ArticlePDF AvailableLiterature Review

Monounsaturated Fatty Acids and Risk of Cardiovascular Disease: Synopsis of the Evidence Available from Systematic Reviews and Meta-Analyses

Authors:

Abstract and Figures

No dietary recommendations for monounsaturated fatty acids (MUFA) are given by the National Institute of Medicine, the United States Department of Agriculture, European Food and Safety Authority and the American Diabetes Association. In contrast, the Academy of Nutrition and Dietetics, and the Canadian Dietetic Association both promote <25% MUFA of daily total energy consumption, while the American Heart Association sets a limit of 20% MUFA in their respective guidelines. The present review summarizes systematic reviews and meta-analyses of randomized controlled trials and cohort studies investigating the effects of MUFA on cardiovascular and diabetic risk factors, cardiovascular events and cardiovascular death. Electronic database Medline was searched for systematic reviews and meta-analyses using "monounsaturated fatty acids", "monounsaturated fat", and "dietary fat" as search terms with no restriction to calendar date or language. Reference lists and clinical guidelines were searched as well. Sixteen relevant papers were identified. Several studies indicated an increase of HDL-cholesterol and a corresponding decrease in triacylglycerols following a MUFA-rich diet. The effects on total and LDL-cholesterol appeared not consistent, but no detrimental effects on blood lipids were observed. Values for systolic and diastolic blood pressure were found to be reduced both during short- and long-term protocols using high amounts of MUFA as compared to low-MUFA diets. In type 2 diabetic subjects, MUFA exerted a hypoglycemic effect and reduced glycosylated hemoglobin in the long term. Data from meta-analyses exploring evidence from long-term prospective cohort studies provide ambiguous results with respect to the effects of MUFA on risk of coronary heart disease (CHD). One meta-analysis reported an increase in CHD events, however, most meta-analyses observed a lesser number of cases in participants subjected to a high-MUFA protocol. Although no detrimental side effects of MUFA-rich diets were reported in the literature, there still is no unanimous rationale for MUFA recommendations in a therapeutic regimen. Additional long-term intervention studies are required to characterized efficacy and effectiveness of recommending MUFA-rich diet among general and clinical populations.
Content may be subject to copyright.
Nutrients 2012, 4, 1989-2007; doi:10.3390/nu4121989
nutrients
ISSN 2072-6643
www.mdpi.com/journal/nutrients
Review
Monounsaturated Fatty Acids and Risk of Cardiovascular
Disease: Synopsis of the Evidence Available from Systematic
Reviews and Meta-Analyses
Lukas Schwingshackl and Georg Hoffmann *
Department of Nutritional Sciences, Faculty of Life Sciences, University of Vienna, Althanstrasse 14,
1090 Vienna, Austria; E-Mail: lukas.schwingshackl@univie.ac.at
* Author to whom correspondence should be addressed; E-Mail: georg.hoffmann@univie.ac.at;
Tel.: +43-1-4277-549-50; Fax: +43-1-4277-9549.
Received: 11 September 2012; in revised form: 14 November 2012 / Accepted: 4 December 2012 /
Published: 11 December 2012
Abstract: No dietary recommendations for monounsaturated fatty acids (MUFA) are given
by the National Institute of Medicine, the United States Department of Agriculture,
European Food and Safety Authority and the American Diabetes Association. In contrast,
the Academy of Nutrition and Dietetics, and the Canadian Dietetic Association both
promote <25% MUFA of daily total energy consumption, while the American Heart
Association sets a limit of 20% MUFA in their respective guidelines. The present review
summarizes systematic reviews and meta-analyses of randomized controlled trials and
cohort studies investigating the effects of MUFA on cardiovascular and diabetic risk
factors, cardiovascular events and cardiovascular death. Electronic database Medline was
searched for systematic reviews and meta-analyses using monounsaturated fatty acids,
monounsaturated fat, and dietary fat as search terms with no restriction to calendar
date or language. Reference lists and clinical guidelines were searched as well. Sixteen
relevant papers were identified. Several studies indicated an increase of HDL-cholesterol
and a corresponding decrease in triacylglycerols following a MUFA-rich diet. The effects
on total and LDL-cholesterol appeared not consistent, but no detrimental effects on blood
lipids were observed. Values for systolic and diastolic blood pressure were found to be
reduced both during short- and long-term protocols using high amounts of MUFA as
compared to low-MUFA diets. In type 2 diabetic subjects, MUFA exerted a hypoglycemic
effect and reduced glycosylated hemoglobin in the long term. Data from meta-analyses
exploring evidence from long-term prospective cohort studies provide ambiguous results
with respect to the effects of MUFA on risk of coronary heart disease (CHD). One
OPEN ACCESS
Nutrients 2012, 4 1990
meta-analysis reported an increase in CHD events, however, most meta-analyses observed
a lesser number of cases in participants subjected to a high-MUFA protocol. Although no
detrimental side effects of MUFA-rich diets were reported in the literature, there still is no
unanimous rationale for MUFA recommendations in a therapeutic regimen. Additional
long-term intervention studies are required to characterized efficacy and effectiveness of
recommending MUFA-rich diet among general and clinical populations.
Keywords: monounsaturated fatty acids; cardiovascular disease; coronary heart disease;
meta-analysis; systematic review; dietary fat
1. Monounsaturated Fatty Acids
Monounsaturated fatty acids (MUFA) are chemically classified as fatty acids containing a single
double bond (in contrast to polyunsaturated fatty acids (PUFA) containing two or more double bonds
and saturated fatty acids (SFA) without double bonds). In the cis-configuration, the hydrogen atoms
are on the same side as the double bond, whereas in trans-configuration the hydrogen atoms and the
double bond are present on opposite sides. The cis-isomers are the predominant form of MUFA in food
sources. The most common cis-configured MUFA in daily nutrition is oleic acid (18:1 n-9), followed
by palmitoleic acid (16:1 n-7), and vaccenic acid (18:1 n-7). Moreover, oleic acid represents the topmost
MUFA provided in the diet (~90% of all MUFAs) [1]. The major trans-configured MUFA is elaidic
acid (trans 18:1 n-9). Some MUFAsuch as mystrioleic (14:1 n-5), gondoic (20:1 n-9), erucic (22:1 n-9)
and nervonic (24:1 n-9) acidare synthesized in minor concentrations endogenously using other MUFAs
as precursors (see Table 1 for a summary of different types of MUFA). Various sources for MUFA in
food are given in Table 2 (for comparison, PUFA and SFA contents are given as well). The most frequently
consumed MUFA rich dietary oils are canola and olive oil. Furthermore, over the last decade
commercial production of high oleic acid modified dietary oils with improved stability for the use in
food processing has been markedly increased in order to replace dietary oils rich in SFA and trans fatty
acids [2]. It should be recognized that in some populations, MUFAs are provided in higher amounts in
the form of erucic acid (C22:1 n-9), e.g., found in culinary oils derived from some Brassica spp. such
as rapeseed and mustard seed [3]. It is therefore not surprising that due to their widespread occurrence
in oils nuts, seeds, fruits and meat, the predominant source of MUFA is largely depending on individual
dietary habits. Like other fatty acids, MUFA are almost completely absorbed by the intestine and are
oxidized for energy production, converted into other fatty acids, or incorporated into tissue lipids.
Table 1. Selected monounsaturated fatty acids.
C-Atoms: Double Bonds
Scientific Name of Acid
Molecular Formula
Chemical Name
11:1
Undecylenic
C10H19COOH
cis-10-undecenoic acid
14:1
Myristoleic
C13H25COOH
cis-9-tetradecenoic acid
16:1
Palmitoleic
C15H29COOH
cis-9-hexadecenoic acid
16:1
Palmitelaidic
C15H29COOH
trans-9-hexadecenoic acid
16:1
/
C15H29COOH
cis-7-hexadecenoic
Nutrients 2012, 4 1991
Table 1. Cont.
18:1
Petroselinic
C17H33COOH
cis-6-octadecenoic acid
18:1
Oleic
C17H33COOH
cis-9-octadecenoic acid
18:1
Elaidic
C17H33COOH
trans-9-octadecenoic acid
18:1
Vaccenic
C17H33COOH
cis-11-octadecenoic acid
20:1
Gondoleic
C19H37COOH
cis-9-eicosenoic acid
20:1
Gondolic
C19H37COOH
cis-11-eicosenoic acid
22:1
Cetoleic
C21H41COOH
cis-11-docosenoic acid
22:1
Erucic
C21H41COOH
cis-13-docosenoic acid
24:1
Nervonic
C23H45COOH
cis-15-tetracosaenoic acid
Table 2. Fatty acid content of different oils, nuts, fruits, seeds and animal products.
Oils
PUFA, %
Olive oil
10.5
Coconut oil
2
Soybean oil
58
Peanut oil
32
Sesame oil
42
Sunflower oil (linoleic acid <60%)
40
High-oleic safflower oil
13
Sunflower oils (linoleic acid >70%)
75
Walnut oil
63
Almond oil
17
Hazelnut oil
10
Avocado oil
13
Canola oil
28
Mustard oil
21
High oleic sunflower
4
Hering oil
16
Fish oil, cold liver
23
Flaxseed oil, cold press
68
Corn and canola oil
29
High oleic sunflower
4
Hazelnut oil
10
Olive oil
10.5
High-oleic safflower oil
13
Avocado oil
13
Almond oil
17
Canola oil
28
Mustard oil
21
Corn and canola oil
29
Hering oil
16
Fish oil, cold liver
23
Peanut Oil
32
Sunflower Oil (linoleic acid <60%)
40
Sesame Oil
42
Nutrients 2012, 4 1992
Table 2. Cont.
Soybean oil
58
Walnut oil
63
Flaxseed oil, cold press
68
Sunflower oils (linoleic acid >70%)
75
Coconut oil
2
Nuts and Seeds
PUFA, %
Macademia
12
Hazelnut
8
Pecanut
22
Almonds
11
cashew nuts, dry roasted
7
Pistacchio nuts
14
Sunflower seed kernels, dried
23
Sesame, whole, roasted and toasted
21
Walnuts
35
Flaxseed
29
Safflower kernels, dried
28
Products of Animal Origin
PUFA, %
Butter, salted
3
Cheese, cheddar
1
Pork, ham
2
Mackerl
3.3
Beef, steak
0.4
Egg
2
Salmon
2.5
Milk, 3.7% fat
0.1
Chicken
0.75
MUFA = monounsaturated fatty acid; PUFA = polyunsaturated fatty acid; SFA = saturated fatty acid [4].
2. Guidelines
2.1. General Nutrition Guidelines
Table 3 summarizes MUFA recommendations of national and international authorities and organizations.
Table 3. National and international MUFA recommendations for healthy adults and
patients with diabetes.
Authority/Society
MUFA (% of TEC)
Target Group/Remarks
References
American Heart Association
<20
Healthy adults
[5]
Academy of Nutrition and Dietetics/Canadian
Dietetic Association
<25
Healthy adults
[6]
Dutch Dietary Guidelines
838
Healthy adults
Upper limit for obese: 25% of TEC
[7]
European Food Safety Authority
No specific
recommendations
Healthy adults
[8]
Nutrients 2012, 4 1993
Table 3. Cont.
Italian Society of Human Nutrition
No specific
recommendations
Healthy adults
[9]
Joint Committees of Germany, Austria, and
Switzerland
10
Healthy adults
[10]
National Cholesterol Educational Program III
<20
Healthy adults
[11]
National Institute of Medicine
No specific
recommendations
Healthy adults
[12]
Nordic Nutrition Dietary Guidelines
1015
Healthy adults
[13]
Nutritional Recommendations for the French
Population
20
Healthy adults
Including pregnant and lactating
women
[14]
UK COMA Committee
12
Healthy adults
[15]
US Department of Agriculture
No specific
recommendations
Healthy adults
[16]
World Health Organization/Food Agriculture
Organization
1520
Healthy adults
Adjusted to total fat intake
[3]
American Association of Clinical
Endocrinologists
No specific
recommendations
Diabetic patients
[17]
American Diabetes Association
No specific
recommendations
Diabetic patients
Initial recommendation:
10%20% of TEC
[18,19]
British Diabetes Association
1015
Diabetic patients
[20]
Canadian Diabetes Association
No specific
recommendations
Diabetic patients
Replacement of SFA by MUFA
[21]
European Association for the Study of
Diabetes
1020
Diabetic patients
Limitation of total fat to 35% of TEC
[22]
International College of Nutrition of India
7
Diabetic patients
[23]
MUFA = monounsaturated fatty acids; SFA = saturated fatty acids; TEC = total energy content.
In 1999, the International Society for the Study of Fatty Acids and Lipids agreed upon a
recommendation table on daily intake of fatty acids as a foundation for further discussions. Adequate
intake levels for adults were specified with respect to α-linolenic acid, eicosapentaenoic acid,
docosahexaenoic acid, as well as upper limits for linoleic acid, trans-fatty acids, and saturated, given
as % of total energy content (TEC), respectively. Given a total fat range from 15% to 40% of TEC,
these recommendations included the suggestion to provide the majority of fatty acids in the form of
MUFAs. However, no precise value (i.e., % of TEC in the form of MUFA) was given by the panel [24].
According to the Joint FAO/WHO Expert Consultation Committee, MUFA intakes should be
determined by calculating the difference: MUFA (% of TEC) = total fat (% of TEC) SFA (% of
TEC) PUFA (% of TEC) TFA (% of TEC). Accordingly, MUFA intakes (% of TEC) will range
with respect to the total fat and fatty acid composition of the diet [3]. Based upon 13 peer-reviewed
background papers dealing with fats and fatty acids in human nutrition, the Joint FAO/WHO Expert
Consultation Committee concluded that replacement of carbohydrates by MUFA beneficially increases
HDL-cholesterol, while the substitution of SFA with MUFA exerts favorable effects on LDL-cholesterol
and the ratio of total cholesterol to HDL-cholesterol [3]. In their position on dietary fatty acids of
Nutrients 2012, 4 1994
2007, the American and Canadian Dietetic Association suggested a high maximum quota of MUFA,
i.e., <25% of TEC [6]. Less than 20% of TEC should be consumed in the form of MUFA as
recommended by the American Heart Association (AHA) in 2006, which is interesting with respect to
the fact that the corresponding value was only <15% in the year 2000-statement of the AHA [5,25].
The National Cholesterol Education Program III suggested that <20% of TEC should be consumed in
the form of MUFA [11]. In their Dietary Guidelines for Americans, edition 2010 [16], the United
States Department of Agriculture (USDA) gives no specific recommendations for MUFA [16]. In
addition, the National Institute of Medicine did not mention any specific recommendations for MUFA.
In their statement, they concluded that n-9 cis Monounsaturated fatty acids are synthesized by the
body and have no known independent beneficial role in human health and are not required in the diet.
Therefore, neither an Adequate Intake nor a Recommended Daily Allowance was set. Since there is
insufficient evidence for an Upper Level as well, the Dietary Reference Intakes did not consider
MUFA at all [12]. In accordance with these proceedings and with a similar rationale, the European
Food and Safety Authority (EFSA) skipped MUFA in their scientific opinions on dietary reference
values for fat [8]. On a national level, the recommendations given in European countries are far from
being conclusive. The Italian Society of Human Nutrition did not list any specific references for
MUFA [9]. The Joint Committees of Germany, Austria, and Switzerland stated that MUFA
consumption should be 10% of TEC, albeit with higher intakes being acceptable [10]. The Nordic
Nutrition Recommendations agreed on 10%15% of TEC in the form of MUFA [13]. The particulars
of the Dutch Dietary Guidelines proposed a limit of 38% of TEC in the form of MUFA and PUFA for
people with optimal body weight, whereas overweight and obese people should be more restrictive and
limit their daily energy uptake in the form of MUFA/PUFA to 28% [7]. The UK COMA Committee
advocated that MUFA (in the form of oleic acid) should provide an average of 12% of TEC [15]. The
Nutritional Recommendations for the French Population promoted an intake of MUFA up to 20% of
TEC for adults including pregnant and lactating women. It was emphasized that the neutrality of oleic
acid represents a benefit and that its consumption was justified [14].
2.2. Specific Guidelines for the Prevention and Treatment of Diabetes
On closer examination, the MUFA recommendations of the American Diabetes Association (ADA)
evolved in a downhill fashion. In 2002, a consumption of 10%20% of TEC in the form of MUFA
was proposed [18]. Two years later, a carbohydrate plus MUFA intake of 60%70% of TEC was
regarded as an evidence-based nutrition principle for the prevention and treatment of diabetes [26]. In
2008, the ADAs position statement did not offer a specific value for MUFA as a preventive or
therapeutic tool any longer [19]. Correspondingly, the American Association of Clinical
Endocrinologists excluded MUFA in their medical guidelines for the management of diabetes [17].
However, the Canadian Diabetes Association suggested frequently replacing SFA with MUFA for a
successful nutritional management of diabetes mellitus [21]. Likewise, the Joslin Diabetes Center
recommended the consumption of MUFA, again without any specific reference values [27]. The
Diabetes and Nutrition Study Group of the European Association for the Study of Diabetes stated that
MUFA should provide 10%20% of TEC with total fat to be limited to 35% of TEC [22]. The British
Diabetes Association, probably referring to the 2004 nutrition principles of the ADA, recommended
Nutrients 2012, 4 1995
a daily amount of 60%70% of TEC in the form of carbohydrates and MUFA, with MUFA values
specified separately to aim at 10%15% of TEC [20]. In Japan, no specific quota of MUFA is given in
as a nutritional reference, while other Asian nations like India allow for up to 7% of TEC in the form
of MUFA [23,28]. In South Africa, the corresponding authorities recommended <13% MUFA for
diabetic subjects [29].
3. Risk Factors for Diabetes and Cardiovascular Disease
The National Cholesterol Education Program guidelines have outlined risk factors that increase
CHD risk over a 10 year period. Elevated LDL-cholesterol (>100 mg/dL) remains the strongest
primary factor in predicting CHD and therefore is a primary target of therapy [11]. However, as
circulating triacyglycerols (TG) and HDL-cholesterol concentrations are critical risk factors in
metabolic syndrome, the TC:HDL-cholesterol ratio has been expressed as a more valuable marker in
determining CHD risk [30]. Summing-up, elevated levels of TC, LDL-cholesterol and TG as well low
levels of HDL-cholesterol are evidence-based risk factors of CVD [3133]. High levels of blood
pressure are also associated with an increased mortality risk [34]. In addition, the Emerging Risk
Factor Collaboration indicated FG levels >100 mg/dL as a predictor of mortality [35]. The
Framingham Heart Study showed that impaired fasting glucose was associated with an aggravated risk
of CHD in women [36]. A meta-analysis of cohort studies including 44,158 individuals without
diabetes found a significant association between glycosylated hemoglobin (HbA1c) and cardiovascular
events as well as death [37]. In another meta-analysis of observational studies, it was concluded that
chronic hyperglycemia is associated with an increased risk of CVD in patients with type 2 diabetes
mellitus (T2D) [38]. Among women, high-sensitive C-reactive protein (CRP) was the strongest
predictor of CVD, accompanied by TC, LDL-cholesterol, TC:HDL-cholesterol, and Apo B 100 [39].
A recent meta-analysis indicated that Apo B is a more accurate marker of cardiovascular risk as
compared to non-HDL-cholesterol (=TC-HDL-cholesterol), while the latter is still more accurate in
comparison to LDL-cholesterol [40]. Strong associations between low serum HDL-cholesterol/high
serum LDL-cholesterol and the onset of abdominal aortic aneurysms prove the continuous validity of
both markers as predictive risk factors [41]. A collaborative analysis of individual data from
36 prospective studies involving more than 126,000 individuals, has demonstrated that circulating
Lp(a) concentrations are correlated with an increased incidence of CHD and stroke independent from
several conventional risk factors (including TC) [42].
4. Methods
4.1. Data Sources and Search Strategy
Electronic database MEDLINE (between 1966 and November 2012) was searched for systematic
review and meta-analysis using following search terms monounsaturated fatty acids,
monounsaturated fat and dietary fat with no restriction to calendar data and language. Reference
lists and relevant clinical guidelines were also searched.
Nutrients 2012, 4 1996
4.2. Inclusion Criteria
Studies were included in this review if they met all of the following criteria: (1) systematic
review/meta-analysis (quantitative analysis) including RCTs, crossover, metabolic, and observational
studies; (2) intervention trials (isocaloric exchange): comparison of MUFA vs. carbohydrates, SFA,
PUFA, and trans-fat; cohort studies: highest MUFA intake vs. lowest MUFA intake; (3) Study
population: >18 years, healthy, patients with type 2 diabetes mellitus (T2D), obese, overweight;
impaired glucose metabolism and cardiovascular disease (CVD); (4) outcome parameters:
anthropometric outcomes, blood lipids, glycemic control parameters, blood pressure, inflammation
markers and cardiovascular events/mortality.
4.3. Study Quality Assessment
Review quality was rated using a modified version of the Overview of Quality Assessment
Questionnaire (OQAQ) including a bias tool [43] (Supplemental material, Table S1) as described
recently [44]. Results of OQAQ assessments are summarized in Table 4. It should be noted that the
analyses considered were in some cases based on overlapping sets of trials.
Table 4. Qualitative aspects of the included systematic reviews and meta-analyses.
Reference
Aim
Methods (Inclusion/Exclusion criteria)
Heterogeneity
Period
Quality
Assessment
Hegsted et al.
1993 [45]
Overall evaluation of the rather extensive
literature on the effects of dietary fatty acid
composition and cholesterol on serum
lipid concentration
Design: metabolic studies (appear to have been
done under rather careful control in which food was
prepared and fed to the subjects); field trials (diet
was modified by instructions or by a combination of
instructions and provision of some foods)
not analyzed
until
1991
8
Mensink et al.
1992 [46]
Combining results to derive equations that
relate changes in the dietary fatty acid
intake to changes in serum HDL-C,
LDL-C, TC and TG
Design: parallel design, crossover or Latin-square;
before and after designs that lacked a control
group were excluded. Diets enriched with
very-long-chain (n-3) PUFA were also excluded
not analyzed
1970
1991
10
Gardner et al.
1995 [47]
The purpose of this investigation was to
address the controversy regarding a
differential effect of MUFA vs. PUFA on
serum lipids
Design: randomized trials comparing a high-mono
and high-poly fat diet; similar in all respects
(isoenergetic, total fat content, SFA) except for
levels of monounsaturated and polyunsaturated fat
intake; minimum 10 subjects on each diet arm
analyzed
1966
1994
12
Yu et al.
1995 [48]
Conducted to more comprehensively
examine the effects of steraic acid,
MUFAs, and other fatty acids on total and
lipoprotein cholesterol concentrations in
both men and women
Studies reported the quantity of individual SFA or
steraic acid, sum of lauric, myristic and palmitic
acids, and sum of MUFA and PUFA of the
experimental diets.
Exclusion. Liquid formula diets; diets that were
specifically enriched with in trans isomers; diets
enriched with very-long-chain PUFA; subject with
familiar hypercholesterolemia
not analyzed
1970
1993
8
Nutrients 2012, 4 1997
Table 4. Cont.
Clarke et al.
1997 [49]
The aim of this meta-analysis of metabolic
ward studies is to provide reliable
quantitative estimates of the relevance of
dietary intake of fatty acids and dietary
cholesterol to blood concentrations of total
cholesterol and cholesterol fraction
Design: dietary intervention studies conducted
under controlled conditions that ensured compliance
not analyzed
/
9
Garg
1998 [50]
Examining the effects of high carbohydrate
low fat diets vs. high MUFA diets on
metabolic indexes in T2D subjects
Design: randomized, crossover trials using
isoenergetic, weight maintaining diets
not analyzed
/
9
Mensink et al.
2003 [30]
Combining results to derive equations that
relate changes in the dietary fatty acid
intake to changes in serum HDL-C,
LDL-C, TC and TG, Apo-B and Apo A-I,
TC:HDL-C
Design: parallel design, crossover or Latin-square;
before and after designs that lacked a control
group were excluded. Diets enriched with
very-long-chain (n-3) PUFA were also excluded
not analyzed
1970
1998
13
Shah et al.
2007 [46]
Comparing high carbohydrate and
high-cis-MUFA interventions trials
conducted to increase understanding of the
effect of carbohydrate and cis-MUFA
on blood pressure
Design: randomized and non-randomized
intervention studies comparing the effects of
high-carbohydrate diets with those of
high-cis-MUFA diets on blood pressure (crossover
or parallel design), comparison of diets isoenergetic,
body weight had to remain stable
analyzed
until
2006
12
Cao et al.
2009 [51]
Objective was to quantify the magnitude of
the changes in lipids and lipoproteins in
response to a MF blood cholesterol-
lowering diet rich in unsaturated fat vs. LF
in subjects with and without diabetes
Design: controlled feeding with a crossover or
parallel design comparing MF vs. LF diets; designed
to lower blood lipids; comparisons were
isoenergetic; participants maintained constant
weight during study; dietary protein and cholesterol
were kept constant between diets
not analyzed
1987
2007
14
Jakobsen et al.
2009 [52]
Associations between energy intake from
MUFA, PUFA, and carbohydrates and risk
of CHD while assessing the potential
effect-modifying role of sex and age
Design: cohort studies; published follow-up study
with 150 incident coronary events; availability of
usual dietary intake; a validation or repeatability
study of the diet-assessment method used
analyzed
/
10
Kodama et al.
2009 [53]
To e lu ci da te th e ef fe ct o f re p la ci ng d ie ta ry
fat with carbohydrate on glucose and
lipid parameters
Design: randomized controlled trials (crossover and
parallel-group design); isoenergetic; only T2D
Exclusion: T1D, diets with change in in the content
or quality of carbohydrates; heterogeneity analyzed
analyzed
1966
2007
16
Mente et al.
2009 [54]
Examining the association between
nutrient intake, dietary components, and
dietary patterns and CHD and its related
clinical outcomes
Design: cohort studies; dietary pattern: higher intake
level is compared with lowest intake level; p-values
for trend, where available, were used to evaluate
dose-response relationship. FFQ, food records, 24 h
recalls; Bradford Hill criteria
analyzed
1950
2007
15
Mozaffarian
and Clarke
2009 [55]
Examining the effects on CHD risk of
replacing partially hydrogenated
formulations on other specific fats on the
basis of the content of TFA, SFA, MUFA
and PUFA
Design: randomized controlled trials (consumption
of fatty acids on risk factors), cohort studies
(association of habitual intake of fatty acids with
incidence of CHD events); isocaloric replacement
not analyzed
until
2008
10
Nutrients 2012, 4 1998
Table 4. Cont.
Skeaff
and Miller
2009 [56]
The purpose of this article was to
summarize the evidence from cohort
studies and randomized controlled trials
of the relation between dietary fat and
risk of CHD
Design: cohort studies; quintiles intake of PUFA,
MUFA, SFA, TFA; The dietary assessment methods
used in the cohort studies included single 24 h
recall, diet records, diet histories and food frequency
questionnaires; For MUFA only studies included in
which exposure was determined by dietary
assessment because blood fatty acids are not good
biomarkers of MUFA intake
analyzed
/
10
Schwingshackl
et al. 2011
[57]
Comparing high MUFA (>12% of TEC)
vs. low MUFA (12% MUFA of TEC) on
cardiovascular risk factors
Design: randomized controlled trials, 6 months,
isocaloric and hypocaloric diets; subgroup analysis
MUFA vs. LF, PUFA, LGI, HGI, Controls
analyzed
1966
2011
13
Schwingshackl
et al. 2011
[58]
Comparing high MUFA (>12% of TEC)
vs. low MUFA (12% MUFA of TEC) on
glycemic control in subjects with
abnormal glucose metabolism
Design: randomized controlled trials, 6 months,
isocaloric and hypocaloric diets, subgroup analysis
MUFA vs. LF, PUFA, LGI, HGI, Controls
analyzed
1966
2011
13
Apo A I: Apolipoprotein A-I; Apo B: Apo lipoprotein B; CHD: coronary heart disease; FFQ: food frequency questionnaire;
HDL-C: high-density lipoprotein cholesterol; HGI: high glycemic index; LDL-C: low-density lipoprotein cholesterol; LF: low fat;
LGI: low glycemic index; MF: moderate fat; MUFA: monounsaturated fat; PUFA: polyunsaturated fat; SFA: saturated fat; T2D: type 2
diabetes subjects; TC: total cholesterol; TEC: total energy content; TFA: trans fat; TG: triacylglycerols.
The present review included meta-analyses of intervention trials (randomized, non-randomized and
crossover trials) and cohort studies. A common problem associated with cross-over trials is that of
carry-over (a type of period-by-intervention interaction), but it seems only justifiable to exclude
cross-over trials from a systematic review if the design is inappropriate within the clinical context [59].
Duration of studies varied remarkably between the different meta-analyses as well as between the
different within each meta-analysis. This represents a major problem especially when comparing
intervention trials. Sensitivity analyses comparing short- vs. long-term studies might be used as an
alternative approach to resolve this issue. Another issue associated with meta-analyses is heterogeneity
of various aspects and characteristics of the study protocols, especially in nutritional intervention trials.
Therefore, it is not surprising that the literature chosen for the present review varies regarding type(s)
of diets used (MUFA vs. carbohydrates/PUFA/SFA/trans fatty acids), definitions of MUFA diets, and
study population (healthy, overweight, or obese subjects, patients with T2D, abnormal glucose
metabolism, or CVD). In addition, in most of the included meta-analyses differential compliance
(drop outs) was not investigated. Another potential source of bias is measurement issues (especially of
self-reported data, e.g., 24 h recalls, food records). Only few systematic reviews screened for the
presence of publication bias by assessing the symmetry of the funnel plots in which mean differences
were plotted against their corresponding standard errors.
Nutrients 2012, 4 1999
5. Evidence from Meta-Analyses
5.1. Healthy Subjects
See Table 5 summarizes the study characteristics of the meta-analyses included in this review. For a
better understanding of the categorization of meta-analyses and other scientific studies, the Levels of
evidence by the Scottish Intercollegiate Guidelines Network are given in Table 6 [60].
Table 5. Study characteristics of meta-analyses.
Reference
No. Studies
Statistical Method
Min. Duration
Participants
Effects of MUFA
Hegsted et al. 1993 [45]
n = 77
Multiple regression
n.d.
n.d.
TC, LDL-C, HDL-C
Mensink et al. 1992 [61]
n = 28
meta-regression
14 days
682
TG, HDL-C:LDL-C
HDL-C
TC, LDL
Gardner et al.
1995 ** [47]
n = 14
Standardized effect size
3 weeks
439
TG *
LDL-C, HDL-C
Yu et al. 1995 [48]
n = 18
Meta-regression analysis
n.d.
804
TC, LDL-C
HDL-C
Clarke et al. 1997 [49]
n = 91
Multilevel regression analysis
2 weeks
5910
HDL-C
TC, LDL-C
Garg 1998 [50]
n = 9
meta-analysis
2 weeks
133
TG, TC, VLDL-C, FG
HDL-C, Apo A-1
LDL-C, Apo B, FI, HbA1c
Mensink et al. 2003 [30]
n = 60
meta-regression
13 days
1672
TG, LDL-C, Apo B, TC:HDL-C
HDL-C, Apo A-1
TC
Shah et al. 2007 [46]
n = 10
Random effect modell
3 weeks
400
SBP, DBP *
Cao et al. 2009 [51]
n = 30
Random effect modell
2 weeks
1213
TG
HDL-C, Apo A 1
LDL-C
Jakobsen et al.
2009 [52]
n = 11
Random effect meta-analysis
4 years
344,696
risk of CHD events
risk of CHD death
Kodama et al. 2009 [53]
n = 11
Fixed effect modell
10 days
329
TG
FG, FI, TC, HDL-C, LDL-C
Mente et al. 2009 [54]
n = 146
Random effect meta-analysis
n.d.
101,521
CHD events
Mozaffarian and Clarke
2009 [55]
n = 13
Multilevel regression analysis
2 weeks
554
TC, TG, LDL-C, Apo B,
TC:HDL-C
HDL-C, Apo A-1
Skeaff et al. 2009 [56]
n = 28
Random effect meta-analysis
4 years
280,000
risk of CHD death/events
Schwingshackl et al.
2011 [57]
n = 12
Random effect meta-analysis
6 months
1990
FM, SBP, DBP
W, WC, TC, LDL-C, HDL-C,
TG, CRP
Schwingshackl et al.
2011 [58]
n = 9
Random effect meta-analysis
6 months
1547
HbA1c, FG
FI, HOMA-IR
significant increase; significant decrease; no significant effects; * p = 0.05; ** MUFA vs. PUFA; MUFA/PUFA for SFA decrease
LDL-Cholesterol; n.d.: no data.
Nutrients 2012, 4 2000
Table 6. Levels of evidence by the Scottish Intercollegiate Guidelines Network.
1++ High quality meta-analyses, systematic reviews of RCTs, or RCTs with a very low risk of bias
1+ Well conducted meta-analyses, systematic reviews, or RCTs with a low risk of bias
1 Meta-analyses, systematic reviews, or RCTs with a high risk of bias
2++ High quality systematic reviews of case control or cohort studies
High quality case control or cohort studies with a very low risk of confounding or bias and a high
probability that the relationship is causal
2+ Well conducted case control or cohort studies with a low risk of confounding or bias and a moderate
probability that the relationship is causal
2 Case control or cohort studies with a high risk of confounding or bias and a significant risk that the
relationship is not causal
3 Non-analytic studies, e.g., case reports, case series
4 Expert opinion
A
At least one meta-analysis, systematic review, or RCT rated as 1++, and directly applicable to
the target population; or
A body of evidence consisting principally of studies rated as 1+, directly applicable to the target
population, and demonstrating overall consistency of results
B
A body of evidence including studies rated as 2++, directly applicable to the target population,
and demonstrating overall consistency of results; or
Extrapolated evidence from studies rated as 1++ or 1+
C
A body of evidence including studies rated as 2+, directly applicable to the target population
and demonstrating overall consistency of results; or
Extrapolated evidence from studies rated as 2++
D
Evidence level 3 or 4; or Extrapolated evidence from studies rated as 2+
In their meta-analysis, Clarke et al. (1997) [49] investigated the effects of MUFA as well as SFA
and PUFA on cardiovascular risk factors in non-diabetic subjects. In addition, liquid formula diets
were included, although they were analyzed separately. Dietary protocols were mostly iso-energetic
but differed with respect to study design: they included randomized crossover, randomized or matched
parallel, non-randomized Latin square and non-randomized sequential attempts. The authors concluded
that substitution of carbohydrates by MUFA (5% of TEC) had no significant effect on TC
and LDL-cholesterol, but managed to increase HDL-cholesterol. With respect to PUFA-rich diets, TC
and LDL-cholesterol were both decreased and HDL-cholesterol was augmented in solid food
experiments [49]. Clarke and Mozaffarian (2009) [55] observed that replacing hydrogenated fats with
MUFA (1% of TEC) resulted in advantageous changes of several CVD risk factors like TC,
LDL-cholesterol, HDL-cholesterol, TG, apoproteins A-1, B as well as B/A1, and lipoprotein (a) in
12 crossover and 1 parallel designed trials. Yu and co-workers (1995) [48] explored the results of
18 studies (again including crossover and parallel designed set-ups) enrolling a total of 804 healthy and
normocholesterolemic participants. Following meta-regression, they observed that MUFA increased
HDL-cholesterol and decreased TC and LDL-cholesterol. The corresponding effects of PUFA were
more pronounced with respect to TC and LDL-cholesterol, but not to HDL-cholesterol [48]. In 1992, a
meta-analysis of short-term RCTs investigated the effects of dietary fatty acids as an iso-caloric
substituent for carbohydrates on CVD risk factors. HDL-cholesterol levels were significantly
augmented following the MUFA-rich diet, while levels of TG and the ratio of TC to HDL-cholesterol
Nutrients 2012, 4 2001
were significantly reduced, respectively [61]. In 2003, the authors published an updated meta-analysis
including 1672 instead of 682 participants and were able to confirm their previous results. In addition,
they observed a significant improvement in LDL-cholesterol, Apo A-1, and Apo B following
high-MUFA regimens [30]. In a recent meta-analysis investigating the long-term (6 months) effects
of high- (>12% MUFA) vs. low- (12% MUFA) MUFA diets on cardiovascular risk factors, we could
show that high-MUFA diets significantly reduced systolic and diastolic blood pressure in
overweight/obese subjects [57] thus confirming data previously reported by Shah et al. in 2007 [46].
When MUFA-rich diets were compared with PUFA-rich onsets, no effects on HDL-cholesterol and
LDL-cholesterol, but a borderline increase (p = 0.05) in TG could be observed [47]. Hegsted et al. [45]
analyzed metabolic studies and field trials and could not observe any impact of MUFA on TC,
LDL-cholesterol, and HDL-cholesterol in their meta-regression.
5.2. Patients with Abnormal Glucose Metabolism/Diabetes Mellitus
In a recent meta-analysis of short-term RCTs (crossover and parallel study designs) with a duration
between 10 days and 6 weeks enrolling 306 subjects with type 2 diabetes mellitus, a significant
decrease in TG values following a MUFA-rich dietary regimen could be observed when compared
with a low-fat/high carbohydrate diet [53]. This is in congruence with data presented by
Garg (1998) [50] reporting reduced fasting TG in patients with type 2 diabetes mellitus subjected to a
weight maintenance diet following replacement of carbohydrates by MUFA [50]. Moreover,
improvements in FG and pre-prandial plasma glucose were shown, while no significant changes in
fasting plasma insulin concentrations, fructosamine and HbA1c were observed. The high-MUFA
protocols were accompanied with significantly lower values for TC and VLDL-cholesterol as well as
increases in HDL-cholesterol, but were not correlated to changes in LDL-cholesterol. Comparison of
high- (>12% MUFA) vs. low- (12% MUFA) MUFA diets on glycemic control in subjects with
abnormal glucose metabolism revealed improvements in HbA1c and fasting glucose in diabetic
subjects, but no differences in blood lipids were found [58,62].
With respect to short-term studies (212 weeks duration), comparison of low vs. moderate dietary
fat content was performed in a meta-analysis by Cao et al. (2009) [51]. Participants with and without
diabetes and a body mass index ranging from 21.1 to 30.2 kg/m2 were enrolled. The mean MUFA
content in a correspondingly modified diet was 23.6% of TEC and 11.4% in the low-fat versions. In
the healthy collective, HDL-cholesterol was significantly increased and TG levels were significantly
decreased in the moderate fat groups as compared to low-fat diets. TC and LDL-cholesterol were
reduced in a similar fashion following both dietary protocols (moderate and low fat). Patients with
diabetes adopting the diet with a higher MUFA content established a significant increase in
HDL-cholesterol as well, accompanied by a significant reduction in TG and a non-significant
reduction in TC as compared to the low fat diets. TG response was even more pronounced in
participants with diabetes as compared to healthy subjects [51].
5.3. Patients with CVD
In a prospective trial investigating the effects of a Mediterranean diet, the Lyon Diet Heart Study
reported a benefit of increased MUFA intake in survivors first time myocardial infarction [63].Three
Nutrients 2012, 4 2002
recent meta-analyses of cohort studies investigated the effects of dietary fats on CHD events and
cardiovascular death. Skeaff and Miller [56] did not observe any effects of MUFA-rich diets on
relative risks of CHD events and death. Moreover, no differences between of high- and low-fat
intake were registered [56]. Jakobsen [52] performed a meta-analysis of cohort studies including
344,696 subjects. They postulated a positive correlation between MUFA-rich diets and risk of coronary
events, but not between MUFA-rich diets and risk of coronary deaths. The authors explain that in the
western diet, the MUFA supply is predominantly of animal origin resulting in a confounder that should
be taken into consideration when comparing dietary fats. The usual source of MUFA/oleic acid is of
vegetable origin. These results are in strong discrepancy with another recent meta-analysis of cohort
studies, were Mente et al. [54] reported a correlation between MUFA uptake and a significant decrease
in the relative risk for CHD. None of these three meta-analyses reported information regarding stroke
or arrhythmic diseases, but included data for hard CHD endpoints like angina pectoris, sudden death,
fatal and non-fatal myocardial infarction. In June 2012, the Cochrane Collaboration updated their
systematic review and meta-analysis on the effects of low vs. modified fat diets on cardiovascular
disease. The findings are suggestive of a small but potentially important reduction in cardiovascular
risk on modification of dietary fat (but not reduction of total fat) in longer trials. However, no
association between total fat content and risk of cardiovascular death and events were reported [64].
6. Conclusions
In comparison, a considerably larger number of meta-analyses explored the effects of PUFAs on
maintenance or reduction of body weight as well as biomarkers of impaired glucose metabolism or
CVD/CHD than there are systematic reviews and meta-analyses dealing with the corresponding impact
of MUFAs. Consequently, the international recommendations for PUFA are more consistent than those
for MUFA, averaging a value of 10% of TEC for healthy persons for the most part. If MUFA
recommendations are given at all, they vary between 12% and 25% of TEC, equaling a remarkable
range of ~3070 g/day for a 2.500 kcal-diet. Prestigious authorities and organizations such as the
National Institute of Medicine, the EFSA, the USDA and the ADA do not provide specific
recommendation for MUFAs either for healthy people or for patients in need of diabetic or
cardiovascular management.
In the present review, only meta-analyses were included, which indicates a high level of evidence,
i.e., from 2+ to 1+++ according to the Scottish Intercollegiate Guidelines Network indicate levels of
evidence (Table 6). Apart from the fact that several meta-analyses and meta-regressions observed
benefits of MUFA on cardiovascular risk factors, it should be noted that most meta-analyses did not
report significant negative effects of a MUFA-rich diet on CVD risk factors. With respect to the
favorable influences of MUFA found in studies recruiting healthy volunteers or patients with diabetes
and CHD respectively, some reservations still remain. Due to various inhomogeneities, the results of
different studies are far from being conclusive. Thus, MUFA were compared to carbohydrate-rich
diets, low fat diets or regimens focusing on PUFA or SFA. Moreover, the term MUFA-rich diet lacks a
concrete definition leading to inconsistent amounts of MUFA used in the corresponding protocols.
Some of the discrepancies in the findings of different studies can be explained by their uneven and
maybe incompatible durations. Long-term biomarkers of glucose metabolism such as HbA1c will be
Nutrients 2012, 4 2003
most likely not or just slightly improved following short-term interventions of 26 weeks
Nevertheless, in view of the importance of dietary interventions for the prevention and therapy of
cardiovascular disease, monounsaturated fatty acid may represent a valuable tool in the modification of
dietary regimens. There is strong evidence that by replacing SFA and carbohydrates with MUFA,
various cardiovascular risk factors will be significantly improved. The results of the different
meta-analyses addressed in this review point to a beneficial effect of MUFA-rich diets on systolic and
diastolic blood pressure as well as parameters of glycemic control. On the other hand, the impact of
MUFA on blood lipids is still discussed controversially. While TG levels were decreased and
HDL-cholesterol levels were increased following short-term interventions with higher amounts of
MUFA, these findings could not be confirmed in long-term study protocols. Thus, there is no
unanimous rationale for MUFAs in a therapeutic regimen. However, since no detrimental effects of
MUFA-rich diets were reported in the literature to date, there is no evidence speaking against the
consideration of MUFAs in dietary guidelines. Further studies dealing with long-term effects of
MUFA on biomarkers of obesity, diabetes, and cardiovascular diseases as well as clinical endpoints
are needed to clarify the potential benefits of MUFA-rich diets in primary and secondary prevention.
Conflict of Interest
The authors declare no conflict of interest.
References
1. Kris-Etherton, P.M. AHA Science Advisory. Monounsaturated fatty acids and risk of cardiovascular
disease. American Heart Association. Nutrition Committee. Circulation 1999, 100, 12531258.
2. Tarrago-Trani, M.T.; Phillips, K.M.; Lemar, L.E.; Holden, J.M. New and existing oils and fats
used in products with reduced trans-fatty acids content. J. Am. Diet. Assoc. 2006, 106, 867880.
3. Fats and Fatty Acids in Human Nutrition. Report of an Expert Consultation. Available online:
http://www.fao.org/docrep/013/i1953e/i1953e00.pdf (accessed on 4 July 2012).
4. Food List. Available online: http://ndb.nal.usda.gov/ndb/foods/list (accessed on 10 June 2012).
5. Lichtenstein, A.H.; Appel, L.J.; Brands, M.; Carnethon, M.; Daniels, S.; Franch, H.A.; Franklin, B.;
Kris-Etherton, P.; Harris, W.S.; Howard, B.; et al. Diet and lifestyle recommendations revision
2006: A scientific statement from the American Heart Association Nutrition Committee.
Circulation 2006, 114, 8296.
6. Kris-Etherton, P.M.; Innis, S.; Ammerican Dietetic Assocition; Dietitians of Canada. Position of
the American Dietetic Association and the Dietitians of Canada: Dietary fatty acids. J. Am. Diet.
Assoc. 2007, 107, 15991611.
7. Spaaij, C.J.K.; Pijls, L.T.J. New dietary reference intakes in the Netherlands for energy, proteins,
fats and digestible carbohydrates. Eur. J. Clin. Nutr. 2004, 58, 191194.
8. European Food Safety Authority (EFSA). Scientific Opinion on Dietary Reference Values for
fats, including saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids,
trans fatty acids, and cholesterol. EFSA J. 2010, 8, 1461.
9. Lipidi. Available online: http://www.sinu.it/larn/lipidi.asp (accessed on 20 June 2012).
Nutrients 2012, 4 2004
10. German Nutrition Society; Austrian Nutrition Society; Swiss Society for Nutrition Research;
Swiss Nutrition Association. Reference Values for Nutrient Intake; Umschau Braus Publishers:
Frankfurt, Germany, 2008.
11. Expert Panel on Detection, Valuation, and Treatment of High Blood Cholesterol in Adults.
Executive summary of the third report of the National Cholesterol Education Program (NCEP)
expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult
treatment panel III). JAMA 2001, 285, 24862497.
12. Institute of Medicine of the National Academies. Dietary Fats: Total Fat and Fatty Acids.
In Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol,
Protein, and Amino Acids (Macronutrients); The National Academy Press: Washington, DC,
USA, 2002; pp. 335342.
13. Nordic Nutrition Recommendations (NNR). Integrating Nutrition and Physical Activity; Nordic
Council of Ministers: Copenhagen, Denmark, 2004; p. 436.
14. AgenceFrancaisedeSécuritéSanitairedesAliments (AFSSA). Apports Nutritionnels Conseillés
pour la Population Francaise; Editions Tec & Doc: Paris, France, 2001; p. 605.
15. Great Britain Department of Health. Dietary Reference Values for Food Energy and Nutrients for
the United Kingdom: Report of the Panel on Dietary Reference Values of the Committee on
Medical Aspects of Food Policy; Stationery Office: London, UK, 1991.
16. US Department of Agriculture; US Department of Health and Human Services. Dietary
Guidelines for Americans, 7th ed.; US Government Printing Office: Washington, DC, USA, 2010.
17. American Association of Clinical Endocrinologists. Medical Guidelines for Clinical Practice for
the Management of Diabetes Mellitus. Available online: http://www.bd.com/resource.aspx?
IDX=3773 (accessed on 20 June 2012).
18. Franz, M.J.; Bantle, J.P.; Beebe, C.A.; Brunzell, J.D.; Chiasson, J.L.; Garg, A.; Holzmeister, L.A.;
Hoogwerf, B.; Mayer-Davis, E.; Mooradian, A.D.; et al. Evidence-based nutrition principles and
recommendations for the treatment and prevention of diabetes and related complications.
Diabetes Care 2003, 26, S51S61.
19. Bantle, J.P.; Wylie-Rosett, J.; Albright, A.L.; Apovian, C.M.; Clark, N.G.; Franz, M.J.;
Hoogwerf, B.J.; Lichtenstein, A.H.; Mayer-Davis, E.; Mooradian, A.D.; et al. Nutrition
recommendations and interventions for diabetes: A position statement of the American Diabetes
Association. Diabetes Care 2008, 31, S61S78.
20. Nutrition Subcommittee of the British Diabetic Associations Professional Advisory Committee.
Dietary recommendations for people with diabetes: An update for the 1990s. Diabet. Med. 1992,
9, 189202.
21. Canadian Diabetes Association. Guidelines for the nutritional management of diabetes mellitus in
the new millennium: A position statement by the Canadian Diabetes Association. Can. J.
Diabetes Care 1999, 23, 5669.
22. Mann, J.I.; de Leeuw, I.; Hermansen, K.; Karamanos, B.; Karlström, B.; Katsilambros, N.;
Riccardi, G.; Rivellese, A.A.; Rizkalla, S.; Slama, G.; et al. Evidence-based nutritional
approaches to the treatment and prevention of diabetes mellitus. Nutr. Metab. Cardiovasc. Dis.
2004, 14, 373394.
Nutrients 2012, 4 2005
23. Singh, R.B.; Rastogi, S.S.; Rao, P.V.; Das, S.; Madhu, S.V.; Das, A.K.; Sahay, B.K.; Fuse, S.M.;
Beegom, R.; Sainani, G.S.; Shah, N.A. Diet and lifestyle guidelines and desirable levels of risk
factors for the prevention of diabetes and its vascular complications in Indians: A scientific
statement of the International College of Nutrition. J. Cardiovasc. Risk. 1997, 4, 201208.
24. Adequate Intakes/Recommendation Table. Available online: http://www.issfal.org/statements/
adequate-intakes-recommendation-table (accessed on 20 June 2012).
25. Krauss, R.M.; Eckel, R.H.; Howard, B.V.; Appel, L.J.; Daniels, S.R.; Deckelbaum, R.J.;
Erdman, J.W., Jr.; Kris-Etherton, P.; Goldberg, I.J.; Kotchen, T.A.; et al. AHA Dietary
Guidelines: Revision 2000: A statement for healthcare professionals from the Nutrition
Committee of the American Heart Association. Stroke 2000, 31, 27512766.
26. Franz, M.J.; Bantle, J.P.; Beebe, C.A.; Brunzell, J.D.; Chiasson, J.L.; Garg, A.; Holzmeister, L.A.;
Hoogwerf, B.; Mayer-Davis, E.; Mooradian, A.D.; et al. Nutrition principles and recommendation
in diabetes. Diabetes Care 2004, 27, S36S46.
27. Joslin Diabetes Center & Joslin Clinic. Clinical Nutrition Guideline for Overweight and Obese
Adults with Type 2 Diabetes, Prediabetes or at High Risk for Developing Type 2 Diabetes.
Available online: http://www.joslin.org/docs/Nutrition_Guideline_Graded.pdf (accessed on
20 June 2012).
28. Kitamura, S. Diet therapy and food exchange lists for diabetic patients. Diabetes Res. Clin. Pract.
1994, 24, S233S240.
29. Silvis, N. Nutrition recommendations for individuals with diabetes mellitus. SAMJ 1992, 81, 162166.
30. Mensink, R.P.; Zock, P.L.; Kester, A.D.; Katan, M.B. Effects of dietary fatty acids and
carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and
apolipoproteins: A meta-analysis of 60 controlled trials. Am. J. Clin. Nutr. 2003, 77, 11461155.
31. Cooney, M.T.; Dudina, A.; de Bacquer, D.; Wilhelmsen, L.; Sans, S.; Menotti, A.; de Backer, G.;
Jousilahti, P.; Keil, U.; Thomsen, T.; et al. SCORE investigators: HDL cholesterol protects
against cardiovascular disease in both genders, at all ages and at all levels of risk. Atherosclerosis
2009, 206, 611616.
32. Lewington, S.; Whitlock, G.; Clarke, R.; Sherliker, P.; Emberson, J.; Halsey, J.; Qizilbash, N.;
Peto, R.; Collins, R. Blood cholesterol and vascular mortality by age, sex, and blood pressure:
A meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths.
Lancet 2007, 370, 18291839.
33. Bayturan, O.; Tuzcu, E.M.; Lavoie, A.; Hu, T.; Wolski, K.; Schoenhagen, P.; Kapadia, S.;
Nissen, S.E.; Nicholls, S.J. The metabolic syndrome, its component risk factors, and progression
of coronary atherosclerosis. Arch. Intern. Med. 2010, 170, 478484.
34. Lloyd-Jones, D.; Adams, R.; Carnethon, M.; Carnethon, M.; Dai, S.; de Simone, G.;
Ferguson, T.B.; Ford, E.; Furie, K.; Gillespie, C.; et al. Heart disease and stroke statistics2010
update: A report from the American Heart Association. Circulation 2010, 121, e46e215.
35. Emerging Risk Factors Collaboration; Seshasai, S.R.; Kaptoge, S.; Thompson, A.;
di Angelantonio, E.; Gao, P.; Sarwar, N.; Whincup, P.H.; Mukamal, K.J.; Gillum, R.F.; et al.
Diabetes mellitus, fasting glucose, and risk of cause-specific death. N. Engl. J. Med. 2011, 364,
829841.
Nutrients 2012, 4 2006
36. Levitzky, Y.S.; Pencina, M.J.; DAgostino, R.B.; Meigs, J.B.; Murabito, J.M.; Vasan, R.S.;
Fox, C.S. Impact of impaired fasting glucose on cardiovascular disease: The Framingham Heart
Study. J. Am. Coll. Cardiol. 2008, 51, 264270.
37. Santos-Oliveira, R.; Purdy, C.; da Silva, M.P.; dos Anjos Carneiro-Leão, A.M.; Machado, M.;
Einarson, T.R. Haemoglobin A1c levels and subsequent cardiovascular disease in persons without
diabetes: A meta-analysis of prospective cohorts. Diabetologia 2011, 54, 13271334.
38. Selvin, E.; Marinopoulos, S.; Berkenblit, G.; Rami, T.; Brancati, F.L.; Powe, N.R.; Golden, S.H.
Meta-analysis: Glycosylated hemoglobin and cardiovascular disease in diabetes mellitus.
Ann. Intern. Med. 2004, 141, 421431.
39. Ridker, P.; Hennekens, C.H.; Buring, J.E.; Rifai, N. C-reactive protein and other markers of
inflammation in the prediction of cardiovascular disease in women. N. Engl. J. Med. 2000, 342,
836843.
40. Sniderman, A.D.; Williams, K.; Contois, J.H.; Monroe, H.M.; McQueen, M.J.; de Graaf, J.;
Furberg, C.D. A meta-analysis of low-density lipoprotein cholesterol, non-high-density
lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk. Circ. Cardiovasc.
Qual. Outcomes 2011, 4, 337345.
41. Takagi, H.; Manabe, H.; Kawai, N.; Goto, S.N.; Umemoto, T. Serum high-density and
low-density lipoprotein cholesterol is associated with abdominal aortic aneurysm presence:
A systematic review and meta-analysis. Int. Angiol. 2010, 29, 371375.
42. The Emerging Risk Factors Collaboration; Erqou, S.; Kaptoge, S.; Perry, P.L.;
di Angelantonio, E.; Thompson, A.; White, I.R.; Marcovina, S.M.; Collins, R.; Thompson, S.G.;
Danesh, J. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke and
nonvascular mortality. JAMA 2009, 302, 412423.
43. Oxmann, A.D.; Guyatt, G.H. Validation of an index of the quality of review articles. J. Clin.
Epidemiol. 1991, 44, 12711278.
44. Greaves, C.J.; Sheppard, K.E.; Abraham, C.; Hardeman, W.; Roden, M.; Evans, P.H.; Schwarz, P.;
IMAGE Study Group. Systematic review of reviews of intervention components associated with
increased effectiveness in dietary and physical activity interventions. BMC Public Health 2011,
11, 119.
45. Hegsted, D.M.; Ausman, L.M.; Johnson, J.A.; Dallal, G.E. Dietary fat and serum lipids:
An evaluation of the experimental data. Am. J. Clin. Nutr. 1993, 57, 875883.
46. Shah, M.; Adams-Huet, B.; Garg, A. Effect of high-carbohydrate or high-cis-monounsaturated fat
diets on blood pressure: A meta-analysis of intervention trials. Am. J. Clin. Nutr. 2007, 85,
12511256.
47. Gardner, C.D.; Kraemer, H.C. Monounsaturated versus polyunsaturated dietary fat and serum
lipids. A meta-analysis. Arterioscler. Thromb. Vasc. Biol. 1995, 15, 19171927.
48. Yu, S.; Derr, J.; Etherton, T.D.; Kris-Etherton, P.M. Plasma cholesterol-predictive equations
demonstrate that stearic acid is neutral and monounsaturated fatty acids are hypocholesterolemic.
Am. J. Clin. Nutr. 1995, 61, 11291139.
49. Clarke, R.; Frost, C.; Collins, R.; Appleby, P.; Peto, R. Dietary lipids and blood cholesterol:
Quantitative meta-analysis of metabolic ward studies. BMJ 1997, 316, 112117.
50. Garg, A. High-monounsaturated-fat diets for patients with diabetes mellitus: A meta-analysis.
Am. J. Clin. Nutr. 1998, 67, 577582.
Nutrients 2012, 4 2007
51. Cao, Y.; Mauger, D.T.; Pelkman, C.L.; Zhao, G.; Townsend, S.M.; Kris-Etherton, P.M. Effects of
moderate (MF) versus lower fat (LF) diets on lipids and lipoproteins: A meta-analysis of clinical
trials in subjects with and without diabetes. J. Clin. Lipidol. 2009, 3, 1932.
52. Jakobsen, M.U.; OReilly, E.J.; Heitmann, B.L.; Pereira, M.A.; Bälter, K.; Fraser, G.E.;
Goldbourt, U.; Hallmans, G.; Knekt, P.; Liu, S.; et al. Major types of dietary fat and risk of
coronary heart disease: A pooled analysis of 11 cohort studies. Am. J. Clin. Nutr. 2009, 89,
14251432.
53. Kodama, S.; Saito, K.; Tanaka, S.; Maki, M.; Yachi, Y.; Sato, M.; Sugawara, A.; Totsuka, K.;
Shimano, H.; Ohashi, Y.; et al. Influence of fat and carbohydrate proportions on the metabolic
profile in patients with type 2 diabetes: A meta-analysis. Diabetes Care 2009, 32, 959965.
54. Mente, A.; de Koning, L.; Shannon, H.S.; Anand, S.S. A systematic review of the evidence
supporting a causal link between dietary factors and coronary heart disease. Arch. Intern. Med.
2009, 169, 659669.
55. 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, 2233.
56. Skeaff, C.M.; Miller, J. Dietary fat and coronary heart disease: Summary of evidence from
prospective cohort and randomised controlled trials. Ann. Nutr. Metab. 2009, 55, 173201.
57. Schwingshackl, L.; Strasser, B.; Hoffmann, G. Effects of monounsaturated fatty acids on
cardiovascular risk factors: A systematic review and meta-analysis. Ann. Nutr. Metab. 2011, 59,
176186.
58. Schwingshackl, L.; Strasser, B.; Hoffmann, G. Effects of monounsaturated fatty on glycemic
control in patients with abnormal glucose metabolism: A systematic review and meta-analysis.
Ann. Nutr. Metab. 2011, 58, 290296.
59. Cochrane Handbook of Systematic Reviews of Interventions. Version 5.1.0 [updated March
2011]. Available online: http://handbook.cochrane.org/ (assessed on 11 November 2012).
60. SIGN 50. A Guideline Developers Handbook. Available online: http://www.sign.ac.uk/
pdf/sign50.pdf (accessed on 10 June 2012).
61. Mensink, R.P.; Katan, M.B. Effect of dietary fatty acids on serum lipids and lipoproteins.
A meta-analysis of 27 trials. Arterioscler. Thromb. 1992, 12, 911919.
62. Schwingshackl, L.; Strasser, B. High-MUFA diets reduce fasting glucose in patients with type 2
diabetes. Ann. Nutr. Metab. 2012, 60, 3334.
63. De Lorgeril, M.; Renaud, S.; Mamelle, N.; Salen, P.; Martin, J.L.; Monjaud, I.; Guidollet, J.;
Touboul, P.; Delaye, J. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of
coronary heart disease. Lancet 1994, 343, 14541459.
64. Hooper, L.; Summerbell, C.D.; Thompson, R.; Sills, D.; Roberts, F.G.; Moore, H.J.;
Davey Smith, G. Cutting down or changing the fat we eat may reduce our risk of heart disease.
Cochrane Database Syst. Rev. 2012, doi:10.1002/14651858.CD002137.
© 2012 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article
distributed under the terms and conditions of the Creative Commons Attribution license
(http://creativecommons.org/licenses/by/3.0/).

Supplementary resource (1)

... The characterization either as an n-3 PUFA or n-6 PUFA refers to the position of the first double bond relative to the methyl end of the fatty acid. In nature, double bonds are usually in the cis form [38]. Monounsaturated fatty acids (MUFA) are chemically classified as fatty acids containing a single, double bond [39]. On the other hand, saturated fatty acids (SFA) have no double bond; the human body can synthesize this type of fat [40]. ...
... As expected, Silverskin (1.21 g·kg −1 ) and Cascara (0.24 g·kg −1 ) showed low levels of them. Schwingshackl and Hoffmann (2012) [39] stated that data from meta-analyses exploring evidence from long-term perspective cohort studies provide ambiguous results with respect to the effects of MUFA on the risk of coronary heart disease (CHD). However, several studies have indicated an increase of HDL cholesterol and a corresponding decrease in triacylglycerols following a MUFA-rich diet. ...
Article
Full-text available
Nowadays, there is an increased interest in coffee derivatives (green beans, roasted beans, and coffee by-products (Cascara and Silverskin)) due to their particular chemical composition. This study aimed to compare the content of dry matter, total fat, fatty acids, and fiber (ADF, NDF) of coffee by-products (Cascara and Silverskin) and coffee beans (green and roasted under different conditions). Coffee beans and their by-products were obtained from 100% C. arabica coffee cherries from Panama by dry process. The lowest concentrations of fat corresponded to Cascara 4.24 g·kg−1 and Silverskin 23.70 g·kg−1, respectively. The major fatty acids detected in all samples were palmitic, stearic, oleic, and linoleic acids, the latter two being essential fatty acids. LDA showed that 89.01% of the variability between beans and by-products was explained by lignoceric, myristic, behenic, tricosanoic, arachidic, and heneicosanoic acids. Silverskin appeared to be a good source of lignoceric, myristic, and behenic acids and had a higher concentration of dietary fiber (314.95 g·kg−1) than Cascara (160.03 g·kg−1). Coffee by-products (Silverskin and Cascara) are low-fat products enriched in dietary fiber. Their incorporation, after adjustment, into the global diet may contribute to nutrition security, the sustainability of the coffee sector, and human health.
... Despite the observed differences between the analyzed samples, quantitative data clearly point out the beneficial properties of hempseed products, including oilseed, flours and corresponding residues, all characterized by low percentages of SFAs, very high percentages of PUFAs with a favorable ω6/ω3 ratio. The moderate percentage of MUFAs, higher than SFAs, also gives a positive contribution to the well-being, due to their potential in reducing the risk of cardiovascular disease [32]. ...
Article
Full-text available
The growing demand in natural matrices that represent a source of dietary and nutraceutical molecules has led to an increasing interest in Cannabis sativa, considered to be a multipurpose, sustainable crop. Particularly, the considerable content in essential fatty acids (FAs) makes its derived-products useful food ingredients in the formulation of dietary supplements. In this research, the FA and triacylglycerol (TAG) composition of hempseed oils and flours were investigated using gas chromatography coupled to mass spectrometry and flame ionization detection as well as liquid chromatography coupled to mass spectrometry (LC-MS), respectively. Furthermore, a recently introduced linear retention index (LRI) approach in LC was successfully employed as a useful tool for the reliable identification of TAG species. A total of 30 FAs and 62 glycerolipids were positively identified in the investigated samples. Relative quantitative analyses confirmed linoleic acid as the most abundant component (50–55%). A favorable omega6/omega3 ratio was also measured in hemp-derived products, with the α-linolenic acid around 12–14%. Whereas, γ-linolenic acid was found to be higher than 1.70%. These results confirm the great value of Cannabis sativa as a source of valuable lipids, and the further improvement of the LRI system paves the way for the automatization of the identification process in LC.
... Beneficial effects of MUFAs such as oleic acid on CV risk factors have been consistently reported in meta-analyses and meta-regressions (Schwingshackl and Hoffmann 2012, Martinez-Gonzalez, Dominguez et al. 2014, Schwingshackl and Hoffmann 2014 although the data available at present are still ambiguous. Polyphenols derived from olive oil are characterized as antioxidants, antiplatelet agents, and anti-inflammatory agents. ...
Thesis
Among the physiological and metabolic changes occurring with ageing, the ageing of heart function is a key determinant of health. The death number from CVDs is expected to reach over 23.6 million by 2030. An estimated 17.9 million people died from CVDs in 2019 in the UK, representing 32% of all global deaths. Evidence suggested that the Mediterranean diet supplemented with extra virgin olive oil (EVOO) (25-50 ml/day) is highly reported as associated with a reduction of CV risk factors. However, the acceptability of the Mediterranean diet and the feasibility of this dietary pattern which includes consumption of olive oil remains unknown among Caucasians and East Asians in Northeast England. An Online Survey with two ethnicities in equal number and similar mean age and BMI that were undertaken for this PhD programme indicating that the acceptability and frequency of olive oil intake among East Asians is higher with a great MD score (8.02±SD1.8) (p<0.001) while Caucasians who consume olive oil were scored higher for MD score (6.51±SD2.2) (p<0.001), scored higher for MD acceptability (10.21±SD2.3) (p=0.017) and reported lower perceived barriers to healthy eating (PBHE) (1.81±SD4.0) (p=0.03) than non-consumers. Olive oil intake is likely to be positively associated with older age, higher MD score, higher MD acceptability and lower PBHE in both ethnicities. Evidence examining the effectiveness of nuts and olive oil, on both traditional and novel CV risk factors, in a comprehensive study in adults with different ethnic background is lacking. Our systematic reviews and meta-analysis of previous relevant literature on nuts that were undertaken for this PhD programme showed that nuts improve TC (MD: -7.54; 95% CI: -10.2 to -4.89; p < 0.00001; I2=59%, n=66), HDL (MD: 0.89; 95% CI: 0.04 to 1.75; P=0.04; I2= 53%; n=67), LDL (MD: -7.21; 95% CI: -9.38 to -5.04; P< 0.00001; I2= 68%; n=68), TG (MD: -8.83; 95% CI: -13.12 to -4.53; P< 0.0001; I2= 64%; n=65) and FMD (MD: 0.74; 95% CI: 0.09 to 1.39; P=0.03; I2=5%, n=10). The non-Asiangroup potentially tends to benefit more CV biomarkers with moderate nut consumption than Asian group. Olive oil systematic review reported that olive oil improves biomarker - PAI-1 (MD: -1.02ng/ml, 95% CI: -1.92 to -0.12; p = 0.03, I2 = 0%). Nevertheless, studies on olive oil on different ethnicities were lacking. A 6-week, cross-over, randomised controlled dietary interventional study with 2 weeks interventional duration was undertaken to test the effects of EVOO on cardiovascular health. Overall, this study provided evidence on the benefits of over a 2-week period produced a positive effect on 24-hour SBP including daytime SBP, night-time DBP and MAP and TC, LDL for all participants. For East Asians, olive oil exerts a beneficial effect on 24-hour SBP and daytime SBP, MAP while night�time DBP was improved among Caucasians following EVOO. EVOO intake also has a positive effect on blood lipids - TC and circulating biomarkers - sE-selectin in East Asians while LDL and non-HDL are improved among Caucasians after EVOO intake. The findings reported in the present thesis could be valuable to health professionals to develop more effective interventions and could also help the public to make better informed food choices relating to cardiovascular health
... The oil extracted from the pistachio kernels is rich in oleic and linolenic acids, both playing a crucial role in therapeutic thanks to their nutritional attractive properties. Expert Consultation Committee determined that replacement of carbohydrates by mono unsaturated fatty acid (MUFA) increases HDLcholesterol [5]. Also, the increase in stability over oxidation of vegetable oil is attributed to oleic acid [6,7]. ...
... Myristic and palmitic acid, members of SFAs, are associated with the risk of hypertension in pregnancy [12]. SFAs may promote pro-coagulation [14] that is associated with placental ischemia [15], and MUFA has a protective role in cardiovascular diseases [16]. However, the information regarding comprehensive fatty acid profiles in pregnancy and preeclampsia is still limited. ...
Article
Full-text available
Background Preeclampsia is a complication during pregnancy characterised by new-onset hypertension and proteinuria that develops after 20 weeks of gestation. Dyslipidemia in pregnancy is correlated with an increased risk of preeclampsia. However, the dynamic changes in lipid metabolic product, particularly fatty acid fraction, in preeclampsia maternal circulation, are not well understood. This study aimed to investigate fatty acid fraction in preeclampsia maternal blood compared with normotensive normal pregnancy. Methods A total of 34 women who developed preeclampsia and 32 women with normotensive normal pregnancy were included in our case-control study. Maternal blood samples were collected for serum fatty acid fractions analysis and other biochemical parameters. Serum fatty acid fractions included long-chain polyunsaturated fatty acid (LCPUFA), monounsaturated fatty acid (MUFA), saturated fatty acid, and total fatty acid, measured with gas chromatography-mass spectrometry (GC-MS). The mean difference of fatty acid level was analysed using parametric and non-parametric bivariate analysis based on normality distributed data, while the risk of preeclampsia based on fatty acid fraction was analysed using a logistic regression model. Results Women with preeclampsia have lower high-density lipoprotein (53.97 ± 12.82 mg/dL vs. 63.71 ± 15.20 mg/dL, p = 0.006), higher triglyceride (284.91 ± 97.68 mg/dL vs. 232.84 ± 73.69 mg/dL, p = 0.018) than that in the normotensive group. Higher palmitoleic acid was found in women with preeclampsia compared to normotensive normal pregnancy (422.94 ± 195.99 vs. 325.71 ± 111.03 μmol/L, p = 0.037). The binary logistic regression model showed that pregnant women who had total omega-3 levels within the reference values had a higher risk of suffering preeclampsia than those with the higher reference value (odds ratio OR (95% CI): 8,5 (1.51–48.07), p = 0.015). Pregnant women who have saturated fatty acid within reference values had a lower risk for suffering preeclampsia than those in upper reference value (OR (95% CI): 0.21 (0.52–0.88), p = 0.032). Conclusion Overall, palmitoleic acid was higher in women with preeclampsia. Further analysis indicated that reference omega-3 in and high saturated fatty acid serum levels are characteristics of women with preeclampsia.
Thesis
L’hyperglycémie chronique est impliquée dans le développement de complications associées au DT2 et la variabilité glycémique (VG) apparait comme une composante à part entière de l'homéostasie du glucose. Les mesures hygiéno-diététiques, en première ligne dans la prise en charge du DT2, passent entre autres par une modification de l’alimentation, dans laquelle les glucides occupent une place prépondérante. Au-delà de la quantité, la qualité des glucides a été mise en avant comme ayant un impact déterminant sur les excursions glycémiques. Notamment, la digestibilité des produits à base d’amidon pourrait alors avoir un impact sur le contrôle glycémique chez les patients atteints de DT2. Mais il y a aujourd’hui un réel besoin d’apporter une caractérisation des produits plus complète sur cet aspect et de mener des études de faisabilité et d’efficacité de tels régimes modulant la digestibilité de l’amidon. Mes travaux de thèse montrent qu’il est possible de concevoir un régime riche en amidon lentement digestible (SDS), grâce à des choix de produits amylacés disponibles dans le commerce, des conseils de cuisson et des recommandations adaptées. Pour la première fois, nous avons montré que le contrôle de la digestibilité de l'amidon de produits amylacés avec des instructions de cuisson appropriées dans une population atteinte de DT2 augmentait la consommation de contenu en SDS dans un contexte de vie réelle et que ce type de régime était bien accepté dans telle population. De plus, nous avons montré que l’augmentation du rapport SDS/glucides était associée à une amélioration du contrôle glycémique postprandial et qu’il existait une corrélation linéaire inverse entre les paramètres de VG et la teneur en SDS. La mise en œuvre d’un régime riche en amidon lentement digestible dans une population atteinte de DT2, a montré une différence significative sur le profil de variabilité glycémique, mais également sur les excursions glycémiques postprandiales, évalués par le CGMS, en comparaison avec un régime pauvre en amidon lentement digestible. Ce type de régime a également permis aux patients d’atteindre des cibles glycémiques postprandiales plus appropriées. Grâce à un travail de revue de la littérature, nous avons mis en évidence que la déviation standard (SD), le coefficient de variation (CV), l’amplitude moyenne des excursions glycémiques (MAGE) et la moyenne glycémique (MBG) étaient les paramètres de VG les plus étudiés en termes de relation avec les paramètres de diagnostic du DT2 et les complications liées au DT2 et qu’ils montraient des relations fortes, en particulier avec l’HbA1c. Dans les études interventionnelles, nous avons pu voir que la SD, le MAGE et le temps dans la cible (TIR) étaient les paramètres les plus utilisés comme critères d’évaluation, montrant des améliorations significatives suite aux interventions pharmacologiques ou nutritionnelles, souvent en lien avec des paramètres de contrôle glycémique comme l’HbA1c, la glycémie à jeun ou en postprandial. La VG apparaît donc comme une composante clé de la dysglycémie du DT2. Au-delà de son utilisation par le patient comme support du contrôle glycémique, le CGMS apparait comme un outil pertinent en recherche clinique pour évaluer l’efficacité des interventions même si à ce jour, il reste encore très peu utilisé pour les interventions nutritionnelles. Des études plus approfondies seront cependant nécessaires pour confirmer l'impact bénéfique de telles interventions alimentaires à long terme. Nous avons conçu une étude à plus grande échelle pour étudier l'impact à long terme d’un régime riche en SDS sur la variabilité et le contrôle glycémiques (CGMS) et les complications et comorbidités associées chez le patient atteint de DT2. La modulation de la digestibilité de l'amidon dans l'alimentation pourrait alors être utilisée comme un outil nutritionnel simple et approprié pour améliorer l'homéostasie glucidique au quotidien dans le DT2.
Article
Rationale The relationship between many fatty acids and respiratory outcomes remains unclear, especially with regard to mechanistic actions. Altered regulation of the process of lung repair is a key feature of chronic lung disease and may impact the potential for pulmonary rehabilitation, but underlying mechanisms of lung repair following injury or inflammation are not well-studied. The epidermal growth factor receptor agonist amphiregulin (AREG) has been demonstrated to promote lung repair following occupational dust exposure in animals. Studies suggest the polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) may enhance the production of AREG. The objective of this study was to determine the relationship between fatty acids and lung function in a population of veterans and determine if fatty acid status is associated with concentrations of AREG. Materials and Methods Data were collected from a cross-sectional study of veterans within the Nebraska-Western Iowa Health Care System. Whole blood assays were performed to quantify AREG concentrations via a commercially available ELISA kit. Fatty acids from plasma samples from the same patients were measured using gas-liquid chromatography. Intakes of fatty acids were quantified with a validated food frequency questionnaire. Linear regression models were used to determine whether plasma fatty acids or intakes of fatty acids predicted lung function or AREG concentrations. A p < 0.05 was considered statistically significant. Results Ninety participants were included in this analysis. In fully adjusted models, plasma fatty acids were associated with AREG production, including the PUFA eicosapentaenoic acid (EPA) (β = 0.33, p = 0.03) and the monounsaturated fatty acid octadecenoic acid: (β = −0.56, p = 0.02). The omega-3 PUFA docosapentaenoic acid (DPA) was positively associated with lung function (β = 0.28, p = 0.01; β = 26.5, p = 0.05 for FEV 1 /FVC ratio and FEV 1 % predicted, respectively), as were the omega-6 PUFAs eicosadienoic acid (β = 1.13, p < 0.001; β = 91.2, p = 0.005 for FEV 1 /FVC ratio and FEV 1 % predicted, respectively) and docosadienoic acid (β = 0.29, p = 0.01 for FEV 1 /FVC ratio). Plasma monounsaturated and saturated fatty acids were inversely associated with lung function. Conclusion Opposing anti- and pro-inflammatory properties of different fatty acids may be associated with lung function in this population, in part by regulating AREG induction.
Article
Full-text available
Milk provides some beneficial fatty acids which in dairy processing are subjected to pasteurization and fermentation. With the aim to assess such changes, aliquot parts of milk from 12 buffaloes were pooled and processed to germinated yoghurt and brined cheese, and to non-germinated curd – the respective samples of raw and dairy material subjected to lipid analysis. The results show that in cheese positive and negative changes are generally balanced, rumenic acid decreasing and other CLAs altered but not total CLA and PUFA; omega ratio and atherogenicity index worsened to little extent, due to adverse change in n-3, myristic and lauric acid. In yoghurt and curd CLA dramatically decreased, excluding rumenic acid; but vaccenic acid increased, though total trans isomers decreased; the worsened n-6/n-3 ratio and atherogenicity index is mostly because of the adverse effect on PUFAn-3 but also on myristic and lauric acid. In all products SFA and MUFA did not change, including palmitic, stearic, and oleic acid. It can be concluded that the decrease of CLA in yoghurt and curd is partially compensated by the increase in the vaccenic acid, while cheese making altered individual isomers but not groups of beneficial acids.
Article
The broad principles of the 1982 British Diabetic Association dietary recommendations remain valid. For the overweight, reduction in energy intake remains the most important aim. Carbohydrate should make up about 50–55% of the dietary energy intake, the majority of this coming from complex sources, preferably foods naturally high in dietary fibre or hydrolysis resistant starch. Up to 25 g of added sucrose may be allowed, provided it is part of a diet low in fat and high in fibre, and that it substitutes for an isocaloric amount of fat or high glycaemic index food or other nutritive sweeteners. Some high-carbohydrate diets have been shown to worsen blood glucose control and serum lipid abnormalities. Some previous recommendations for fibre intake have proved unrealistically high and of limited value. A modest increase to 30 g day−1, concentrating on soluble fibre, is recommended. Reduction of fat intake to 30–35% of energy intake remains an important goal which should help to reduce the incidence of cardiovascular disease in people with diabetes and aid weight loss. Of this only 10% of total energy should be saturated fat, 10% polyunsaturated fat, and 10–15% may be mono-unsaturated fat. The latter has been shown to provide a useful alternative energy source which may have beneficial effects on blood glucose control and serum lipids. Cholesterol intake should not exceed 300 mg day−1. Protein should comprise about 10–15% of energy intake. Reduction in intake of protein and associated nutrients may help to slow down progression of nephropathy. Limitation of salt intake to 6 g day−1 is recommended. Reduction in fat intake may be relatively more important in Type 2 diabetic patients, whereas limitation in protein intake may be more important in Type 1 diabetes.
Book
Part of the authoritative series on reference values for nutrient intakes , this new release establishes a set of reference values for dietary energy and the macronutrients: carbohydrate (sugars and starches), fiber, fat, fatty acids, cholesterol, protein, and amino ...
Article
Age, sex, and blood pressure could modify the associations of total cholesterol (and its main two fractions, HDL and LDL cholesterol) with vascular mortality. This meta-analysis combined prospective studies of vascular mortality that recorded both blood pressure and total cholesterol at baseline, to determine the joint relevance of these two risk factors. METHODS Information was obtained from 61 prospective observational studies, mostly in western Europe or North America, consisting of almost 900,000 adults without previous disease and with baseline measurements of total cholesterol and blood pressure. During nearly 12 million person years at risk between the ages of 40 and 89 years, there were more than 55,000 vascular deaths (34,000 ischaemic heart disease [IHD], 12,000 stroke, 10,000 other). Information about HDL cholesterol was available for 150,000 participants, among whom there were 5000 vascular deaths (3000 IHD, 1000 stroke, 1000 other). Reported associations are with usual cholesterol levels (ie, corrected for the regression dilution bias). FINDINGS 1 mmol/L lower total cholesterol was associated with about a half (hazard ratio 0.44 [95% CI 0.42-0.48]), a third (0.66 [0.65-0.68]), and a sixth (0.83 [0.81-0.85]) lower IHD mortality in both sexes at ages 40-49, 50-69, and 70-89 years, respectively, throughout the main range of cholesterol in most developed countries, with no apparent threshold. The proportional risk reduction decreased with increasing blood pressure, since the absolute effects of cholesterol and blood pressure were approximately additive. Of various simple indices involving HDL cholesterol, the ratio total/HDL cholesterol was the strongest predictor of IHD mortality (40% more informative than non-HDL cholesterol and more than twice as informative as total cholesterol). Total cholesterol was weakly positively related to ischaemic and total stroke mortality in early middle age (40-59 years), but this finding could be largely or wholly accounted for by the association of cholesterol with blood pressure. Moreover, a positive relation was seen only in middle age and only in those with below-average blood pressure; at older ages (70-89 years) and, particularly, for those with systolic blood pressure over about 145 mm Hg, total cholesterol was negatively related to haemorrhagic and total stroke mortality. The results for other vascular mortality were intermediate between those for IHD and stroke. INTERPRETATION Total cholesterol was positively associated with IHD mortality in both middle and old age and at all blood pressure levels. The absence of an independent positive association of cholesterol with stroke mortality, especially at older ages or higher blood pressures, is unexplained, and invites further research. Nevertheless, there is conclusive evidence from randomised trials that statins substantially reduce not only coronary event rates but also total stroke rates in patients with a wide range of ages and blood pressures.
Article
To calculate the effect of changes in carbohydrate and fatty acid intake on serum lipid and lipoprotein levels, we reviewed 27 controlled trials published between 1970 and 1991 that met specific inclusion criteria. These studies yielded 65 data points, which were analyzed by multiple regression analysis using isocaloric exchanges of saturated (sat), monounsaturated (mono), and polyunsaturated (poly) fatty acids versus carbohydrates (carb) as the independent variables. For high density lipoprotein (HDL) we found the following equation: delta HDL cholesterol (mmol/l) = 0.012 x (carb----sat) + 0.009 x (carb----mono) + 0.007 x (carb---- poly) or, in milligrams per deciliter, 0.47 x (carb----sat) + 0.34 x (carb----mono) + 0.28 x (carb----poly). Expressions in parentheses denote the percentage of daily energy intake from carbohydrates that is replaced by saturated, cis-monounsaturated, or polyunsaturated fatty acids. All fatty acids elevated HDL cholesterol when substituted for carbohydrates, but the effect diminished with increasing unsaturation of the fatty acids. For low density lipoprotein (LDL) the equation was delta LDL cholesterol (mmol/l) = 0.033 x (carb----sat) - 0.006 x (carb----mono) - 0.014 x (carb----poly) or, in milligrams per deciliter, 1.28 x (carb----sat) - 0.24 x (carb----mono) - 0.55 x (carb---- poly). The coefficient for polyunsaturates was significantly different from zero, but that for monounsaturates was not. For triglycerides the equation was delta triglycerides (mmol/l) = -0.025 x (carb----sat) - 0.022 x (carb----mono) - 0.028 x (carb---- poly) or, in milligrams per deciliter, -2.22 x (carb----sat) - 1.99 x (carb----mono) - 2.47 x (carb----poly).(ABSTRACT TRUNCATED AT 250 WORDS)
Article
This report summarizes our current understanding of how monounsaturated fatty acids (MUFAs) affect risk for cardiovascular disease (CVD). This is a topic that has attracted considerable scientific interest,1 2 3 in large part because of uncertainty regarding whether MUFA or carbohydrate should be substituted for saturated fatty acids (SFAs) and the desirable quantity of MUFA to include in the diet. MUFAs are distinguished from the other fatty acid classes on the basis of having only 1 double bond. In contrast, polyunsaturated fatty acids (PUFAs) have 2 or more double bonds, and SFAs have none. The position of the hydrogen atoms around the double bond determines the geometric configuration of the MUFA and hence whether it is a cis or trans isomer. In a cis MUFA, the hydrogen atoms are present on the same side of the double bond, whereas in the trans configuration, they are on opposite sides. The American Heart Association Nutrition Committee recently published a scientific statement regarding the relationship of trans MUFA to CVD risk,4 and the present statement, therefore, will be limited to a discussion of dietary cis MUFAs, of which oleic acid ( cis C18:1) comprises ≈92% of cis MUFAs. In the United States, average total MUFA intake is 13% to 14% of total energy intake, an amount that is comparable to (or slightly greater than) SFA intake. In contrast, PUFAs contribute less (ie, 7% of energy). The major emphasis of current dietary guidelines involves replacing SFAs with complex carbohydrates to achieve a total fat intake of ≤30% of calories. There is evidence suggesting that the substitution of MUFA instead of carbohydrate for SFA calories may favorably affect CVD risk.5 6 7 The American Heart Association dietary guidelines for healthy American adults recommend a diet that provides <10% of calories from SFA, up …
Article
THE SECOND report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II, or ATP II) presents the National Cholesterol Education Program's updated recommendations for cholesterol management. It is similar to the first in general outline, and the fundamental approach to treatment of high blood cholesterol is comparable. This report continues to identify low-density lipoproteins (LDL) as the primary target of cholesterol-lowering therapy. As in the first report, the second report emphasizes the role of the clinical approach in primary prevention of coronary heart disease (CHD). Dietary therapy remains the first line of treatment of high blood cholesterol, and drug therapy is reserved for patients who are considered to be at high risk for CHD. However, the second report contains new features that distinguish it from the first. These include the following: Increased emphasis on See also pp 3002 and 3009.
Article
Explains the contents of the COMA Report – COMA (Committee on Medical Aspects of Food Policy) has thoroughly evaluated the requirements for different nutrients. The term “dietary reference values” has been devised and it replaces recommended dietary intakes. Considers the problems of implementing the new recommendations.