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Effects of dietary saturated, monounsaturated, and n⫺3 fatty acids
on blood pressure in healthy subjects
Birthe M Rasmussen, Bengt Vessby, Matti Uusitupa, Lars Berglund, Eva Pedersen, Gabrielle Riccardi,
Angela A Rivellese, Linda Tapsell, and Kjeld Hermansen for The KANWU Study Group
Background: The quantity and quality of fats consumed in the diet
influence the risk of cardiovascular disease (CVD). Although the
effect of diet on plasma lipids and lipoproteins is well documented,
less information exists on the role of fats on blood pressure (BP).
Objective: The objective was to evaluate the effects of different
types of dietary fat on BP in healthy subjects.
Design: Healthy subjects (n҃162) were randomly assigned for 3
mo to follow 1 of 2 isoenergetic diets: 1 rich in monounsaturated fatty
acids (MUFA diet) and the other rich in saturated fatty acids (SFA
diet). Each group was further randomly assigned to receive supple-
mentation with fish oil (3.6 g nҀ3 fatty acids/d) or placebo.
Results: Systolic BP (SBP) and diastolic BP (DBP) decreased with
the MUFA diet [Ҁ2.2% (P҃0.009) and Ҁ3.8% (P҃0.0001),
respectively] but did not change with the SFA diet [Ҁ1.0% (P҃
0.2084) and Ҁ1.1% (P҃0.2116)]. The MUFA diet caused a sig-
nificantly lower DBP than did the SFA diet (P҃0.0475). Interest-
ingly, the favorable effects of MUFA on DBP disappeared at a total
fat intake above the median (쏜37% of energy). The addition of nҀ3
fatty acids influenced neither SBP nor DBP.
Conclusions: Changing the proportions of dietary fat by decreasing
SFAs and increasing MUFAs decreased diastolic BP. Interestingly,
the beneficial effect on BP induced by fat quality was negated by the
consumption of a high total fat intake. The addition of nҀ3 fatty
acids to the diet had no significant effect on BP. Am J Clin Nutr
KEY WORDS Diet, saturated fatty acids, monounsaturated
fatty acids, nҀ3 fatty acids, blood pressure
The quantity and quality of fats consumed in the diet are
important features that influence the risk of cardiovascular dis-
ease (CVD) (1). The paradigm that dietary fats act exclusively via
effects on serum lipids and lipoproteins has been challenged
(2– 6). Evidence suggesting the beneficial health effects of the
Mediterranean diet has emerged from the classic studies of Keys
(7), which indicate that the consumption of diets enriched in
monounsaturated fat (MUFA) relates to a lower incidence of
coronary heart disease. The Lyon Diet Heart Study (3) showed
that a Mediterranean-type diet reduces the rate of recurrence after
a first myocardial infarction. The replacement of saturated fat
(SFA) with MUFA and
-linolenic acids (nҀ3 fatty acids) seems
to induce beneficial effects in persons with CVD without chang-
ing plasma lipid concentrations. The Diet and Reinfarction Trial
(DART; 5) supported the ability of diets rich in eicosapentaenoic
acid (EPA) to lower ischemic complications of arteriosclerosis.
The study by Trichopoulou et al (8) corroborated the Lyon Diet
Heart Study (3) and showed that strict adherence to a Mediter-
ranean diet is associated with a significant reduction in total
Studies focusing on surrogate risk markers for CVD other than
plasma lipids and lipoproteins are needed to clarify the effects of
dietary fat on CVD. In this regard, it seems prudent to evaluate
the effect of dietary fat on CVD risk factors such as blood pres-
sure (BP), insulin sensitivity, endothelial function, hemostatic
factors, and microalbuminuria.
Genetic factors seem to be responsible for as much as 20 – 40%
of BP variations in the general population (9). However, epide-
miologic data implicate that lifestyle factors (eg, dietary habits)
are a major contributor to the high prevalence of hypertension
(10). Nevertheless, our knowledge of the influence of macronu-
trients such as fat on BP is limited. Data suggest that both the fat
quantity and quality of the diet could be important for the devel-
opment of insulin resistance (11). In the KANWU study (12, 13)
we showed that MUFA, in contrast with SFA, improved the
insulin sensitivity in healthy subjects (12) and concomitantly
From the Department of Clinical Endocrinology and Metabolism C,
Aarhus University Hospital, Aarhus, Denmark (BMR, EP, and KH); the Unit
for Clinical Nutrition Research, Department of Public Health and Caring
Sciences/Geriatrics, University of Uppsala, Uppsala, Sweden (BV); the De-
partment of Clinical Nutrition, University of Kuopio, Kuopio, Finland (MU);
the Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden
(LB); the Department of Clinical and Experimental Medicine, School of
Medicine, Federico II University, Naples, Italy (GR and AAR); and the
Department of Biomedical Sciences and Smarts Food Centre, University of
Wollongong, Wollongong, Australia (LT).
Supported by the Danish Medical Research Council, the Swedish Coun-
cil for Forestry and Agricultural Research, Health Research Council Acad-
emy of Finland, Helga and Peter Kornings Foundation, and International
Council of Olive Oil. The food for the study was generously supplied by MD
Foods (ARLA), Denmark; Carlshamn Mejeri AB, Svenska Nestlé AB, and
Van den Bergh Foods AB, Sweden; Eridania Beghin-Say, Belgium; and
Meadow Lea Foods, Australia. The Pikasol capsules were supplied by Lube
Ltd, Hadsund, Denmark.
Reprints not available. Address correspondence to K Hermansen, De-
partment of Clinical Endocrinology and Metabolism C, Aarhus University
Hospital, Aarhus Sygehus, Tage-Hansens Gade 2, DK 8000 Aarhus C, Den-
mark. E-mail: email@example.com.
Received May 23, 2005.
Accepted for publication October 24, 2005.
221Am J Clin Nutr 2006;83:221– 6. Printed in USA. © 2006 American Society for Nutrition
by guest on June 2, 2013ajcn.nutrition.orgDownloaded from
reduced plasma cholesterol and triacylglycerol concentrations
(13). More recently, it was shown that insulin sensitivity im-
proved when dietary SFA was substituted for polyunsaturated fat
(PUFA) (14). An important question is whether the quantity or
quality of fat also affects BP and thereby the risk of hypertension.
The aim of this study was to investigate whether dietary MUFA,
compared with SFA, affects BP in healthy subjects. Second, we
investigated whether the addition of long-chain nҀ3 fatty acids
had a modifying effect.
SUBJECTS AND METHODS
The study was a 3-mo controlled, parallel, multicenter study,
performed at 5 different centers (Kuopio, Finland; Aarhus, Den-
mark; Naples, Italy; Wollongong, Australia; and Uppsala, Swe-
den). The design was reported in detail previously (12).
Healthy subjects were randomly assigned to a diet containing
either a high proportion of SFAs (SFA diet) or a high proportion
of MUFAs (MUFA diet). Within each of these 2 groups, the
subjects were randomly assigned to receive supplementary cap-
sules containing fish oil [3.6 g nҀ3 fatty acids/d providing 2.4 g
EPA and docosahexaenoic fatty acids (DHA); Pikasol, Lube Ltd,
Hadsund, Denmark] or placebo capsules containing the same
amount of olive oil.
The test period was preceded by a 2-wk run-in period during
which the subjects consumed their habitual diets supplemented
with placebo capsules. Routine clinical tests, including an oral-
glucose-tolerance test (15), were carried out during this period.
The subjects kept a 3-d dietary record (2 weekdays and 1 week-
end day) to document pretrial dietary habits. Two additional 3-d
dietary records were kept at the beginning of the second and third
months of the test period. Tests and laboratory analyses were
carried out at baseline and at the end of the study. Blood pressure
was measured at baseline and at the end of study.
A total of 162 healthy white subjects (n҃95 men and 67
women) aged 30 –65 y and with normal or moderately increased
body weight [BMI (in kg/m
)҃22–32] were included. Health
status was screened via medical history and routine laboratory
examinations. Subjects with impaired glucose tolerance (15) but
without diabetes were included. Other reasons for exclusion
were specific eating habits due to cultural or religious beliefs,
high habitual physical activity, high alcohol intake (ie, binge
drinking or a regular alcohol intake 쏜40 g/d), and hepatic, car-
diac, thyroid, and disabling diseases. Body weight during the past
3 mo should not have changed 쏜4 kg. Subjects taking acetyl
salicylic acid, thiazide diuretics,
drugs, and corticosteroids were also excluded. If a subject was
taking any other medication, the dose had to remain constant
during the test period. Alcohol consumption, weight, and the
degree of physical activity were kept stable during the study.
Smoking was allowed, but smoking habits had to remain un-
changed during the study. Premenopausal women had all tests
made during the same period of their menstrual cycle.
All subjects were fully informed of the experimental nature of
the investigation, which had been approved by the local ethics
committees. Informed consent was obtained before the study
began, and all subjects complied fully with the protocol.
All subjects were instructed to eat isoenergetic diets contain-
ing the same amount of macronutrients: 37% of energy as fat with
a high proportion of SFAs (SFA diet) or MUFAs (MUFA diet).
The SFA diet contained 17% of energy as SFAs, 14% of energy
as MUFAs, and 6% of energy as PUFAs, whereas the MUFA diet
contained 8% of energy as SFAs, 23% of energy as MUFAs, and
6% of energy as PUFAs, respectively. Trained dietitians in-
structed all subjects on the preparation of their diets. To ensure
good adherence to the diets, the subjects met the dietitians at least
every second week until the end of the study. The participants
were supplied with edible fats to be used as spreads on bread, for
cooking, and in dressings. Core foods such as margarine, oils,
and a range of other staple items were provided. Butter, marga-
rines, and oils to be used in the diets were prepared centrally and
distributed to the different European centers. The SFA diet in-
cluded butter and table margarine containing a relatively high
proportion of SFAs. The MUFA diet included spread and mar-
garine with a high proportion of oleic acid, derived from high–
oleic acid sunflower oil and negligible amounts of trans fatty
acids, nҀ3 fatty acids, and olive oil. The study center in Australia
obtained similar oil from local suppliers. The intake during the
test period was calculated as the mean values from the dietary
records provided during the second and third months of the study.
The dietary records were estimated, not weighed. Local nutrient
analysis software programs containing country-specific food da-
tabases were used in the analyses. Data on margarine and other
specially prepared foods were entered into these databases for
inclusion in the analyses. The adherence to the test fats was
verified by analyses of the phospholipid fatty acid composition of
Blood pressure and body weight
Blood pressure was measured at baseline and at the end of the
study to the nearest 5 mm Hg with a sphygmomanometer. Sys-
tolic and diastolic BP was defined as phase I and V Korotkoff
sounds, respectively. Blood pressure was measured from the
same arm, with subjects in a sitting position, after 10 min of rest
from the time the cuff had been placed on the arm. Measurements
were made 3 times at 2-min intervals in each case. The data
analyzed were the means of the 3 BP values. Body weight was
measured at each visit to ensure that the participants were weight
Results are presented as mean 앐SD. The study was an inten-
tion to treat study, ie all randomized subjects, with at least one
measurement during treatment were included in the analyses.
The treatment effects were estimated from a statistical model in
which treatment categories (SFA or MUFA diet with or without
nҀ3 fatty acids) and their interaction were analyzed factors,
whereas center, age, sex, and baseline value of the outcome
variable were covariates. The difference between groups for
adjusted mean treatment effects are presented with Pvalues and
A post hoc subgroup analysis was made according to the
relative intake of total fat during treatment (above or below the
median of 37% of energy). The abovementioned model was used
with the addition of an interaction term between treatment and
relative fat intake (above or below the median).
222 RASMUSSEN ET AL
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Of the 83 subjects assigned to the SFA diet, 42 subjects were
in the SFA ѿplacebo group (1 dropout) and 41 subjects were
in the SFA ѿnҀ3 fatty acid group (1 dropout). Of the 79 subjects
assigned to the MUFA diet, 40 subjects were in the MUFA ѿ
placebo group (no dropouts) and 39 subjects were in the
MUFA ѿnҀ3 fatty acid group (1 dropout).
The clinical characteristics of the 162 subjects (n҃76 women
and 86 men) assigned randomly to the SFA and MUFA diets did
not differ significantly (Table 1). Mean (앐SD) body mass index
(BMI; in kg/m
) and body weight remained unchanged during
the study. BMIs at baseline and at end of the SFA diet period were
26.6 앐2.9 and 26.7 앐2.9 and at the end of the MUFA diet were
26.6 앐3.1 and 26.3 앐3.2, respectively.
The average nutrient composition before the study, as calcu-
lated from the dietary records (Table 2), was not different be-
tween the SFA and MUFA diet groups, respectively. During the
test period there was a slight increase in the proportion of dietary
fat in both groups. The recorded mean intake of fat and fatty acids
during the study was similar to the target values. During the study
the amount of fiber was significantly higher (P҃0.0444), and
the amount of cholesterol was significantly lower (P҃0.0006),
in the MUFA than in the SFA diet. The estimated proportions of
trans fatty acids were low and not different between the diets.
Adherence to the diets was not different between the SFA and
MUFA diet groups. These data were reported previously (12).
Effects on blood pressure
A significant decrease in SBP (Ҁ2.2%; P҃0.009) and DBP
(Ҁ3.8%; P҃0.0001) was observed during the MUFA diet,
whereas no significant changes were seen during the SFA diet.
The MUFA diet caused a significantly lower DBP than did the
SFA diet (P҃0.0475) (data not shown). We also looked at the
effects of a low compared with a high fat intake, ie, a fat intake
below or above the median fat intake of 37% of energy (Table 3).
In subjects with a total fat intake below the median, the MUFA
diet reduced the SBP (P҃0.0408) and the DBP (P҃0.0023)
significantly. Interestingly, the differences in SBP and in DBP
disappeared with a total fat intake above the median. Addition of
nҀ3 fatty acids did not influence SBP or DBP. Thus, the mean
(앐SD) changes in DBP in response to nҀ3 fatty acids and to
placebo were Ҁ2.2 앐0.7 and Ҁ1.6 앐0.7 mm Hg (P҃0.5700),
respectively, and the corresponding changes in SBP were
Ҁ2.2 앐1.1 and Ҁ1.8 앐1.1 mm Hg (P҃0.7567), respectively
Clinical characteristics of the healthy subjects at entry
Age (y) 49.3 앐7.1 48.5 앐8.0 47.0 앐8.8 49.5 앐7.3
)26.3 앐2.7 26.9 앐3.0 26.1 앐3.2 26.5 앐3.1
SBP (mm Hg) 121.6 앐11.5 122.7 앐11.4 123.1 앐16.6 122.4 앐12.9
DBP (mm Hg) 77.2 앐7.6 77.1 앐9.0 77.8 앐9.9 74.6 앐9.1
All values are x앐SD. SFA, saturated fatty acid; MUFA, monounsaturated fatty acid. No statistically significant differences in the clinical characteristics
were observed between the groups (Student’s unpaired ttests).
Dietary nutrient composition in the healthy subjects before and during the study
Pfor adjusted mean
differences in treatment
effects (SFA versus
MUFA diet period)
Target values for fat
composition during the
During SFA diet MUFA diet
Energy (kcal) 2250 앐550
2140 앐390 2120 앐500 2150 앐450 0.0768 — —
Protein (% of energy) 15.6 앐3.0 15.2 앐2.5 15.8 앐2.8 14.8 앐2.3 0.1005 — —
Carbohydrate (% of energy) 45.8 앐6.7 44.1 앐5.2 47.3 앐7.0 45.9 앐4.2 0.0519 — —
Fat (% of energy) 33.7 앐6.5 37.1 앐4.1 33.3 앐6.1 37.1 앐4.2 0.7975 37 37
SFA 13.5 앐3.6 17.6 앐2.5 13.3 앐3.7 9.6 앐1.8 쏝0.0001 17 8
MUFA 13.0 앐3.7 13.1 앐2.5 13.1 앐3.2 21.1 앐4.0 쏝0.0001 14 23
PUFA 4.8 앐1.6 4.7 앐1.5 4.7 앐1.5 4.6 앐0.8 0.1768 6 6
Fiber (g/d) 23.8 앐7.7 22.4 앐6.6 23.0 앐8.4 23.0 앐8.4 0.0444 — —
Cholesterol (mg/d) 316 앐126 322 앐91 310 앐139 254 앐80 0.0006 — —
PUFA, polyunsaturated fat; SFA, saturated fatty acid; MUFA, monounsaturated fatty acid. Statistical method: intention-to-treat study in which the
categories (SFA or MUFA diet with or without nҀ3 fatty acids) and their interactions were analyzed; center, age, sex, and the baseline value of the outcome
variables were covariates.
The average nutrient composition before the study was not significantly different in the subjects randomly assigned to the SFA and MUFA diets.
x앐SD (all such values).
FATTY ACIDS AND BLOOD PRESSURE 223
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(data not shown). As seen in Table 3, the addition of nҀ3 fatty
acids had no influence on SBP or DBP. In the main model (with-
out % of energy as fat), no interactions were found between SFA
and MUFA and nҀ3 fatty acids. In the post hoc analysis, how-
ever, the 3-factor interaction between SFA or MUFA, nҀ3 fatty
acids, and % of energy as fat (above or below the median) was
significant for the change in DBP (P҃0.048). There were no
significant interactions with SBP.
Comparison of the effects of MUFA and SFA on blood
In the present study we found that a MUFA-rich diet, in con-
trast with an SFA-rich diet, reduced the DBP in healthy, normo-
tensive subjects. Although the type of fat, rather than the amount
of fat, in the diet may be more important in terms of determining
health outcomes, it is noteworthy that a MUFA-rich diet causes
a reduction in both SBP and DBP at a fat intake below 37% of
energy, whereas the positive effect of MUFA on BP seems to be
lost at a high total fat intake. Whether the slightly higher dietary
fiber content and the lower cholesterol content may have con-
tributed to the positive effect of MUFA on BP cannot be ruled
out. The calculated dietary intakes of calcium, sodium, potas-
sium, and alcohol did not differ significantly between the MUFA
and SFA diet groups; this finding supports the suggestion that the
difference in health outcomes was related to the quality of dietary
fat. Body weight was stable in both diet groups.
In the Multiple Risk Factor Intervention Trial (MRFIT; 16,
17), the main findings in the multivariate analysis of the 6-y
observational data were significant, independent, positive rela-
tions between dietary SFA and DBP and between dietary cho-
lesterol and SBP and DBP and an inverse relation of the PUFA-
SFA ratio to DBP. A BP-lowering effect of MUFA has been
suggested in some epidemiologic studies among populations
with a high intake of MUFA (7, 18 –20). Although limited in
number, intervention studies also suggest a BP-lowering effect
when MUFA is substituted for SFA (21, 22). In a small group of
hypertensive women, a diet rich in MUFA from olive oil showed
beneficial effects on BP (23). However, other trials in normo-
tensive subjects showed no evidence of a BP-reducing effect of
MUFA (16). Interestingly, substituting dietary PUFA with
MUFA lowered both systolic and diastolic BP in 16 type 2 dia-
betic subjects (24), whereas only a minor lowering in DBP could
be detected in healthy subjects (25). A diet rich in olive oil
lowered the SBP and DBP by 4 –5 and 3 mm Hg, respectively, as
compared with a carbohydrate-rich diet in normotensive type 2
diabetic subjects (26), whereas such an effect was not detected in
a small group of insulin-treated type 2 diabetic subjects with
microalbuminuria (27). Finally, a slight reduction in SFA intake
along with a supplement of olive oil markedly lowered the daily
dose of antihypertensive drugs needed by hypertensive subjects
Effect of a 12-wk dietary intervention and nҀ3 fatty acids on diastolic (DBP) and systolic (SBP) blood pressure in the healthy subjects
Differences in treatment
effects (SFA versus MUFA
Difference 95% CI P
DBP (mm Hg)
쏝37 % of energy 76.2 앐6.8
1.9 앐8.2 2.5 0.0663 78.3 앐11.8
Ҁ4.8 앐8.5 Ҁ6.1 0.0160 6.4 2.3, 10.5 0.0023
쏜37 % of energy 78.2 앐8.4
Ҁ2.7 앐5.3 Ҁ3.5 0.0144 77.3 앐8.1
Ҁ2.1 앐7.8 Ҁ2.7 0.1789 Ҁ1.7 Ҁ5.6, 2.2 0.3973
nҀ3 Fatty acids
쏝37 % of energy 74.4 앐8.7
Ҁ1.0 앐6.4 Ҁ1.3 0.6059 74.2 앐9.0
Ҁ2.3 앐6.3 Ҁ3.1 0.0897 1.7 Ҁ2.3, 5.7 0.4107
쏜37 % of energy 79.7 앐8.6
Ҁ1.3 앐6.1 Ҁ1.6 0.2030 74.9 앐9.6
Ҁ3.4 앐5.1 Ҁ4.5 0.0224 1.8 Ҁ2.4, 5.9 0.3940
SBP (mm Hg)
쏝37 % of energy 122.4 앐10.3
3.5 앐11.6 2.9 0.1568 125.8 앐16.8
Ҁ4.8 앐8.2 Ҁ3.8 0.1520 6.6 0.3, 12.9 0.0408
쏜37 % of energy 120.8 앐12.8
Ҁ3.2 앐5.7 Ҁ2.7 0.0524 120.7 앐16.4
Ҁ2.4 앐11.6 Ҁ2.0 0.2642 Ҁ1.9 Ҁ7.9, 4.1 0.5286
nҀ3 Fatty acids
쏝37 % of energy 121.1 앐11.1
Ҁ2.1 앐13.2 Ҁ1.7 0.2940 125.0 앐10.1
Ҁ2.3 앐10.9 Ҁ1.8 0.2865 Ҁ0.1 Ҁ6.3, 6.0 0.9691
쏜37 % of energy 124.1 앐11.7
Ҁ1.4 앐7.1 Ҁ1.1 0.5575 119.5 앐15.4
Ҁ3.2 앐11.9 Ҁ2.7 0.2793 1.3 Ҁ5.0, 7.7 0.6802
SFA, saturated fatty acid; MUFA, monounsaturated fatty acid. Statistical method: intention-to-treat study in which the categories (SFA or MUFA diet
with or without nҀ3 fatty acids) and their interactions were analyzed; center, age, sex, and the baseline value of the outcome variables were covariates. Post
hoc analysis: a subgroup analysis was made according to the relative intake of total fat during the treatment (above or below the median of 37% of energy). The
model was used with the addition of an interaction term between treatment and relative fat intake (above or below the median). A significant 3-factor interaction
between SFA or MUFA diet, nҀ3 fatty acids, and % of energy (above or below the median) for the change in DBP (P҃0.048) was found. There were no
significant interactions with SBP.
All values are x앐SD.
All values are least-squares x앐SD.
224 RASMUSSEN ET AL
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(28). We showed that the present change in the proportion of
dietary fatty acids, ie, a decrease in SFAs and an increase in
MUFAs, improves insulin sensitivity (12). Prolonged insulin
resistance has been shown to be associated with structural alter-
ations of arterial vascular smooth muscle, which may provide the
anatomic substrate for the propagation of hypertension (29).
Insulin is a growth factor that stimulates the synthesis of vascular
smooth muscle cells and results in proliferative changes in the
arteries. Elevated circulating concentrations of insulin are asso-
ciated with activation of the sympathetic nervous system and
increased peripheral resistance and sodium retention (10, 30).
The beneficial effect on BP of MUFA, in contrast with SFA, may
thus, at least in part, be mediated via an improvement in insulin
sensitivity. Interestingly, the beneficial effect of the MUFA diet
on insulin sensitivity was not seen when the absolute fat intake
was high (쏜37% of energy) (12). In line with this, the effect of
MUFA on BP faded away at a high fat intake (쏜37% of energy).
Another possibility could be that the olive oil phenolics, which
are powerful antioxidants, partially accounted for the BP-
lowering effect (30).
Some of the discrepancies among studies investigating similar
dietary changes may be due to differences in populations (eg, an
effect of dietary factors may be easier to find in hypertensive than
in normotensive individuals) or in methods of measuring BP.
Thus, ambulatory BP monitoring with repeated measurements
over 24 h much more accurately detects small changes in BP than
do clinical BP measurements. Interestingly, we previously found
that the diurnal BP was unaffected by a change in the quality of
SFAs, ie, between the 2 most important SFAs, stearic and
palmitic acids, in type 2 diabetic subjects (31). Mediterranean
diets are associated with a reduced risk of CVD, and additional
research on the effects of MUFA on BP is warranted to elucidate
the potential of MUFA-rich diets to lower BP via diurnal BP
measurements, sufficient population samples, and different pop-
nⴚ3 Fatty acids and blood pressure
In the present study we found that the addition of 3.6 g nҀ3
fatty acids/d did not affect DBP or SBP in normotensive subjects,
regardless of whether they were consuming a high-fat (쏜37% of
energy) or a low-fat diet. In a meta-analysis (32), relatively high
doses of nҀ3 PUFAs, typically 쏜3 g/d, reduced BP but only in
hypertensive subjects. Weighted pooled estimates of SBP and
DBP changes (mm Hg) and 95% CIs were Ҁ1.0 (Ҁ2.0, 0.0) and
Ҁ0.5 (Ҁ1.2, 0.2) in normotensive subjects and were Ҁ5.5 (Ҁ8.1,
Ҁ2.9) and Ҁ3.5 (Ҁ5.0, Ҁ2.1) in the trials of untreated hyper-
tensive subjects. The magnitude of BP reduction was greatest at
a high BP but was not significantly associated with dose of nҀ3
fatty acids. In contrast, another meta-analysis showed a dose-
response effect of fish oil on BP with an amount of nҀ3 fatty
acids of 쏜3.3 g/d needed to be associated with an effect on BP
(33). However, the effect of nҀ3 fatty acids on BP occurred only
in subjects with hypertension, hypercholesterolemia, and athero-
sclerosis and not in healthy normotensive subjects. In subjects
with peripheral arterial disease, a recent Cochrane analysis (34)
found that nҀ3 fatty acid supplementation reduced DBP but not
SBP. Interestingly, the Lugalawa Study (35) found that a daily
fish consumption of 300 – 600 g increased plasma nҀ3 fatty
acids and decreased BP. The effect of nҀ3 fatty acids on BP in
normotensive subjects is not convincing. Thus, in a 9-mo inter-
vention study the addition of nҀ3 fatty acids lowered SBP and
DBP in normotensive subjects (36). However, a 12-mo study of
the addition of nҀ3 fatty acids in normotensive subjects found no
effect on SBP or DBP (37).
Dietary fats may modulate BP through different mechanisms.
Also, nҀ3 and nҀ6 PUFAs are converted to prostaglandins,
which reduce BP by affecting arterial vasodilation, electrolyte
balance, and renal release of renin or pressor hormones. The
incorporation of unsaturated fatty acids into cell membranes
increases membrane permeability, thus stimulating the transport
of sodium and cations across the membrane. In summary, nҀ3
fatty acids seem to have a small dose-dependent, hypotensive
effect, the extent of which seems to be dependent on the degree
of hypertension. In view of the high dose required to lower BP,
an increased intake of nҀ3 fatty acids has a limited role in the
management of hypertension.
Changing the proportions of dietary fat by decreasing SFAs
and increasing MUFAs decreased diastolic BP. Interestingly, the
beneficial effect on BP induced by fat quality was negated by
the consumption of a high total fat intake (쏜37% of energy). The
addition of nҀ3 fatty acids did not alter the BP.
BMR, BV, MU, GR, AAR, LT, and KH were the daily project leaders,
were involved in the study scheme and data interpretation, and wrote the
manuscript. LB was involved in the study scheme and data interpretation and
provided significant advice. EP was involved in carrying out the study and
provided significant advice. The KANWU Study Group consists of B
Vessby, M Uusitupa, K Hermansen, G Riccardi, AA Rivellese, LC Tapsell,
L Berglund, BM Rasmussen, and E Pedersen. None of the authors had a
conflict of interest.
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