ArticlePDF AvailableLiterature Review

Role of cis-Monounsaturated Fatty Acids in the Prevention of Coronary Heart Disease


Abstract and Figures

The effects of cis-monounsaturated fatty acids (cis-MUFAs) on the risk of coronary heart disease (CHD) and on CHD mortality are not clear. Also, dietary recommendations for cis-MUFA as derived by various organizations are not in agreement. Earlier studies have mainly focused on the effects of cis-MUFA on serum lipids and lipoproteins. More recent studies, however, have also addressed effects of cis-MUFA on other non-traditional CHD risk markers such as vascular function markers, postprandial vascular function, and energy intake and metabolism. Although well-designed randomized controlled trials with CHD events as endpoints are missing, several large prospective cohort studies have recently been published on the relationship between cis-MUFA and CHD risk. The aim of this paper is to review these new studies that have been published in the last 3 years on the effects of cis-MUFA on cardiovascular risk markers and CHD.
This content is subject to copyright. Terms and conditions apply.
Role of cis-Monounsaturated Fatty Acids in the Prevention
of Coronary Heart Disease
Peter J. Joris
&Ronald P. Mensink
Published online: 24 May 2016
#The Author(s) 2016. This article is published with open access at
Abstract The effects of cis-monounsaturated fatty acids (cis-
MUFAs) on the risk of coronary heart disease (CHD) and on
CHD mortality are not clear. Also, dietary recommendations
for cis-MUFA as derived by various organizations are not in
agreement. Earlier studies have mainly focused on the effects
of cis-MUFA on serum lipids and lipoproteins. More recent
studies, however, have also addressed effects of cis-MUFA on
other non-traditional CHD risk markers such as vascular func-
tion markers, postprandial vascular function, and energy in-
take and metabolism. Although well-designed randomized
controlled trials with CHD events as endpoints are missing,
several large prospective cohort studies have recently been
published on the relationship between cis-MUFA and CHD
risk. The aim of this paper is to review these new studies that
have been published in the last 3 years on the effects of cis-
MUFA on cardiovascular risk markers and CHD.
Keywords Monounsaturated fatty acids .Oleic acid .Risk
markers .Coronary heart disease .Cardiovascular disease
Optimizing dietary fatty-acid intake is an integral part of die-
tary guidelines to prevent coronary heart disease (CHD) [1]. In
fact, unequivocal evidence exists that eliminating trans-fatty
acids from hydrogenated oils in the diet lowers the prevalence
of CHD [2]. A decrease in the intake of saturated fatty acids
(SFA) is also recommended, but in this respect, the type of
macronutrient that replaces SFA is important. Replacement of
SFA by carbohydrates from refined starches/added sugars
may not decrease CHD risk, while replacement by carbohy-
drates from whole grains or cis-polyunsaturated fatty acid (cis-
PUFA) does [3,4]. The effects of cis-monounsaturated fatty
acids (MUFA; Fig. 1) on CHD risk and CHD mortality are
however less clear [5]. Also, dietary recommendations as de-
rived by various health agencies for trans-fatty acids, SFA,
and cis-PUFA are generally more in agreement than those
for cis-MUFA. For example, no specific dietary reference
values for cis-MUFA have been formulated in the very recent
20152020 Dietary Guidelines for Americans [6], while other
organizations have set reference values for cis-MUFA [7]. In
2012, Schwingshackl and Hoffmann have reviewed the avail-
able evidence from systemic reviews and meta-analyses re-
garding cis-MUFA intake and cardiovascular risk [8]. It was
concluded that there was no clear justification to formulate
specific dietary recommendations for cis-MUFA for the pri-
mary and secondary prevention of cardiovascular disease
(CVD). On the other hand, as no harmful effects of cis-
MUFA-rich diets are known, more longer term intervention
studies were suggested to clarify potential benefits of cis-
MUFA-rich diets. Since then, several new studies have been
published during the last 3 years on the relationship between
cis-MUFAs and cardiovascular risk markers or CHD, which
will be discussed in the present review.
Food Sources Of cis-Monounsaturated Fatty Acids
Worldwide,themeanintakeofcis-MUFA ranges from 3.5 %
of total energy in certain regions of China to about 22 % in
This article is part of the Topical Collection on Nutrition
*Ronald P. Mensink
Department of Human Biology, NUTRIM School of Nutrition and
Translational Research in Metabolism, Maastricht University
Medical Center, PO Box 616, Maastricht 6200 MD, The Netherlands
Curr Atheroscler Rep (2016) 18: 38
DOI 10.1007/s11883-016-0597-y
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Greece. Oleic acid (18:1; n-9) is the predominant cis-MUFA,
accounting for more than 92 % of all MUFAs consumed.
Other cis-MUFAs are also present in the diet, but only in very
small amounts (Table 1). Except for erucic acid (22:1; n-9),
their health effects have hardly been studied. Animal studies
have suggested that erucic acid at high intakes may cause
myocardial lipidosis due to poor mitochondrial β-oxidation.
However, rapeseed oil varieties low in erucic acid are nowa-
days part of the food chain. Therefore, cis-MUFA intakes in
the studies discussed mainly refer to intakes of oleic acid.
Some vegetable oils, such as olive oil (75 %), mid-oleic
sunflower oil (70 %), and rapeseed oil (65 %), consist of
more than 50 % of cis-MUFA, followed by other products
such as palm oil, nuts and seeds, avocados, and animal fats
[9]. In fact, animal fats are the main source of cis-MUFA in a
typical American diet, and high cis-MUFA and SFA intakes
may thus be correlated. The six food groups with the highest
contribution to total MUFA intake among US adults based on
the National Health and Nutrition Examination Survey
(NHANES) 20032006 were other fats and oils (10.5 %), beef
(9.2 %), cakes/cookies/quick bread/pastry/pie (8.9 %), frank-
furters/sausages/luncheon meats (7.5 %), cheese (6.6 %), and
margarine and butter (6.4 %) [10].
cis-Monounsaturated Fatty Acid
and Cardiovascular Risk Markers
cis-MUFA may affect cardiovascular health through effects on
a wide variety of markers associated with CHD [11]. This
paragraph reviews current evidence on the effects of cis-
MUFA on serum lipids and lipoproteins, vascular function
markers, postprandial vascular function, and energy intake
and metabolism.
Serum Lipids and Lipoproteins
Data from the many earlier well-controlled randomized inter-
vention studies have shown that cis-MUFA has a favorable
effect on the serum lipoprotein profile. In studies that replaced
fats or oils high in SFAwith oils rich in cis-MUFA, significant
decreases were found in serum concentrations of total choles-
terol, LDL-cholesterol, and apoB100 and the total to HDL-
cholesterol ratio. Serum HDL-cholesterol, apo-AI, and triac-
ylglycerol concentrations hardly changed. Overall, the effects
of oils rich in cis-PUFA were slightly more favorable than
those of oils rich in cis-MUFA, especially on LDL-
cholesterol and the total to HDL-cholesterol ratio. In these
studies, the diets were enriched with cis-MUFA from different
sources such as olive oil, high-oleic acid sunflower oil, high-
oleic acid safflower oil, and rapeseed oil. More recently, other
intervention trials have been carried out specifically focusing
on cis-MUFA. Gilmore et al. reported that in 17 postmeno-
pausal women, consumption of high-MUFA or low-MUFA
ground beef for 6 weeks had comparable effects on the serum
lipoprotein profile [12]. However, the difference in cis-MUFA
intake provided by the two types of ground beef was less than
2 g/day, which may have been too small to observe any ef-
fects. In a randomized, double-blind, crossover design with
131 abdominally obese volunteers, five oils with comparable
amounts of SFA, but differing in the amounts of oleic acid,
linoleic acid, α-linolenic acid, or docosahexaenoic acid
(DHA) were consumed for 4-week periods [13••]. Effects on
serum LDL-cholesterol, HDL-cholesterol, and triacylglycerol
concentrations were comparable, confirming the findings that
Fig. 1 Monounsaturated fatty acids (MUFAs) are chemically classified
as fatty acids that have one double bond in the carbon chain. In the cis-
configuration, the hydrogen atoms attached to the double bond point into
the same direction (top:oleicacid,acis-MUFAwith18carbonatoms),
while in the trans-configuration, the hydrogen atoms are located on op-
posite sides (bottom:elaidicacid,atrans-MUFA with 18 carbon atoms)
Tabl e 1 Overview of different types of cis-monounsaturated fatty acids
cis-MUFA Food sources
Caproleic acid (10:1) Ruminant fats
Lauroleic acid (12:1; n-3) Ruminant fats
Myristoleic acid (14:1; n-5) Ruminant fats
Palmitoleic acid (16:1; n-7) Ruminant fats, fats from fish and
marine mammals, macadamia oil,
sea buckthorn oil and milkweed
seed oil
Oleic acid (18:1; n-9) Vegetable oils such as olive oil,
mid-oleic sunflower oil and
low-erucic acid rapeseed oil, nuts
and seeds, avocados, palm oil,
and animal fats
Gadoleic acid (20:1; n-11) Fish oils such as ray, shark and
cod, and mustard oil
Erucic acid (22:1; n-9) Mustard oil
Nervonic acid (24:1; n-9) Mustard oil, fish oils such as salmon
Oleic acid is the predominant cis-MUFA in the diet, accounting for more
than 92 % of all MUFAs consumed
MUFA monounsaturated fatty acid
38 Page 2 of 7 Curr Atheroscler Rep (2016) 18: 38
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
cis-unsaturated fatty acids with 18 carbon atoms have compa-
rable effects on serum lipids. An oil rich in cis-MUFA and
DHA, however, increased LDL-cholesterol and HDL-
cholesterol and lowered serum triacylglycerol concentrations
as compared with the other four oils [13••]. In a subset of the
population, no evidence was found that consumption of the
oils had an adverse effect on LDL proteoglycan binding [14],
as observed in animal studies after consumption of oils rich in
cis-MUFA [15]. As expected, a high-palmitic acid diet in-
creased concentrations of total LDL-cholesterol and HDL-
cholesterol and had no effects on serum triacylglycerol as
compared with a high-oleic acid diet in 18 healthy subjects
[16]. Also, olive oil and rapeseed oil were found to have
similar effects on the serum lipoprotein profile [17]. In a 24-
week parallel study in individuals with type 2 diabetes, a
peanut-enriched American Diabetic Association (ADA) meal
plan had similar effects on the serum lipoprotein profile com-
pared with a nut-free ADA meal plan [18]. Dietary SFA and
total fat intakes between the two groups were not different. In
the Dietary Intervention and Vascular Function (DIVAS) trial,
a randomized, single-blind, parallel-group intervention study
with 195 adults at moderate CVD risk, three groups of sub-
jects consumed for 16 weeks a diet that was rich in SFA, cis-
MUFA, or cis-PUFA. Except for commercially available
foods, specially formulated oils and spreads were used high
in cis-MUFA (refined olive oil and rapeseed oil) and cis-
PUFA (safflower oil). The high-SFA group received butter.
As compared with the high-SFA groups, serum total and
LDL-cholesterol concentrations were reduced to the same ex-
tent on the high-MUFA and high-PUFA diets. Effects on se-
rum HDL-cholesterol and triacylglycerol were comparable
[19••]. Overall, these recent studies are in line with the earlier
The mechanistic aspects of cis-MUFA were examined by
Labonté and colleagues [20]. In a randomized parallel study,
the effects of exchanging carbohydrates for cis-MUFA as part
of an experimental portfolio diet on apolipoprotein kinetics
were investigated in 16 dyslipidemic subjects. The experimen-
tal diets were fed for 4 weeks after a 4-week run-in period. The
high-MUFA diet increased apo-AI pool size, mainly due to a
reduced apo-AI fractional catabolic rate. LDL apoB100 pool
size tended to be reduced on the cis-MUFA diet through an
increase in LDL apoB100 fractional catabolic rate.
Vascular Function Markers
The DIVAS study was adequately powered to investigate the
long-term impact of replacing SFAs with cis-MUFAs on var-
ious fasting vascular function markers [19••]. It was found that
replacing dietary SFAs with cis-MUFAs did not affect fasting
flow-mediated vasodilation (FMD) of the brachial artery
[19••]. These findings are in agreement with those of
Sanders and colleagues, who replaced 5.2 % of energy from
dietary SFAs by cis-MUFAs for 24 weeks in 121 insulin-
resistant men and women [21••]. Furthermore, replacement
of SFAs had no effect on arterial stiffness, supporting the
earlier findings of Sanders et al. reporting no change in
carotid-to-femoral pulse wave velocity (PWV
were replaced with cis-MUFAs [21••]. Of the secondary out-
come measures, substitution of dietary SFAs by cis-MUFAs
significantly reduced circulating E-selectin concentrations by
7.8 %, suggesting an improvement in endothelial activity,
while night systolic blood pressure was reduced by 4.9 mm
of Hg. As discussed by the authors [19••], the large range of
recorded daily activity levels may have masked any effects of
the intervention on 24-h or daytime ambulatory blood pres-
sure recordings.
Postprandial Vascular Function
Postprandial vascular responses were compared between
normal-weight and obese men following three isocaloric
high-fat challenges differing in fatty-acid composition [22].
For this, 18 normal-weight and 18 obese middle-aged men
received in a random order a milkshake providing 95 g of
fat, which was either high in SFAs, cis-MUFAs, or n-3long-
chain PUFAs. Compared with the SFA and n-3PUFA shakes,
it was found that the cis-MUFA milkshake resulted in a more
pronounced decrease in the augmentation index (AIx)a
measure of the arterial pressure waveform that depends on
the tone of peripheral resistance arteriesand blood pressure.
Milkshake consumption resulted in increased plasma
sICAM1, sICAM3, and sVCAM1 concentrations 4 h post-
prandially, with no differences in responses between the
shakes for these and other (E-selectin and vWF) plasma bio-
markers of endothelial function. Lithander et al. [23] com-
pared the effects of a test meal rich in oleic acid with an
isoenergetic meal rich in palmitic acid on postprandial vascu-
lar function in younger male participants. No differences in
, AIx or blood pressure were found between the two
test meals providing 56 g of fat. Except for subject character-
istics, the difference in findings with the study of Esser and
colleagues [22] may also be explained by meal composition,
because the mixed meal provided by Lithander was higher in
carbohydrates and lower in dietary fat (56 g of fat versus 95 g
of fat).
Energy Intake and Metabolism
Mennella and colleagues fed 15 healthy normal-weight sub-
jects in random order 30 mL of high-oleic acid sunflower oil,
virgin olive oil, or sunflower oil plus 30 g of bread. After
consumption of the oils rich in oleic acid, energy intake was
reduced at the subsequent self-chosen lunch, possible related to
the increased postprandial concentrations of
oleoylethanolamide (OEA), a compound produced by the small
Curr Atheroscler Rep (2016) 18: 38 Page 3 of 7 38
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
intestine that is involved in appetite regulation. However, ener-
gy intake over the next 24 h as assessed by food diaries was
comparable between the three treatments [24]. Total energy
intake as measured during 4 days was lower in a randomized
controlled trial (RCT) with 24 healthy elderly overweight par-
ticipants following consumption of high-oleic acid peanuts and
regular peanuts compared with isoenergetic amounts of a high-
carbohydrate snack (potato crisps). Despite these reductions in
energy intake, no differences in hunger and satiety that were
assessed following snack consumption using visual analog
scales were observed [25]. Comparable results were reported
in another study with high-oleic acid peanuts [26].
In their recent review [27], Krishnan and Cooper conclud-
ed that acute-meal studies suggested that diet-induced thermo-
genesis and fat oxidation were increased on high unsaturated-
fat diets as compared with SFA-rich diets. In this respect, no
differences were found between MUFA and PUFA. It was
further concluded that also long-term dietary interventions
may suggest that MUFA-rich diets induced a greater energy
expenditure, diet-induced thermogenesis or fat oxidation as
compared with SFA-rich diets [27]. More recently, however,
Clevenger et al. found no differences in the effects of SFA,
MUFA, and PUFA on diet-induced thermogenesis or post-
prandial substrate oxidation in obese women [28]. On the
other hand, Kien and colleagues reported in healthy volunteers
a higher rate of fat oxidation during the fasted state on a
palmitic-acid rich diet as compared with an oleic-acid rich
diet. Diets were provided for 3 weeks [29••]. Overall, there
is no unanimous agreement that cis-MUFA affects energy
metabolism compared with other dietary fatty acids. The few
short-term studies that used peanuts are more consistent in this
respect and effects may therefore not necessarily be related to
cis-MUFA intake. Also, it is not known if the effects are
sustained on the longer term and are ultimately translated into
a lower body weight and an improved cardiometabolic profile.
cis-Monounsaturated Fatty Acid
and Cardiovascular Disease
The Mediterranean diet is well known for its high cis-
MUFA content (16 to 29 % of energy) with olive oil being
the predominant source of fat and intakes of SFA below 8 %
[30]. The Mediterranean dietary pattern is associated with a
reduced cardiovascular risk. Even though not designed to
specially evaluate the effects of cis-MUFA, the
PREvención con DIEeta MEDiterraneá (PREDIMED) trial
found that a Mediterranean diet supplemented with extra-
virgin olive oil (50 g/day) or mixed nuts (30 g/day) reduced
in individuals at high cardiovascular risk the incidence of
major cardiovascular events (a composite of myocardial in-
farction, stroke, or death from CVD causes) as compared
with a control diet low in fat [31••]. A meta-analysis of 15
RCTs, that involved more than 50,000 participants, aimed to
estimate the effect of replacing dietary SFA for carbohy-
drates, cis-PUFA, cis-MUFA, or protein on cardiovascular
morbidity and mortality [5]. It was concluded that the effects
of cis-MUFA were unclear as only one small trial from 1965
was identified [32], in which no effects were observed. In
this respect, the results of recently published large prospec-
tive cohort studies evaluating the association between cis-
MUFA intake with the risk of CVD and cardiovascular
death may be more informative (Table 2).
Subjects within the PREDIMED trial were also prospec-
tively studied. While the trial was conducted from 2003 to
2010, the present data were based on an expanded follow-up
until 2012 [33]. The mean intake of cis-MUFAs (expressed as
percentage of energy) was high: 13.4 % in the lowest quintile
compared with 26.1 % in the top quintile. After 6 years of
follow-up, 336 CVD cases and 414 total deaths were reported.
It was found that higher intakes of cis-MUFA were inversely
associated with CVD, cardiovascular death, and all-cause
death. In fact, isocaloric substitution of 5 % of energy from
SFAs or trans-FAs with cis-MUFAs was associated with a 37
and 40 % lower risk of total CVD events. In agreement, an
updated analysis of the NursesHealth Study (19802010; 84,
628 US women) and the Health Professional Follow-Up
Study (19862010; 42,908 US men) showed a reduction in
CHD risk when SFA was exchanged for cis-MUFA [3]. In
these two large, independent prospective cohorts of men and
women, 7667 cases of CHD (4931 nonfatal myocardial infarc-
tions and 2736 CHD deaths) were documented over 24 to
30 years of follow-up. Replacing 5 % of energy from dietary
SFAwithanequivalentamountofcis-MUFA was associated
with a 15 % (95 % CI, 3 to 26 %) lower risk of CHD. In a large
prospective cohort study carried out within the Alpha-
Tocopherol, Beta-Carotene Cancer Prevention Study
(ATBC), the associations between glycemic index, substitu-
tions of total, low-, medium-, and high-glycemic-index carbo-
hydrates for dietary fat and the risk of CHD were examined
[34]. During a 19-year follow-up, 4379 CHD cases, including
a total of 2377 non-fatal myocardial infarctions and 2002
CHD deaths, were documented among approximately 22,
000 middle-aged Finnish male smokers. Substituting carbo-
hydrates for cis-MUFAs was associated with a decreased risk.
It was estimated that isoenergetic replacements of 2 % of
energy from total, low-, or high-glycemic-index carbohy-
drates for cis-MUFAs were associated with 8 % (95 % CI, 1
to 16 %), 9 % (95 % CI 2 to 16 %), and 8 % (95 % CI 1 to
15 %) lower CHD risks. The isocaloric replacement of
medium-glycemic-index carbohydrates with cis-MUFA
tended to decrease the risk of CHD by 7 % (95 % CI 0 to
15 %). Dietary fiber intake modified the association between
the replacement of carbohydrates with cis-MUFA and the risk
of CHD in the stratified analyses. In fact, increasing cis-
MUFA intake at the expense of carbohydrates was more
38 Page 4 of 7 Curr Atheroscler Rep (2016) 18: 38
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
beneficial among the subjects with a higher fiber intake. In
patients with type 2 diabetes, the association between dietary
carbohydrate intake and substitution for cis-MUFA with car-
diovascular and all-cause mortality was also investigated
[35]. A total of 6192 type 2 diabetic patients from 15 cohorts
of the European Prospective Investigation into Cancer and
Nutrition (EPIC) were included. After a mean follow-up of
about 9 years, 268 CVD deaths and 791 total deaths were
reported. Substituting 5 % of energy from carbohydrates with
cis-MUFA may be associated with a lower all-cause mortality
risk (HR, 0.87; 95 % CI, 0.76 to 1.00), while no effects were
reported for CVD mortality risk.
Surprisingly, a lower CHD risk with a higher intake of
SFAs was recently observed that did not depend on the
type of substituting macronutrient [36]. The EPIC-
Netherlands (EPIC-NL) cohort included 35,597 Dutch
men and women. In this prospective cohort study, a total
of 1807 incident CHD cases and 158 CHD deaths (8.7 %)
occurred over a median follow-up time of 12 years. After
full adjustment, the substitution of 5 % of energy from SFA
with cis-MUFA was associated with 30 % (95 % CI: 2 %
to 65 %) increased risk to develop CHD. These results,
however, should be interpreted with caution. As discussed
by the authors [36], residual confounding by unmeasured
initiation of cholesterol-lowering therapy during follow-up
may explain these findings as adults with high SFA intake
have high serum cholesterol concentrations and will be-
come eligible for lipid-lowering therapy during follow-up,
which would reduce CHD risk. In addition, the limited
variation in dietary SFA intake or the source of SFA may
also have attributed to the observed risk differences in this
Dutch population.
In summary, recent studies are in line with the earlier studies
showing that cis-MUFAs have a favorable effect on the serum
lipoprotein profile as compared with a mixture of SFA, while
effects are comparable to those of linoleic and α-linolenic acid.
Effects on fasting and postprandial vascular function have not
been studied extensively and no consistent differences between
the various fatty acids are evident. Longer-term studies should
address whether products rich in cis-MUFA affect energy intake
and metabolism compared with other macronutrients. In fact,
studies addressing the effects of food sources and matrices are
of interest, as this may impact the results. Well-designed RCTs
with CVD events as endpoints are lacking. Evidence from large
prospective cohort studies regarding effects of cis-MUFA on the
risk to develop CHD is limited, but several studies do suggest
that replacements of SFA or high-glycemic index foods for cis-
MUFA lowers CHD risk. In this respect, however, cis-MUFA is
not more beneficial than linoleic acid. More research is thus
required on the long-term effects of cis-MUFA as compared
with other macronutrients on CHD risk markers as well as on
clinical endpoints to clarify the potential role of cis-MUFAs in
the primary and secondary prevention of CHD.
Compliance with Ethical Standards
Conflict of Interest Peter J. Joris declares no conflict of interest.
Ronald P. Mensink declares grant support from Top Institute for Food
and Nutrition (Wageningen, the Netherlands) and from Unilever
Research and Development (Vlaardingen, the Netherlands).
Human and Animal Rights and Informed Consent This article does
not contain any studies with human or animal subjects performed by any
of the authors.
Tabl e 2 Summary of recent studies assessing the effects of cis-MUFAs on cardiovascular disease
Study Research question Study design Results
PREDIMED Study [33] Dietary fat intake and risk of total
CVD events in a population at
high risk of CVD
Prospective cohort study Dietary SFA for cis-MUFA
(5 % of energy) HR 0.63
(95 % CI 0.430.94)
NHS and the HPFS [3] Dietary fat intake and risk of CHD
in men and women free of
diabetes, CVD, and cancer
Prospective cohort study Dietary SFA for cis-MUFA
(5 % of energy) HR 0.85
(95 % CI 0.740.97)
ATBC Cancer Prevention
Study [34]
Carbohydrate substitution for
dietary fat and risk of CHD in
Finnish male smokers
Prospective cohort study Total carbohydrates for cis-
MUFA (2 % of energy)
RR 0.92 (95 % CI 0.840.99)
EPIC Study [35] Carbohydrate substitution for
dietary fat on mortality risk in
patients with type 2 diabetes
Prospective cohort study Carbohydrates for cis-MUFA
(5 % of energy) HR 0.87
(95 % CI 0.761.00). No
effects on CVD mortality risk
EPIC-NL Study [36] Dietary fat intake and risk of
CHD in a Dutch population
Prospective cohort study Dietary SFA for cis-MUFA
(5 % of energy) HR 1.30
(95 % CI 1.021.65)
CVD cardiovascular disease, CHD coronary heart disease, N/A not applicable, SFA saturated fatty acid, MUFA monounsaturated fatty acid, HR hazards
ratio, RR relative risk
Curr Atheroscler Rep (2016) 18: 38 Page 5 of 7 38
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Open Access This article is distributed under the terms of the
Creative Commons Attribution 4.0 International License (http://, which permits unrestricted use,
distribution, and reproduction in any medium, provided you give appro-
priate credit to the original author(s) and the source, provide a link to the
Creative Commons license, and indicate if changes were made.
Papers of particular interest, published recently, have been
highlighted as:
Of importance
•• Of major importance
1. Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S,
Franch HA, et al. Diet and lifestyle recommendations revision
2006: a scientific statement from the American Heart Association
Nutrition Committee. Circulation. 2006;114:8296.
2. Mozaffarian D, Clarke R. Quantitative effects on cardiovascular
risk factors and coronary heart disease risk of replacing partially
hydrogenated vegetable oils with other fats and oils. Eur J Clin
Nutr. 2009;63:S2233.
3.Li Y, Hruby A, Bernstein AM, Ley SH, Wang DD, Chiuve SE, etal.
Saturated fats compared with unsaturated fats and sources of carbo-
hydrates in relation to risk of coronary heart disease: a prospective
cohort study. J Am Coll Cardiol. 2015;66:153848. This prospec-
tive cohort study suggests that replacement of saturated fatty
acids for unsaturated fatty acids and/or high-quality carbohy-
drates reduces CHD risk.
4. Mozaffarian D, Micha R, Wallace S. Effects on coronary heart
disease of increasing polyunsaturated fat in place of saturated fat:
a systematic review and meta-analysis of randomized controlled
trials. PLoS Med. 2010;7, e1000252.
5. Hooper L, Martin N, Abdelhamid A, Davey Smith G. Reduction in
saturated fat intake for cardiovascular disease. Cochrane Database
Syst Rev. 2015;6, CD011737.
6. U.S. Department of Health and Human Services and U.S.
Department of Agriculture. 20152020 Dietary Guidelines for
Americans. 8th Edition. December 2015. Available at: http:// Accessed on
March 3, 2016.
7. Aranceta J, Perez-Rodrigo C. Recommended dietary reference in-
takes, nutritional goals and dietaryguidelines for fat and fatty acids:
a systematic review. Br J Nutr. 2012;107:S822.
8. Schwingshackl L, Hoffmann G. Monounsaturated fatty acids and
risk of cardiovascular disease: synopsis of the evidence available
from systematic reviews and meta-analyses. Nutrients. 2012;4:
9. Degirolamo C, Rudel LL. Dietary monounsaturated fatty acids ap-
pear not to provide cardioprotection. Curr Atheroscler Rep.
10. O'Neil CE, Keast DR, Fulgoni VL, Nicklas TA. Food sources of
energy and nutrients among adults in the US: NHANES 2003
2006. Nutrients. 2012;4:2097120.
11. Hammad S, Pu S, Jones PJ. Current evidence supporting the link
between dietary fatty acids and cardiovascular disease. Lipids. doi:
12. Gilmore LA, Crouse SF, Carbuhn A, Klooster J, Calles JA, Meade
T, et al. Exercise attenuates the increase in plasma monounsaturated
fatty acids and high-density lipoprotein cholesterol but not high-
density lipoprotein 2b cholesterol caused by high-oleic ground beef
in women. Nutr Res. 2013;33:100311.
13.•• Jones PJ, Senanayake VK, Pu S, Jenkins DJ, Connelly PW,
Lamarche B, et al. DHA-enriched high-oleic acid canola oil im-
proves lipid profile and lowers predicted cardiovascular disease risk
in the canola oil multicenter randomized controlled trial. Am J Clin
Nutr. 2014;100:8897. This well-controlled study shows that oils
rich in unsaturated fatty acids with 18 carbon atoms have com-
parable effects on the serum lipoprotein profile.
14. Jones PJ, MacKay DS, Senanayake VK, Pu S, Jenkins DJ,
Connelly PW, et al. High-oleic canola oil consumption enriches
LDL particle cholesteryl oleate content and reduces LDL proteo-
glycan binding in humans. Atherosclerosis. 2015;238:2318.
15. Melchior JT, Sawyer JK, Kelley KL, Shah R, Wilson MD, Hantgan
RR, et al. LDL particle core enrichment in cholesteryl oleate in-
creases proteoglycan binding and promotes atherosclerosis. J Lipid
Res. 2013;54:2495503.
16. Kien CL, Bunn JY, Stevens R, Bain J, Ikayeva O, Crain K, et al.
Dietary intake of palmitate and oleate has broad impact on systemic
and tissue lipid profiles in humans. Am J Clin Nutr. 2014;99:43645.
17. Kruse M, von Loeffelholz C, Hoffmann D, Pohlmann A, Seltmann
AC, Osterhoff M, et al. Dietary rapeseed/canola-oil supplementa-
tion reduces serum lipids and liver enzymes and alters postprandial
inflammatory responses in adipose tissue compared to olive-oil
supplementation in obese men. Mol Nutr Food Res. 2015;59:
18. Wien M, Oda K, Sabate J. A randomized controlled trial to evaluate
the effect of incorporating peanuts into an American Diabetes
Association meal plan on the nutrient profile of the total diet and
cardiometabolic parameters of adults with type 2 diabetes. Nutr J.
19.•• Vafeiadou K, Weech M, Altowaijri H, Todd S, Yaqoob P, Jackson
KG, et al. Replacement of saturated with unsaturated fats had no
impact on vascular function but beneficial effects on lipid bio-
markers, E-selectin, and blood pressure: results from the randomized,
controlled Dietary Intervention and VAScular function (DIVAS)
study. Am J Clin Nutr. 2015;102:408. This is a large randomized
controlled trial reporting that replacement of saturated with un-
saturated fats has no impact on vascular function.
20. Labonte ME, Jenkins DJ, Lewis GF, Chiavaroli L, Wong JM,
Kendall CW, et al. Adding MUFA to a dietary portfolio of
cholesterol-lowering foods reduces apoAI fractional catabolic rate
in subjects with dyslipidaemia. Br J Nutr. 2013;110:42636.
21.•• Sanders TA, Lewis FJ, Goff LM, Chowienczyk PJ, Group RS.
SFAs do not impair endothelial function and arterial stiffness. Am
J Clin Nutr. 2013;98:67783. This well-controlled trial shows in a
large group of healthy individuals that replacement of saturat-
edfattyacidwithcis-monounstatured fatty acid does not affect
vascular function.
22. Esser D, van Dijk SJ, Oosterink E, Muller M, Afman LA. A high-
fat SFA, MUFA, or n3 PUFA challenge affects the vascular re-
sponse and initiates an activated state of cellular adherence in lean
and obese middle-aged men. J Nutr. 2013;143:84351.
23. Lithander FE, Herlihy LK, Walsh DM, Burke E, Crowley V,
Mahmud A. Postprandial effect of dietary fat quantity and quality
on arterial stiffness and wave reflection: a randomised controlled
trial. Nutr J. 2013;12:93.
24. Mennella I, Savarese M, Ferracane R, Sacchi R, Vitaglione P. Oleic
acid content of a meal promotes oleoylethanolamide response and
reduces subsequent energy intake in humans. Food Funct. 2015;6:
25. Barbour JA, Howe PR, Buckley JD, Wright GC, Bryan J, Coates
AM. Lower energy intake following consumption of Hi-oleic and
regular peanuts compared with iso-energetic consumption of potato
crisps. Appetite. 2014;82:12430.
26. Duarte Moreira Alves R, Boroni Moreira AP, Silva Macedo V,
Brunoro Costa NM, Goncalves Alfenas Rde C, Bressan J. High-
38 Page 6 of 7 Curr Atheroscler Rep (2016) 18: 38
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
oleic peanuts increase diet-induced thermogenesis in overweight
and obese men. Nutr Hosp. 2014;29:102432.
27. Krishnan S, Cooper JA. Effect of dietary fatty acid composition on
substrate utilization and body weight maintenance in humans. Eur J
Nutr. 2014;53:691710.
28. Clevenger HC, Stevenson JL, Cooper JA. Metabolic responses to
dietary fatty acids in obese women. Physiol Behav. 2015;139:739.
29.•• Kien CL, Bunn JY, Tompkins CL, Dumas JA, Crain KI, Ebenstein
DB, et al. Substituting dietary monounsaturated fat for saturated fat
is associated with increased daily physical activity and resting en-
ergy expenditure and with changes in mood. Am J Clin Nutr.
2013;97:68997. In this article, Kien and colleagues demon-
strate that substituting monounsaturated fat for saturated fat
is associated with an increased resting energy expenditure.
30. Gillingham LG, Harris-Janz S, Jones PJ. Dietary monounsaturated
fatty acids are protective against metabolic syndrome and cardio-
vascular disease risk factors. Lipids. 2011;46:20928.
31.•• Estruch R, Ros E, Salas-Salvado J, Covas MI, Corella D, Aros F, et al.
Primary prevention of cardiovascular disease with a Mediterranean
diet. N Engl J Med. 2013;368:127990. The PREDIMED study is
the first large randomized controlled trial showing the benefit of a
Mediterranean diet pattern on CVD risk.
32. Rose GA, Thomson WB, Williams RT. Corn oil in treatment of
ischaemic heart disease. Br Med J. 1965;1:15313.
33.Guasch-Ferre M, Babio N, Martinez-Gonzalez MA, Corella D, Ros
E, Martin-Pelaez S, et al. Dietary fat intake and risk of
cardiovascular disease and all-cause mortality in a population at
high risk of cardiovascular disease. Am J Clin Nutr. 2015;102:
156373. This recently published prospective cohort study
found that intakes of monounsaturated fatty acids are associat-
ed with a lower risk of CVD and death.
34.Simila ME, Kontto JP, Mannisto S, Valsta LM, Virtamo J.
Glycaemic index, carbohydrate substitution for fat and risk of
CHD in men. Br J Nutr. 2013;110:170411. Within the Alpha-
Tocopherol, Beta-Carotene Cancer Prevention Study, a pro-
spective cohort study in male smokers, replacements of carbo-
hydrates for cis-MUFA reduced the risk of CHD.
35.Campmans-Kuijpers MJ, Sluijs I, Nothlings U, Freisling H,
Overvad K, Boeing H, et al. The association of substituting carbo-
hydrates with total fat and different types of fatty acids with mor-
tality and weight change among diabetes patients. Clin Nutr. 2015.
doi:10.1016/j.clnu.2015.08.003.In patients with type 2 diabetes,
substitution of carbohydrates with MUFAs may be associated
with lower CVD mortality.
36.Praagman J, Beulens JW, Alssema M, Zock PL, Wanders AJ, Sluijs I,
et al. The association between dietary saturated fatty acids and ischemic
heart disease depends on the type and source of fatty acid in the
European Prospective Investigation into Cancer and Nutrition-
Netherlands cohort. Am J Clin Nutr. 2016;103:35665. Replacement
of saturated fatty acids for other macronutrients was associated
with a lower risk of CHD in this Dutch cohort from the
European Prospective Investigation into Cancer and Nutrition.
Curr Atheroscler Rep (2016) 18: 38 Page 7 of 7 38
Content courtesy of Springer Nature, terms of use apply. Rights reserved.
Terms and Conditions
Springer Nature journal content, brought to you courtesy of Springer Nature Customer Service Center GmbH (“Springer Nature”).
Springer Nature supports a reasonable amount of sharing of research papers by authors, subscribers and authorised users (“Users”), for small-
scale personal, non-commercial use provided that all copyright, trade and service marks and other proprietary notices are maintained. By
accessing, sharing, receiving or otherwise using the Springer Nature journal content you agree to these terms of use (“Terms”). For these
purposes, Springer Nature considers academic use (by researchers and students) to be non-commercial.
These Terms are supplementary and will apply in addition to any applicable website terms and conditions, a relevant site licence or a personal
subscription. These Terms will prevail over any conflict or ambiguity with regards to the relevant terms, a site licence or a personal subscription
(to the extent of the conflict or ambiguity only). For Creative Commons-licensed articles, the terms of the Creative Commons license used will
We collect and use personal data to provide access to the Springer Nature journal content. We may also use these personal data internally within
ResearchGate and Springer Nature and as agreed share it, in an anonymised way, for purposes of tracking, analysis and reporting. We will not
otherwise disclose your personal data outside the ResearchGate or the Springer Nature group of companies unless we have your permission as
detailed in the Privacy Policy.
While Users may use the Springer Nature journal content for small scale, personal non-commercial use, it is important to note that Users may
use such content for the purpose of providing other users with access on a regular or large scale basis or as a means to circumvent access
use such content where to do so would be considered a criminal or statutory offence in any jurisdiction, or gives rise to civil liability, or is
otherwise unlawful;
falsely or misleadingly imply or suggest endorsement, approval , sponsorship, or association unless explicitly agreed to by Springer Nature in
use bots or other automated methods to access the content or redirect messages
override any security feature or exclusionary protocol; or
share the content in order to create substitute for Springer Nature products or services or a systematic database of Springer Nature journal
In line with the restriction against commercial use, Springer Nature does not permit the creation of a product or service that creates revenue,
royalties, rent or income from our content or its inclusion as part of a paid for service or for other commercial gain. Springer Nature journal
content cannot be used for inter-library loans and librarians may not upload Springer Nature journal content on a large scale into their, or any
other, institutional repository.
These terms of use are reviewed regularly and may be amended at any time. Springer Nature is not obligated to publish any information or
content on this website and may remove it or features or functionality at our sole discretion, at any time with or without notice. Springer Nature
may revoke this licence to you at any time and remove access to any copies of the Springer Nature journal content which have been saved.
To the fullest extent permitted by law, Springer Nature makes no warranties, representations or guarantees to Users, either express or implied
with respect to the Springer nature journal content and all parties disclaim and waive any implied warranties or warranties imposed by law,
including merchantability or fitness for any particular purpose.
Please note that these rights do not automatically extend to content, data or other material published by Springer Nature that may be licensed
from third parties.
If you would like to use or distribute our Springer Nature journal content to a wider audience or on a regular basis or in any other manner not
expressly permitted by these Terms, please contact Springer Nature at
... Monounsaturated fatty acids (MUFA) present an aliphatic chain with only one C=C double bond; in particular, in MUFA in cis configuration, the two hydrogens adjacent to the double bond are on the same side of the aliphatic chain [79]. The average worldwide intake of MUFA ranges from 10% of daily total energy consumption to 22%: generally, southern European Countries had a higher MUFA intake compared to central and northern ones [80]. Other differences are related to the dietary sources: although vegetable oils, mainly olive oil, represent the main MUFA sources in Greece, Italy, and Spain by providing up to 64% of total MUFA intake [36], in other countries, MUFA are introduced through meat, meat products, added fats, and dairy products [81,82]. ...
... Oleic acid is the most important MUFA, accounting for about 92% of all MUFA introduced through the diet [37][38][39]. In recent years, various studies have analyzed the effect of olive oil on CVD-related outcomes in humans, highlighting an overall antiatherogenic and antithrombotic effect, by increasing the HDL-C/LDL-C ratio, decreasing TC plasma levels [80,83], reducing blood pressure [84], and exerting a beneficial anti-inflammatory effect [85]. However, other studies have reported a neutral or negative association between CVD and MUFA. ...
Full-text available
Reverse cholesterol transport (RCT) is a physiological mechanism protecting cells from an excessive accumulation of cholesterol. When this process begins in vascular macrophages, it acquires antiatherogenic properties, as has been widely demonstrated in animal models. Dietary lipids, despite representing a fundamental source of energy and exerting multiple biological functions, may induce detrimental effects on cardiovascular health. In the present review we summarize the current knowledge on the mechanisms of action of the most relevant classes of dietary lipids, such as fatty acids, sterols and liposoluble vitamins, with effects on different steps of RCT. We also provide a critical analysis of data obtained from experimental models which can serve as a valuable tool to clarify the effects of dietary lipids on cardiovascular disease.
... However, recent research has indicated that this might not always be the case . On the other hand, it was found that a high MUFA intake together with a reduction in SFA intake might reduce LDL cholesterol (associated with the development of atherosclerosis) and total cholesterol (Joris & Mensink, 2016). However, there is not yet enough evidence to link this fact with the prevention of CHD. ...
... This is critical as vascular endothelial cells depend on insulin activity for proper function. Also, the fatty acid profile likely reduces the risk of LDL oxidation, thus protecting against atherosclerosis [13,[38][39][40][41][42][43]. For weight control, higher oleic acid intake leads to lower fat storage compared to long-chain saturated fats, especially when consumed in a moderate refined carbohydrate diet [44,45]. ...
Full-text available
This first comprehensive review of fresh Hass avocados includes 19 clinical trials, five observational studies, and biological mechanisms. We identified four primary avocado health effects: (1) reducing cardiovascular disease risk in healthy overweight or obese adults with dyslipidemia by lowering non-HDL-C profiles, triglycerides, LDL oxidation, small atherogenic LDL particles and promoting postprandial vascular endothelial health for better peripheral blood flow; (2) lowering the risk of being overweight or obese, supporting weight loss, and reducing visceral fat tissue in overweight or obese women; (3) improving cognitive function in older normal-weight adults and in young to middle age overweight or obese adults especially in frontal cortex executive function; and (4) stimulating improved colonic microbiota health in overweight or obese adults by promoting healthier microflora and fecal metabolites. We also identified a unique combination of four Hass avocado nutritional features that appear to be primarily responsible for these health effects: (1) a 6 to 1 unsaturated (rich in oleic acid) to saturated fat ratio similar to olive oil; (2) a source of multifunctional prebiotic and viscous fiber; (3) a relatively low energy density of 1.6 kcal/g (79% of edible Hass avocado weight consists of water and fiber with a creamy, smooth texture); and (4) its oleic acid and water emulsion increases carotenoid absorption from low-fat fruits and vegetables (e.g., salsa or salad) when consumed with avocados. They are also a good source of micronutrients and polyphenols, and are very low in sodium and available carbohydrates supporting secondary health and wellness benefits. Hass avocado health effects are best demonstrated when consumed in a healthy dietary plan such as the Mediterranean diet. More extensive and longer clinical trials are needed to further enhance our understanding of the Hass avocado’s health effects.
... Chei et al. [24] found that high levels of palmitoleic acid increased the risk of IHD. On the contrary, data from some controlled randomized trials have shown that MUFAs have a beneficial effect on the profile of lipoproteins in the blood, and as a consequence, on reducing the risk of CVD [28]. The results obtained may cast doubt on the supposed positive effects of MUFAs in the body, particularly in IHD. ...
Full-text available
Objective: To identify associations of fatty acids (FAs) with the antioxidant enzymes in the blood of men with coronary atherosclerosis and ischemic heart disease (IHD). Methods: The study included 80 patients: control group-20 men without IHD, the core group-60 men with IHD. The core group was divided into subgroups: subgroup A-with the presence of vulnerable atherosclerotic plaques, subgroup B-with the absence of vulnerable atherosclerotic plaques. We analyzed the levels of FAs, free radicals, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) in the blood. Results: Patients with IHD, compared with the control group: (1) had higher levels of SOD, CAT, myristic, palmitic, palmitoleic, and octadecenoic FAs; (2) had lower levels of GPx, α-linolenic, docosapentaenoic, docosahexaenoic, and arachidonic FAs. In subgroup A there were found: (1) negative associations of SOD-with linoleic, eicosatrienoic, arachidonic, eicosapentaenoic, docosapentaenoic and docosahexaenoic FAs, positive associations-with palmitic acid; (2) positive correlations of CAT level with palmitoleic and stearic acids; (3) negative associations between of GPx and palmitic, palmitoleic, stearic and octadecenoic FAs. Conclusions: Changes in the levels of antioxidant enzymes, and a disbalance of the FAs profile, probably indicate active oxidative processes in the body and may indicate the presence of atherosclerotic changes in the vessels.
... Previous studies reported similar MUFA and UFA results for GPO (Mokhtar et al., 2018) and GSO (Ramadan & Morsel, 2003). In fact, MUFAs have a favorable effect on the serum lipoprotein profile compared with saturated fatty acids (SFAs), and they have a significant effect in reducing coronary heart diseases (Joris & Mensink, 2016). GPO and GSO had high ratios of polyunsaturated/saturated acids (PUFA/SFA, 7.1 and 5.1%, respectively), which has been recommended to reduce serum cholesterol and prevent cardiovascular diseases (Rudel, Kelly, Sawyer, Shah, & Wilson, 1998). ...
The chemical and thermal characteristics of goldenberry pomace oil (GPO) and goldenberry seed oil (GSO) were investigated. GPO and GSO contained high levels of unsaturated fatty acids (90.1% and 85.1%, respectively), and the major fatty acid was linoleic (62.0% and 72.8%, respectively). Additionally, GPO contained eleven triacylglycerol (TAG) species, three of which represented 82.7%, namely C54:6, C54:4 and C52:4, and trilinolein was the dominant one (35.5%). GSO contained nine TAG species, two of which represented 80.3%, namely C54:6 and C52:4, and trilinolein was dominant (53.3%). The DSC analysis of GPO and GSO revealed that three exothermal peaks were detected during cooling. Three endothermal peaks (one of which is exothermal for GSO) were detected during melting, and the most significant peaks occurred at low temperatures. FTIR spectra indicated that GPO and GSO did not contain peroxides or trans fatty acids, but they did contain low concentrations of free fatty acids.
Full-text available
MicroRNA (miRNA)-130b, as a regulator of lipid metabolism in adipose and mammary gland tissues, is actively involved in lipogenesis, but its endogenous role in fatty acid synthesis remains unclear. Here, we aimed to explore the function and underlying mechanism of miR-130b in fatty acid synthesis using the CRISPR/Cas9 system in primary goat mammary epithelial cells (GMEC). A single clone with deletion of 43 nucleotides showed a significant decrease in miR-130b-5p and miR-130b-3p abundances and an increase of target genes PGC1α and PPARG. In addition, knockout of miR-130b promoted triacylglycerol (TAG) and cholesterol accumulation, and decreased the proportion of monounsaturated fatty acids (MUFA) C16:1, C18:1 and polyunsaturated fatty acids (PUFA) C18:2, C20:3, C20:4, C20:5, C22:6. Similarly, the abundance of fatty acid synthesis genes ACACA and FASN and transcription regulators SREBP1c and SREBP2 was elevated. Subsequently, interference with PPARG instead of PGC1α in knockout cells restored the effect of miR-130b knockout, suggesting that PPARG is responsible for miR-130b regulating fatty acid synthesis. Moreover, disrupting PPARG inhibits PGC1α transcription and translation. These results reveal that miR-130b directly targets the PPARG–PGC1α axis, to inhibit fatty acid synthesis in GMEC. In conclusion, miR-130b could be a potential molecular regulator for improving the beneficial fatty acids content in goat milk.
Polyunsaturated and monounsaturated fatty acids, respectively known as PUFA and MUFA, are considered bioactive compounds. Nuts and seeds, fish, and other marine products are the main sources of PUFA and MUFA. Epidemiological studies support many health benefits of PUFA and MUFA. Accordingly, this contribution summarizes the general chemical aspects as well as the reported health benefits in cell model systems, animals, and humans attributed to these compounds. The main biological mechanisms involved in the role of MUFA and PUFA are provided and discussed. The protective role of these compounds against cardiovascular diseases has been widely recognized in previous works. However, more studies are needed regarding potential health benefits of MUFA and PUFA against diabetes, cancer, Alzheimer’s disease, and dementia due to current controversies.
Purpose: Parental nutrition can influence the early stages of offspring development, leading to fetal programming. During this critical period, fatty acids play an important role in the regulation of lipid metabolism, essential for the proper development of offspring. Epigenetic mechanisms seem to be involved in the changes in structure and function of several tissues due to poor nutrition, as long as deficient or excessive maternal exposure to saturated fatty acids (SFA), polyunsaturated fatty acids (PUFA), and monounsaturated fatty acids (MUFA) seem to be able to alter offspring metabolism and influence long-term chronic diseases. This review addresses an update on the influence of SFA, PUFA, and/or MUFA in the epigenetic mechanisms on fetal programming. Methods: The literature search was performed in the database PubMed and original papers in the English language were selected, containing the effects of different types of fatty acids in epigenetic programming mechanisms of chronic diseases. The time limit was not set for a broader identification of papers published within the field. Results: SFA present in maternal high-fat diets (HFD) has been shown to cause epigenetic alterations in the liver, adipose tissue, heart, and brain, leading to changes in glucose, lipid, and cardiovascular metabolism of the offspring. Maternal consumption of MUFA oleic acid during pregnancy and lactation can be beneficial especially to lipid metabolism, as long as PUFA intake exerts positive outcomes on offspring neurodevelopment and epigenome reshape, preventing chronic diseases. Conclusions: The present data showed that maternal intake of different types of SFA, MUFA, and PUFA can influence the offspring programming of epigenetic machinery through histone modifications, DNA methylation, and miRNA regulation. More studies including both male and female offspring are needed in order to compare differences between sexes, as well as epigenetic studies in the offspring from male progenitors exposed to different types of fatty acids. © 2021, The Author(s), under exclusive licence to Springer Nature Switzerland AG.
Obesity is a relevant health hazard characterized as a chronic noncommunicable disease, with severe comorbidities that cause mortality worldwide. Acrocomia aculeata is a Brazilian palm with edible fruits. Its pulp contains fibers, monounsaturated fatty acids (MUFAs), such as oleic acid and carotenoids. In this context, our study aimed to elucidate the protective effect of the lyophilized A. aculeata pulp added at the rates of 1%, 2%, and 4% to a high-fat (HF) diet (rich in saturated fats and cholesterol), for 90 days, in mice. The treatment with 4% pulp induced a significant increase in the biochemical parameters of serum cholesterol HDL-C (high-density lipoprotein) compared with the control. According to the evaluation of the epididymal tissue, the groups treated with A. aculeata pulp exhibited smaller fat deposits compared with the HF diet group. Therefore, we infer that the predominant components in A. aculeata, particularly fibers and MUFAs, promote beneficial effects on health parameters during simultaneous exposure to food rich in saturated fat and cholesterol, typical of the Western diet. This is the first study to correlate the presence of fatty acids from A. aculeata pulp in different proportions added in a HF diet with metabolic and histological parameters in Swiss mice.
Full-text available
Background: The association between saturated fatty acid (SFA) intake and ischemic heart disease (IHD) risk is debated. Objective: We sought to investigate whether dietary SFAs were associated with IHD risk and whether associations depended on 1) the substituting macronutrient, 2) the carbon chain length of SFAs, and 3) the SFA food source. Design: Baseline (1993-1997) SFA intake was measured with a food-frequency questionnaire among 35,597 participants from the European Prospective Investigation into Cancer and Nutrition-Netherlands cohort. IHD risks were estimated with multivariable Cox regression for the substitution of SFAs with other macronutrients and for higher intakes of total SFAs, individual SFAs, and SFAs from different food sources. Results: During 12 y of follow-up, 1807 IHD events occurred. Total SFA intake was associated with a lower IHD risk (HR per 5% of energy: 0.83; 95% CI: 0.74, 0.93). Substituting SFAs with animal protein, cis monounsaturated fatty acids, polyunsaturated fatty acids (PUFAs), or carbohydrates was significantly associated with higher IHD risks (HR per 5% of energy: 1.27-1.37). Slightly lower IHD risks were observed for higher intakes of the sum of butyric (4:0) through capric (10:0) acid (HRSD: 0.93; 95% CI: 0.89, 0.99), myristic acid (14:0) (HRSD: 0.90; 95% CI: 0.83, 0.97), the sum of pentadecylic (15:0) and margaric (17:0) acid (HRSD: 0.91: 95% CI: 0.83, 0.99), and for SFAs from dairy sources, including butter (HRSD: 0.94; 95% CI: 0.90, 0.99), cheese (HRSD: 0.91; 95% CI: 0.86, 0.97), and milk and milk products (HRSD: 0.92; 95% CI: 0.86, 0.97). Conclusions: In this Dutch population, higher SFA intake was not associated with higher IHD risks. The lower IHD risk observed did not depend on the substituting macronutrient but appeared to be driven mainly by the sums of butyric through capric acid, the sum of pentadecylic and margaric acid, myristic acid, and SFAs from dairy sources. Residual confounding by cholesterol-lowering therapy and trans fat or limited variation in SFA and PUFA intake may explain our findings. Analyses need to be repeated in populations with larger differences in SFA intake and different SFA food sources.
Full-text available
Lack of consensus exists pertaining to the scientific evidence regarding effects of various dietary fatty acids on cardiovascular disease (CVD) risk. The objective of this article is to review current evidence concerning cardiovascular health effects of the main dietary fatty acid types; namely, trans (TFA), saturated (SFA), polyunsaturated (PUFA; n-3 PUFA and n-6 PUFA), and monounsaturated fatty acids (MUFA). Accumulating evidence shows negative health impacts of TFA and SFA; both may increase CVD risk. Policies have been proposed to reduce TFA and SFA consumption to less than 1 and 7 % of energy intake, respectively. Cardiovascular health might be promoted by replacing SFA and TFA with n-6 PUFA, n-3 PUFA, or MUFA; however, the optimal amount of PUFA or MUFA that can be used to replace SFA and TFA has not been defined yet. Evidence suggests of the potential importance of restricting n-6 PUFA up to 10 % of energy and obtaining an n-6/n-3 ratio as close as possible to unity, along with a particular emphasis on consuming adequate amounts of essential fatty acids. The latest evidence shows cardioprotective effects of MUFA-rich diets, especially when MUFA are supplemented with essential fatty acids; namely, docosahexaenoic acid. MUFA has been newly suggested to be involved in regulating fat oxidation, energy metabolism, appetite sensations, weight maintenance, and cholesterol metabolism. These favorable effects might implicate MUFA as the preferable choice to substitute for other fatty acids, especially given the declaration of its safety for up to 20 % of total energy.
Full-text available
ABSTRACT Background: Dietary fat quality and fat replacement are more important for cardiovascular disease (CVD) prevention than is total dietary fat intake. Objective: The aim was to evaluate the association between total fat intake and fat subtypes with the risk of CVD (myocardial infarc- tion, stroke, or death from cardiovascular causes) and cardiovascular and all-cause death. We also examined the hypothetical effect of the isocaloric substitution of one macronutrient for another. Design: We prospectively studied 7038 participants at high CVD risk from the PREvención con DIeta MEDiterránea (PREDIMED) study. The trial was conducted from 2003 to 2010, but the present analysis was based on an expanded follow-up until 2012. At baseline and yearly thereafter, total and specific fat subtypes were repeatedly measured by using validated food-frequency questionnaires. Time-dependent Cox proportional hazards models were used. Results: After 6 y of follow-up, we documented 336 CVD cases and 414 total deaths. HRs (95% CIs) for CVD for those in the highest quintile of total fat, monounsaturated fatty acid (MUFA), and poly- unsaturated fatty acid (PUFA) intake compared with those in the lowest quintile were 0.58 (0.39, 0.86), 0.50 (0.31, 0.81), and 0.68 (0.48, 0.96), respectively. In the comparison between extreme quintiles, higher saturated fatty acid (SFA) and trans-fat intakes were associated with 81% (HR: 1.81; 95% CI: 1.05, 3.13) and 67% (HR: 1.67; 95% CI: 1.09, 2.57) higher risk of CVD. Inverse associations with all-cause death were also observed for PUFA and MUFA intakes. Iso- caloric replacements of SFAs with MUFAs and PUFAs or trans fat with MUFAs were associated with a lower risk of CVD. SFAs from pastries and processed foods were associated with a higher risk of CVD. Conclusions: Intakes of MUFAs and PUFAs were associated with a lower risk of CVD and death, whereas SFA and trans-fat intakes were associated with a higher risk of CVD. The replacement of SFAs with MUFAs and PUFAs or of trans fat with MUFAs was inversely associated with CVD.
Full-text available
Substitution of carbohydrates with fat in a diet for type 2 diabetes patients is still debated. This study aimed to investigate the association between dietary carbohydrate intake and isocaloric substitution with (i) total fat, (ii) saturated fatty acids (SFA), (iii) mono-unsaturated fatty acids (MUFA) and (iv) poly-unsaturated fatty acids (PUFA) with all-cause and cardiovascular (CVD) mortality risk and 5-year weight change in patients with type 2 diabetes. The study included 6192 patients with type 2 diabetes from 15 cohorts of the European Prospective Investigation into Cancer and Nutrition (EPIC). Dietary intake was assessed at recruitment with country-specific food-frequency questionnaires. Cox and linear regression were used to estimate the associations with (CVD) mortality and weight change, adjusting for confounders and using different methods to adjust for energy intake. After a mean follow-up of 9.2 y ± SD 2.3 y, 791 (13%) participants had died, of which 268 (4%) due to CVD. Substituting 10 g or 5 energy% of carbohydrates by total fat was associated with a higher all-cause mortality risk (HR 1.07 [1.02-1.13]), or SFAs (HR 1.25 [1.11-1.40]) and a lower risk when replaced by MUFAs (HR 0.89 [0.77-1.02]). When carbohydrates were substituted with SFAs (HR 1.22 [1.00-1.49]) or PUFAs (HR 1.29 [1.02-1.63]) CVD mortality risk increased. The 5-year weight was lower when carbohydrates were substituted with total fat or MUFAs. These results were consistent over different energy adjustment methods. In diabetes patients, substitution of carbohydrates with SFAs was associated with a higher (CVD) mortality risk and substitution by total fat was associated with a higher all-cause mortality risk. Substitution of carbohydrates with MUFAs may be associated with lower mortality risk and weight reduction. Instead of promoting replacement of carbohydrates by total fat, dietary guideline should continue focusing on replacement by fat-subtypes; especially SFAs by MUFAs. Copyright © 2015 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
Full-text available
Reducing saturated fat reduces serum cholesterol, but effects on other intermediate outcomes may be less clear. Additionally it is unclear whether the energy from saturated fats that are lost in the diet are more helpfully replaced by polyunsaturated fats, monounsaturated fats, carbohydrate or protein. This review is part of a series split from and updating an overarching review. To assess the effect of reducing saturated fat intake and replacing it with carbohydrate (CHO), polyunsaturated (PUFA) or monounsaturated fat (MUFA) and/or protein on mortality and cardiovascular morbidity, using all available randomised clinical trials. We updated our searches of the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE (Ovid) and EMBASE (Ovid) on 5 March 2014. We also checked references of included studies and reviews. Trials fulfilled the following criteria: 1) randomised with appropriate control group; 2) intention to reduce saturated fat intake OR intention to alter dietary fats and achieving a reduction in saturated fat; 3) not multifactorial; 4) adult humans with or without cardiovascular disease (but not acutely ill, pregnant or breastfeeding); 5) intervention at least 24 months; 6) mortality or cardiovascular morbidity data available. Two review authors working independently extracted participant numbers experiencing health outcomes in each arm, and we performed random-effects meta-analyses, meta-regression, subgrouping, sensitivity analyses and funnel plots. We include 15 randomised controlled trials (RCTs) (17 comparisons, ˜59,000 participants), which used a variety of interventions from providing all food to advice on how to reduce saturated fat. The included long-term trials suggested that reducing dietary saturated fat reduced the risk of cardiovascular events by 17% (risk ratio (RR) 0.83; 95% confidence interval (CI) 0.72 to 0.96, 13 comparisons, 53,300 participants of whom 8% had a cardiovascular event, I² 65%, GRADE moderate quality of evidence), but effects on all-cause mortality (RR 0.97; 95% CI 0.90 to 1.05; 12 trials, 55,858 participants) and cardiovascular mortality (RR 0.95; 95% CI 0.80 to 1.12, 12 trials, 53,421 participants) were less clear (both GRADE moderate quality of evidence). There was some evidence that reducing saturated fats reduced the risk of myocardial infarction (fatal and non-fatal, RR 0.90; 95% CI 0.80 to 1.01; 11 trials, 53,167 participants), but evidence for non-fatal myocardial infarction (RR 0.95; 95% CI 0.80 to 1.13; 9 trials, 52,834 participants) was unclear and there were no clear effects on stroke (any stroke, RR 1.00; 95% CI 0.89 to 1.12; 8 trials, 50,952 participants). These relationships did not alter with sensitivity analysis. Subgrouping suggested that the reduction in cardiovascular events was seen in studies that primarily replaced saturated fat calories with polyunsaturated fat, and no effects were seen in studies replacing saturated fat with carbohydrate or protein, but effects in studies replacing with monounsaturated fats were unclear (as we located only one small trial). Subgrouping and meta-regression suggested that the degree of reduction in cardiovascular events was related to the degree of reduction of serum total cholesterol, and there were suggestions of greater protection with greater saturated fat reduction or greater increase in polyunsaturated and monounsaturated fats. There was no evidence of harmful effects of reducing saturated fat intakes on cancer mortality, cancer diagnoses or blood pressure, while there was some evidence of improvements in weight and BMI. The findings of this updated review are suggestive of a small but potentially important reduction in cardiovascular risk on reduction of saturated fat intake. Replacing the energy from saturated fat with polyunsaturated fat appears to be a useful strategy, and replacement with carbohydrate appears less useful, but effects of replacement with monounsaturated fat were unclear due to inclusion of only one small trial. This effect did not appear to alter by study duration, sex or baseline level of cardiovascular risk. Lifestyle advice to all those at risk of cardiovascular disease and to lower risk population groups should continue to include permanent reduction of dietary saturated fat and partial replacement by unsaturated fats. The ideal type of unsaturated fat is unclear.
Background: Arterial stiffness is a component of vascular function and an established risk factor for cardiovascular disease. There is a lack of conclusive evidence on the effect of a meal rich in monounsaturated fat (MUFA) compared with an isoenergetic meal rich in saturated fat (SFA) on postprandial vascular function and specifically on arterial stiffness. Methods: Twenty healthy, non-smoking males (BMI 24 ± 2 kg/m²; age 37.7 ± 14.4 y) participated in this single-blind, randomised, cross-over dietary intervention study. Each subject was randomised to receive a high-fat test-meal (3 MJ; 56 ± 2 g fat) at breakfast on 2 separate occasions, one rich in oleic acid (MUFA-meal) and one rich in palmitic acid (SFA-meal), and the meals were isoenergetic. Blood pressure (BP), arterial stiffness (PWV) and arterial wave reflection (augmentation index, AIx) were measured using applanation tonometry at baseline and every 30 minutes up to 4 hours after the ingestion of the test-meals. Results: All subjects completed both arms of the dietary intervention. There was no significant difference in BP parameters, PWV or AIx at baseline between the two treatments (P > 0.05). There was a significant increase in brachial and aortic BP, mean arterial pressure (MAP), heart rate and PVW (time, P < 0.05) over the four hours after consumption of the fat-rich test-meal although the increase in PWV was no longer significant when adjusted for the increase in MAP. There was no difference in PWV between the two treatments (treatment time, P > 0.05). There was a significant reduction in AIx (time, P < 0.05) over the four hour postprandial period although this was no longer significant when adjusted for the increase in heart rate and MAP (time, P > 0.05). There was no difference in AIx between the two treatments (treatment time, P > 0.05). However, the reduction in heart rate corrected augmentation index (AIx75) was significant when corrected for the increase in MAP (time, P < 0.01) with no differential effect of the treatments (treatment time, P > 0.05). Conclusions: This study has demonstrated a BP dependent increase in PWV and a decrease in arterial wave reflection in the four hour period in response to a high-fat meal. There was no evidence however that replacement of some of the SFA with MUFA had a differential effect on these parameters. The study highlights the need for further research to understand the effects of the substitution of SFA with MUFA on non-serum, new and emerging risk factors for CVD such as arterial stiffness.
Background: The associations between dietary saturated fats and the risk of coronary heart disease (CHD) remain controversial, but few studies have compared saturated with unsaturated fats and sources of carbohydrates in relation to CHD risk. Objectives: This study sought to investigate associations of saturated fats compared with unsaturated fats and different sources of carbohydrates in relation to CHD risk. Methods: We followed 84,628 women (Nurses' Health Study, 1980 to 2010), and 42,908 men (Health Professionals Follow-up Study, 1986 to 2010) who were free of diabetes, cardiovascular disease, and cancer at baseline. Diet was assessed by a semiquantitative food frequency questionnaire every 4 years. Results: During 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates from whole grains were significantly associated with a lower risk of CHD comparing the highest with lowest quintile for PUFAs (hazard ratio [HR]: 0.80, 95% confidence interval [CI]: 0.73 to 0.88; p trend <0.0001) and for carbohydrates from whole grains (HR: 0.90, 95% CI: 0.83 to 0.98; p trend = 0.003). In contrast, carbohydrates from refined starches/added sugars were positively associated with a risk of CHD (HR: 1.10, 95% CI: 1.00 to 1.21; p trend = 0.04). Replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from whole grains was associated with a 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10). Conclusions: Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk.
Public health strategies to lower cardiovascular disease (CVD) risk involve reducing dietary saturated fatty acid (SFA) intake to ≤10% of total energy (%TE). However, the optimal type of replacement fat is unclear. We investigated the substitution of 9.5-9.6%TE dietary SFAs with either monounsaturated fatty acids (MUFAs) or n-6 (ω-6) polyunsaturated fatty acids (PUFAs) on vascular function and other CVD risk factors. Using a randomized, controlled, single-blind, parallel-group dietary intervention, 195 men and women aged 21-60 y with moderate CVD risk (≥50% above the population mean) from the United Kingdom followed one of three 16-wk isoenergetic diets (%TE target compositions, total fat:SFA:MUFA:n-6 PUFA) that were rich in SFAs (36:17:11:4, n = 65), MUFAs (36:9:19:4, n = 64), or n-6 PUFAs (36:9:13:10, n = 66). The primary outcome measure was flow-mediated dilatation; secondary outcome measures included fasting serum lipids, microvascular reactivity, arterial stiffness, ambulatory blood pressure, and markers of insulin resistance, inflammation, and endothelial activation. Replacing SFAs with MUFAs or n-6 PUFAs did not affect the percentage of flow-mediated dilatation (primary endpoint) or other measures of vascular reactivity. Of the secondary outcome measures, substitution of SFAs with MUFAs attenuated the increase in night systolic blood pressure (-4.9 mm Hg, P = 0.019) and reduced E-selectin (-7.8%, P = 0.012). Replacement with MUFAs or n-6 PUFAs lowered fasting serum total cholesterol (-8.4% and -9.2%, respectively), low-density lipoprotein cholesterol (-11.3% and -13.6%), and total cholesterol to high-density lipoprotein cholesterol ratio (-5.6% and -8.5%) (P ≤ 0.001). These changes in low-density lipoprotein cholesterol equate to an estimated 17-20% reduction in CVD mortality. Substitution of 9.5-9.6%TE dietary SFAs with either MUFAs or n-6 PUFAs did not significantly affect the percentage of flow-mediated dilatation or other measures of vascular function. However, the beneficial effects on serum lipid biomarkers, blood pressure, and E-selectin offer a potential public health strategy for CVD risk reduction. This trial was registered at as NCT01478958. © 2015 American Society for Nutrition.
Oleic acid consumption is considered cardio-protective according to studies conducted examining effects of the Mediterranean diet. However, animal models have shown that oleic acid consumption increases LDL particle cholesteryl oleate content which is associated with increased LDL-proteoglycan binding and atherosclerosis. The objective was to examine effects of varying oleic, linoleic and docosahexaenoic acid consumption on human LDL-proteoglycan binding in a non-random subset of the Canola Oil Multi-center Intervention Trial (COMIT) participants. COMIT employed a randomized, double-blind, five-period, cross-over trial design. Three of the treatment oil diets: 1) a blend of corn/safflower oil (25:75); 2) high oleic canola oil; and 3) DHA-enriched high oleic canola oil were selected for analysis of LDL-proteoglycan binding in 50 participants exhibiting good compliance. LDL particles were isolated from frozen plasma by gel filtration chromatography and LDL cholesteryl esters quantified by mass-spectrometry. LDL-proteoglycan binding was assessed using surface plasmon resonance. LDL particle cholesterol ester fatty acid composition was sensitive to the treatment fatty acid compositions, with the main fatty acids in the treatments increasing in the LDL cholesterol esters. The corn/safflower oil and high-oleic canola oil diets lowered LDL-proteoglycan binding relative to their baseline values (p = 0.0005 and p = 0.0012, respectively). At endpoint, high-oleic canola oil feeding resulted in lower LDL-proteoglycan binding than corn/safflower oil (p = 0.0243) and DHA-enriched high oleic canola oil (p = 0.0249), although high-oleic canola oil had the lowest binding at baseline (p = 0.0344). Our findings suggest that high-oleic canola oil consumption in humans increases cholesteryl oleate percentage in LDL, but in a manner not associated with a rise in LDL-proteoglycan binding.
Obesity is associated with hyperlipidemia, hepatic steatosis and low-grade inflammation. Studies have shown that MUFA as well as PUFA have beneficial effects on blood lipids and the inflammatory state. This study investigates a daily supplementation of either 50 g of rapeseed/canola (RA) or olive (OL) oil over four weeks on serum lipids, serum liver enzymes and inflammatory gene expression in subcutaneous (s. c.) adipose tissue in obese men. Consuming RA resulted in increased serum n-3 fatty acids and a reduction in total cholesterol, LDL cholesterol and serum aspartate aminotransferase compared to OL. In s. c. adipose tissue gene expression of the pro-inflammatory cytokine IL6 was reduced in RA compared to OL. However, after four hours after a test meal, containing the appropriate oil, white bread and 400 mL of liquid diet drink (835 kcal in total), gene expression of IL6, IL1B and EMR1 was increased in RA and of monocyte chemoattractant protein-1 (CCL2) in both, RA and OL. This demonstrates that consuming RA for four weeks improves serum lipids, liver enzymes and basal inflammation in s. c. adipose tissue, but mediates an acute pro-inflammatory response in adipose tissue upon consuming a meal. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.