but directly associated, and PUFA were
inversely associated with coronary events. The ef-
fect was not modified by either age or gender.
Thus, consistent with conventional wisdom,
this group argued that “replacing SFA intake with
PUFA intake rather than MUFA or carbohydrate in-
take prevents CHD over a wide range of intakes
and among all middle-aged and older men and
women.” Although such distinctions were not
tested, Jakobsen also suggested that CHO quality—
i.e., fiber content, extent of processing, and
glycemic index—might alter the analysis.
But the modern-day macronutrient wars posi-
tively erupted a year later when four American re-
searchers led by Patty Siri-Tarino published a
meta-analysis of 21 studies finding “insufficient evi-
dence … to conclude that dietary saturated fat is
associated with an increased risk of CHD, stroke, or
CVD.”16
In other words, this group’s rousing judg-
ment had threatened to undercut the very founda-
tion upon which the diet-heart hypothesis (D-Hh)
had been built.
Arguably, however, the Americans’ findings
were not entirely hostile to those of Jakobsen. They
acknowledged, for example, that a decreased risk
often results when SFA are replaced with PUFA. But
their interpretation of the data suggested not that
SFA were independently problematic, but rather that
the benefit of replacement might derive from either
increased PUFA or the PUFA to SFA ratio.
In a companion opinion piece, the Americans
commented further on the relationships between
SFA, CHO, and CVD risk.17
Therein, Siri-Tarino as-
sailed not only existing and proposed guidelines,
but the long-standing use of low-density lipopro-
tein-cholesterol (LDL-C) as the primary biomarker
for CVD risk as well:
volume 20 number 2 2015 WWW.SKEPTIC.COM 5

5. Recommendations for further reductions in satu-
rated fat intake (e.g., to 7% of total energy) are
based primarily on the prediction of a progressive
reduction in CVD risk associated with greater re-
ductions in LDL cholesterol. However, from the
standpoint of implementation, further reductions in
saturated fat intake usually involve…increased pro-
portion of carbohydrate…. [But] the effect of higher
carbohydrate diets, particularly those enriched in
refined carbohydrates, coupled with the rising inci-
dence of overweight and obesity, creates a metabolic
state characterized by elevated triglycerides, re-
duced HDL cholesterol, and increased concentra-
tions of small, dense LDL particles.
Similarly, this group noted that CHO restriction (or
weight loss absent restriction) had been shown to
yield reductions in the total-cholesterol to high-den-
sity lipoprotein-cholesterol (HDL-C) ratio, apolipo-
protein B, and the number of small, dense LDL
particles. In Siri-Tarino’s estimation, these markers
were more closely associated with reduced CVD risk
than LDL-C, which “appears to be specific to [less
dangerous and] larger, more buoyant particles.”
The Americans finally emphasized the data’s
failure to support recommendations for reductions
in SFA below 10% of total calories. While conceding
that SFA might raise CVD risk by increasing inflam-
mation and reducing insulin sensitivity, they insisted
that their relative effect should be reevaluated “given
the changing landscape of CVD risk factors.” Dietary
efforts to curb CVD, they urged, “should primarily
emphasize limitation of refined carbohydrate intakes
and reduction in excess adiposity.”
But the professional response was both swift
and severe.18
Oxford University nutritionist Peter
Scarborough denounced the Americans’ method-
ological design along with their failure to recognize
the “well established” association between SFA,
serum cholesterol, and CVD. Siri-Tarino countered
that her “overall results” remained “robust” and un-
affected by “different analytic strategies” even after
adjustment for the alleged methodological weakness.
Dutch researcher Martijn Katan criticized Siri-
Tarino et al.’s reliance on the underlying studies’
use of single-day dietary assessments, as opposed to
multiday diet records. He insisted as well that,
since fat-reduction recommendations had been is-
sued 50 years ago, falling LDL-C concentrations
had resulted in conspicuous declines in CHD. Fi-
nally, he questioned the private interests of Siri-
Tarino’s colleague, Ronald Krauss, relative to his
“advisory activities for the dairy industry.” Siri-
Tarino acknowledged the underlying studies’ limi-
tations, but argued that all dietary assessments had
been subjected to a “quality score” which con-
firmed her final results. She also informed Katan
that Krauss had discontinued his dairy industry as-
sociations years prior to publication.
In a separate editorial, Northwestern Univer-
sity preventive-medicine specialist, Jeremiah Stam-
ler—who had served with Ancel Keys on the AHA
nutrition committee during the early 1960s—vigor-
ously defended what he deemed an unwarranted at-
tack on the D-Hh:
Do they doubt the validity of the equations of Keys
… which are based on dozens of metabolic ward-
type feeding experiments, showing independent re-
lations of dietary SFA and cholesterol (direct) and
[PUFA] (inverse) to cholesterol …, findings that are
repeatedly confirmed in observational and interven-
tional studies in free-living people? … Do they
bring into question the classical findings?19
Stamler accused Siri-Tarino’s group of ignoring
several important investigations, including the Seven
Countries, Ni-Hon-San, and National Diet-Heart
studies, along with the DASH/Omni-Heart and Mul-
tiple Risk Factor Intervention trials. He also chal-
lenged Siri-Tarino’s emphasis on CHO-induced
dyslipidemia, wondering how she might explain why
native Japanese have demonstrated favorable lipid
profiles relative to American Japanese, despite their
distinctly low-fat, high-CHO diets.
Finally, Stamler denied that the “limited
data” supporting the differential effects of SFA
and CHO on smaller or larger LDL particles could
justify significant changes to the official guide-
lines. Indeed, nothing Siri-Tarino had to say,
Stamler maintained, could “warrant modification
of recommendations … beyond intensified em-
phasis on prevention and control of obesity.”
But the macronutrient guidelines would be
challenged again in 2010 by NIH biochemist
Christopher Ramsden. Although the AHA, for ex-
ample, recommended substantial replacement of
SFA with Omega-6 (n-6) PUFA-rich vegetable oils,
Ramsden suspected that the underlying literature
had failed to either, one, distinguish between inter-
ventions increasing n-6 PUFA specifically and those
boosting both Omega-3 (n-3) and n-6 PUFA, or,
two, compare the relative effects of these interven-
tions on CHD outcomes.
Indeed, following their meta-analysis of “all
randomized controlled trials that increased PUFA
and reported relevant CHD outcomes,” Ramsden’s
team calculated a 22% reduction in CHD risk for
6 SKEPTIC MAGAZINE volume 20 number 2 2015

6. mixed n-3/n-6 PUFA diets, but a 13% increase in risk
for specific n-6 diets.20
“These analyses were thus
not appropriate,” Ramsden decided, “for formulat-
ing advice specific to n-6 PUFA.” Recommendations
to increase n-6 PUFA “should be reconsidered,” he
warned, “because there is no indication of benefit,
and there is a possibility of harm.”
One year later—in apparent disregard of
Ramsden’s findings—a diverse group consisting of
members from both Jakobsen’s and Siri-Tarino’s
2010 teams and led by Danish nutritionist, Arne
Astrup, decided to reevaluate SFA in light of re-
cently published evidence.21
While now confessing
the over-simplicity of the D-Hh, this group pre-
dictably confirmed prior claims that SFA should be
replaced with PUFA, but not refined CHO. The
data regarding MUFA, they added, were too limited
to be instructive.
Astrup conceded as well that biomarkers other
than LDL-C—to include the total cholesterol-to-
HDL-C ratio, non-HDL-C, and apolipoprotien B—
can be more enlightening of CVD risk. He also
acknowledged evidence indicating that distinct SFA
have different physiological effects, depending on
their complement of carbon atoms. For example, in
terms of raising serum cholesterol levels, stearic
acid (found in meat and cocoa butter) appears neu-
tral, while lauric and palmitic acids (found, for ex-
ample, in tropical oils and dairy, respectively)
might be far more problematic.
So the consensus as of 2011, according to As-
trup, was that “the effect of a specific food on risk
of CVD cannot be determined simply on the basis
of the fatty acid profile.” Indeed, “the total matrix of
a food is more important.” Nevertheless, he ad-
vised, a “healthy dietary pattern is primarily plant-
based and low in SFA.”
Perhaps, but 2011 was a lifetime ago in the in-
creasingly volatile world of nutrition science. Im-
portant questions about fats, CHO, and various
biomarkers and risk factors for CHD were raised
and recognized. But ensuing research would reveal
quite clearly that the macronutrient wars were just
warming up.
The Macronutrient Wars Rage On
Controversy has beset the diet-heart hypothesis from
its very inception. Throughout the 1950s and 1960s,
the idea’s founder, Ancel Keys, was accused of
“cherry picking” evidence to advance his career. If
the Masai warriors of Kenya and Tanzania can sub-
sist healthfully on raw milk, meat, and blood, the de-
tractors prodded, why should Westerners shun
butter, omelets, and cheeseburgers?22
Since then,
every official recommendation urging Americans to
consume less cholesterol and saturated fatty acids to
reduce their risks of coronary heart disease and car-
diovascular disease has suffered incessant criticism.
In recent months, the attacks have only intensi-
fied. Cardiologist Aseem Malhotra scolded re-
searchers for their allegedly outdated obsession over
the link between SFA and low-density lipoprotein
cholesterol (LDL-C). Yes, consumption of SFA tends
to elevate blood LDL-C levels, he conceded. But that
increase “seems to be specific to large, buoyant
(type A) LDL particles,” and not the “small, dense
(type B) particles” implicated in CVD.23
More dan-
gerous type B particles are actually “responsive to
carbohydrate intake,” Malhotra insisted. Indeed,
“saturated fat has been found to be protective.”
So, while the majority continues to condemn
the SFA typically found in animal products and
tropical oils, the minority has instead begun to im-
pugn carbohydrates, particularly the refined variety
favored by Western palates. Most researchers agree
that excess energy from whatever sources leads to
obesity, diabetes, and CHD. But authors of the offi-
cial guidelines spurn minority influences and con-
tinue to recommend replacement of SFA with their
polyunsaturated counterparts.
In response, indignant writers have pummeled
the professional literature with papers hostile to of-
ficial policies. For example, following a meta-analy-
sis of 12 studies involving 7,150 participants,
Austrian nutritionist Lukas Schwingshackl argued
that replacing SFA with PUFA “showed no signifi-
cant benefit in the secondary prevention of coro-
nary heart disease.”24
NIH biochemist Christopher
Ramsden raised the stakes after examining newly-
recovered data from the Sydney Diet Heart Study.
He decided not only that linoleic acid (LA), a com-
mon omega-6 (n-6) PUFA, “did not provide the
intended benefits,” but also that its substitution for
SFA “increased all-cause mortality, cardiovascular
death, and death from coronary heart disease.”25
Swedish researcher Uffe Ravnskov concurred, em-
phasizing studies associating consumption of PUFA
with inflammation, immune system suppression,
decreased high-density lipoprotein cholesterol lev-
els, and an increased risk of many cancers.26
At that point, CVD researcher (and Ravnskov
co-author) James DiNicolantonio stepped in to
summarize the detractors’ position. First, he
stressed that the current outbreak of Western dia-
betes and obesity derives from overconsumption of
CHO, not SFA. Second, the replacement of SFA
volume 20 number 2 2015 WWW.SKEPTIC.COM 7

7. with CHO only increases small, dense LDL parti-
cles and shifts the overall lipid profile toward de-
creased HDL-C, elevated triglycerides, and an
increase in the apolipoprotein B-to-apolipoprotein
A-1 ratio (ApoB/ApoA-1). Third, the substitution of
SFA with n-6 PUFA only reduces HDL-C and raises
the risk of cancer, CHD, and overall mortality. Fi-
nally, he argued, the PREDIMED and Lyon Diet
Heart studies had demonstrated that Mediter-
ranean-style diets reduce cardiovascular events, car-
diovascular mortality, and all-cause mortality
relative to either low-fat diets or the AHA’s “pru-
dent” diet. Thus, DiNicolantonio concluded, those
responsible for the official guidelines “should assess
the totality of evidence and strongly reconsider
their recommendations.”27
When I contacted him, DiNicolantonio main-
tained that the D-Hh “has never been proven.” SFA
acids might raise LDL-C levels, he advised, but an in-
creased risk of CHD simply doesn’t follow. Small,
dense LDL particles are more atherogenic, or “more
capable of penetrating a damaged endothelium”—
which likely results from a “high refined carb/sugar
diet,” among other things. To the contrary, he ar-
gued, the SFA found in whole, unprocessed foods
like red meat can provide immune-boosting proper-
ties and stability against oxidation.
Meanwhile, minority support continued to
mount. In his very controversial meta-analysis of 49
observational studies and 27 randomized controlled
trials, Cambridge University epidemiologist Rajiv
Chowdhury found null associations between coro-
nary risk and both total SFA and monounsaturated
fatty acids (MUFA), along with a statistically non-
significant association between coronary risk and
PUFA supplementation.28
Likewise, Tulane Univer-
sity epidemiologist Lydia Bazzano, conducted a 12-
month randomized, parallel-group diet
intervention trial of 148 healthy men and women,
and found that participants who completed the
low-CHO regime lost more weight and presented
with fewer CVD risk factors compared to subjects
who completed the low-fat program.29
Predictably, the majority’s response was imme-
diate. Harvard University nutritionist Maryam
Farvid performed her own systematic review and
meta-analysis of prospective cohort studies to ex-
amine the effect of increased LA consumption in
healthy subjects. Contrary to Ramsden’s and
Chowdhury’s findings, Farvid revealed a linear in-
verse association between the predominant n-6
PUFA and CHD. LA’s “cardio-protective effects,”
she argued, included a “9% lower risk of total CHD
and 13% lower risk of CHD deaths” with a “5% in-
crease in energy from LA, replacing SFA.”30
While acknowledging Ramsden’s and Ravn-
skov’s concerns relating to LA, Farvid nevertheless
resolved that such fears remained unsupported by
both prospective studies and randomized controlled
feeding trials. Even so, she conceded, “the effects of
LA on heart disease risks are difficult to predict,”
and diets high in LA may increase lipid oxidation
and “play a role in the pathogenesis of cancer.”
Farvid also distinguished her analysis from
those of her minority predecessors. Ramsden, she
noted, based his results primarily on one short-
term trial from the 1960s restricted to a small sam-
ple of unhealthy men. And because the partial
hydrogenation of vegetable oils was then common,
she suggested, Ramsden’s findings might have been
confounded by the trans-fats found in margarines
high in LA. Chowdhury, on the other hand, had
based his analysis on a limited number of studies
and was unable to compare LA with SFA or any
other macronutrient. In a separate critique, Walter
Willet—Farvid’s co-author and Harvard col-
league—accused Chowdhury of committing “multi-
ple serious errors and omissions” and creating
unnecessary confusion. When SFA are replaced
with PUFA or MUFA in the form of olive oil, nuts
and other plant oils, he disputed, “we have much
evidence that risk will be reduced.”31
The Bazzano study’s relevance to the D-Hh
and the guidelines are less clear than many imag-
ine. While certain popular media outlets seized on
these results to extol the virtues of bacon and egg
breakfasts, for example, Bazzano had actually urged
subjects in both the low-fat and low-CHO interven-
tion groups to consume less SFA and more unsatu-
rated fat.32
Further, the low-fat cohort was advised
merely to diminish overall fat intake to 30% of total
calories, which is “hardly low,” as NYU professor of
nutrition Marion Nestle reminded me.
Finally, an interesting variation on the minority
theme alleges first, that dietary SFA do not affect
plasma SFA levels, and second, that excessive intake
of refined CHO does raise either SFA or palmitoleic
MUFA plasma levels via de novo lipogenesis in the
liver, thereby increasing the risk of CHD.33, 34
But
James Kenny, nutrition researcher at the low-fat ad-
vocacy Pritikin Longevity Center judges this argu-
ment a “gross over-interpretation of the data.” Yes,
the liver will convert sugar to both SFA and MUFA
when its glycogen stores are maximized. Nonethe-
less, Kenney told me, even under these circum-
stances, mere trivial portions of ingested CHO will
8 SKEPTIC MAGAZINE volume 20 number 2 2015

8. be converted and only when consumed far in excess
of energy needs. Regardless, he added, “low-
fat/high-CHO diets composed of vegetables, whole-
grains, and fruit decrease total cholesterol and
ApoB-containing lipoproteins, reduce inflamma-
tion, and may actually reverse atherosclerosis.”
What Should We Eat?
So where does the D-Hh stand at the dawn of 2015?
My conversations with the experts could not have
yielded more starkly conflicting opinions. Accord-
ing to Ravnskov, for example, “the diet-heart idea is
the greatest medical scandal in modern time.” By
contrast, Tufts University researcher Alice Lichten-
stein—instrumental in generating the AHA’s most
recent guidelines—wouldn’t dignify minority rheto-
ric with a response. She maintains that “the obser-
vational and intervention data are entirely
consistent” and “support substituting PUFA for sat-
urated fat to decrease the risk of CVD.” Kenney was
less reluctant to characterize minority views as
“fringe” and “pseudoscientific.”
Nonetheless, important inferences can be
drawn from a century’s worth of diet-heart litera-
ture. With respect to biomarkers, for example, we
might soon reconsider our preoccupations with
LDL-C and HDL-C per se. Non-HDL-C (total cho-
lesterol minus HDL-C) and total ApoB containing
lipoproteins likely provide more revealing indica-
tors of cardiovascular risk and, correspondingly,
particle quantity is more critical than size. Concern
also grows that, while SFA and MUFA increase
HDL-C, much of that HDL-C can become dysfunc-
tional and actually pro-atherogenic.
As intense friction between research commu-
nities continues to mount, the USDA Dietary
Guidelines Advisory Committee has proposed
meaningful revisions for 2015.35
Recommended
ceilings for the consumption of dietary choles-
terol—currently set at 300 milligrams per day—
will likely be rescinded, overturning forty years of
advisory precedent. Further restriction of refined
sugars was also advised. On the other hand, the
Committee apparently remains committed to the
D-Hh and long-standing recommendations to re-
duce intake of SFA, though not total fat.
In an editorial response to Zoe Harcombe’s re-
cent condemnation of the original (and persisting)
government guidelines, British cardiologist Rahul
Bahl reflected on their empirical support overall.
Given the results of more recent analyses detailed
here, he found Harcombe et al.’s results and conclu-
sions “unsurprising” but not necessarily convinc-
ing.36
“There remain reasons to postulate a causal
connection” he argued, “between fat consumption
and heart disease.” First, the epidemiological and
ecological evidence suggest such a link and, second,
we should expect certain randomized controlled
trials to produce negative results given the capri-
ciousness of human behavior. On the other hand,
Bahl reasoned,
There is certainly a strong argument that an overre-
liance in public health on saturated fat as the main
dietary villain for cardiovascular disease has dis-
tracted from the risks posed by other nutrients such
as carbohydrates. Yet replacing one caricature with
another does not feel like a solution. It is plausible
that both can be harmful or indeed that the rela-
tionship between diet and cardiovascular risk is
more complex than a series of simple relationships
with the proportions of individual macronutrients.
Beyond that, the inherent limitations of nutri-
tion science tend to frustrate the public’s demand
for concrete conclusions. Confounding factors, in-
cluding genetics, are difficult to both identify and
account for. Assessing the significance of any sin-
gle risk factor for a chronic disease of multifactor-
ial etiology is a knotty problem at best. And
because people consume foods rather than mere
nutrients, intake itself complicates the issue. High-
fat diets, for example, might be loaded with sugar
too, and are often low in fiber, antioxidants,
flavonoids, folate, and carotenes. Study method-
ologies vary considerably as well, and participant
behaviors often render findings non-replicable and
scientifically suspect. Finally, given the establish-
ment of a paradigm like the D-Hh, ethical consid-
erations often make meaningful test conditions
impossible.
Even so, a sensible combination of nutrition sci-
ence and sound reasoning proves very helpful. First,
ignore the popular media. Some truths simply don’t
sell advertising. Second, nutritionally irredeemable
trans-fats should be eliminated from our diets uncer-
emoniously. Otherwise, as Bahl and others suggest,
focus on whole foods over fatty acids and remember
that humans never evolved to consume processed
foods, including refined fats and oils. Third, learn to
prepare and spice lean, unprocessed meats and fresh
vegetables to otherwise unembellished satisfaction.
Add a few fruits and nuts and avoid everything
else—especially refined sugars and starches. Finally,
exercise regularly and vigorously, avoid excess adi-
posity, and don’t smoke. With that, what within our
control could possibly go wrong?
volume 20 number 2 2015 WWW.SKEPTIC.COM 9

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