Lipid, lipoprotein, and hemostatic effects of fish vs fish-oil n-3 fatty acids in mildly hyperlipidemic males13 Lynne
Cobiac,
Peter
ABSTRACT
The
mostasis,
and
blood
perlipidemic
(EPA)
M Clifton,
men
plus
effects
subjects
served
triglycerides
20%
protein
(VLDL)
cholesterol increased by creases in the proportion respectively. lipoprotein
and
significantly
different
lowered
from
fibrinogen
KEY
WORDS
lipids,
plasma
dition, fish oil appears (17) and protect against
acid
for 5 wk. Six
and
N-3
P
(all
(HDL)
rise
The
fish
fish
oil
produced
but
only the Nutr l99l;53:
J C/in n-3
comparable
fatty acids,
lipoproteins,
lipid
fish improved 12 10-16.
plasma
fatty fatty
and
hemostatic
acids
fish and
fish may
health
benefits
of fish
the observations extended
been
effects
It is therefore oil and
content. We men in whom plus
DHA
were
compared.
in Eskimos.
correlated
with
the Eskimos’
have
played
that
have
other
a role high
(3).
(1) highlighted
large
of whale
lifestyle
showed
disease
(4)
of Japanese
popula-
a similar
reduced
and
as little as 30 g lean fish/d may development of heart disease (5). Nevertheless, sumption
and
not
to
(1 1). n-3 fatty
acids
sahexaenoic responsible (3, flesh 1210
reportedly
fatty lower
more
are likely biological
reported
coronary fish
fish con-
(6, 7) whereas
study
heart
or
eicosapentaenoic
acid (DHA) for the many
12, 1 3). N-3
clinical
eat
suggested against the prospective
between
risk
intervention
with
advised
it was
protect some
an association
heart-disease
A recent
in patients
been
ments The
showed
reduced
(8-10).
mortality had
studies
were
intake
even
epidemiologic
findings
of the Eskimos’
of fish
heart
the
lipid profile,
These
Investigations
intakes
of coronary
aspects
investigated
favorable
time
may
did
differ
In ad-
EPA (19)
ar-
either
other
the
fatty
or con-
acids.
EPA-DHA
and
DHA
were
effects
differences
such study in mildly on lipids and hemostatic
supplied
that
and
the
account
flesh
biological
give
reported
(20) and hemostasis
to compare into
fish
in their
because
on lipid metabolism
report one the effects
extract
produce with
metabolites
to take
g EPA
(eg,
may It is possible
may
important
also
forms
in conjunction
consideration
to have different
Subjects
hemostasis
widely
Dyerberg
disease,
bleeding
tions
prevalence
have
and
heart
seal fat (2) although
that
oils
of Bang
ofcoronary
subsequently
and
(16).
atherosclerosis ventricular
as fatty
offish
with
in fatty
acid
hyperlipidemic factors of 4.5
fish
or as a fish-oil
and methods
Subjects
low prevalence and
(15). act
eicosanoid
Thirty-one since
in different
the oils consumed
an important
(21).
actions
supplements)
magnitudes
in the
to different
fish
supplied offish-oil
of various
ratio,
antithrombotic
to prevent experimental experimentally induced
fish, fish oil, plasma acids,
Introduction The
produce
forms
stituents
LDL cholesterol, apofish and fish oil were not diet.
fatty
effects
The
and
(18).
the various
respectively
for the control
(15),
rhythmias
fish oil lowered
and thromboxane (10.5%) and in(10.8%) (P < 0.05 compared with control).
changes,
Am
profiles
(15.7%)
bleeding time fatty fish and
lipoprotein factors.
changes
J Nestel
he-
9%, with 34% and 32% inparticles for fish and fish oil,
Changes in total cholesterol, B, and blood pressure with
Paul
hy-
very-bow-density-lipo52%,
and
lipids,
High-density-lipoprotein
10% and of HDL2
Beiing,
in 25 mildly
oil on
daily
and
42%
G Bryan
g eicosapentaenoic Fish
28%
with control).
fish
(DHA)
as controls.
triglycerides
0.05 compared
and
4.5
acid and
Abbey,
compared
received
plasma
creased Eating
were
docosahexaenoic
additional
20
Committee South
at
Australia.
participant.
who
suppleand
doco-
constituents of fish ascribed to the oils
blood
mmol/L, pressure
excessive
aged
(plasma cholesterol 6.7 ± 0. 1 1 mmol/L, I 5.8-8.0 mmol/L; plasma triglycerides 1.9 ± 0.14
reduced
fish-oil (EPA)
men
hyperlipidemic ± SEM) range
fish oil or fish plasma
Am J C/in Nutr
lipid 1991;53:1210-16.
Downloaded from https://academic.oup.com/ajcn/article-abstract/53/5/1210/4731818 by Denise Hannibal user on 03 June 2018
I From the CSIRO Division Australia. 2 Supported by the National
of Human Heart
Nutrition,
Foundation
Address reprint requests to L Cobiac, CSIRO Nutrition, P0 Box 10041 Gouger Street, Adelaide Received June 27, 1990. Accepted for publication October 31, 1990. 3
Printed
in USA.
© 1991 American
Society
Adelaide,
South
of Australia. Division of Human SA 5000, Australia.
for Clinical
Nutrition
n-3
Study
ACIDS
AND
design
The
study
each
consisted
subject
supplement
of a 3-wk
adapted
and
a 5-wk period,
to the
maintaining
of their
systolic
and
baseline
a constant
blood
for all three
allocated
to receive
treatment. group
(n
groups.
(SBP
Two
and
A third
matched
6). The
interventions
=
separate
parallel
fish with
fish oil, a small
to monitor
possible
larger
the fish (n
either
groups.
DBP,
were
Although
allocated therefore
ofcontrol
background
carried
out
globulin
(8.50
(4.08
nm),
the
acid
perchloric
of
study.
Hewlett
Packard
Each
subject’s
samples
and blood
on 3 consecutive
days
pressure
at the end
measurements
ofthe
baseline
were taken
and
intervention
phases.
were
by transesterification
prepared chloride/L
tercurrent
illnesses
were
monitored
alcohol for medications,
routinely
the 24 h and in-
throughout
the
study. Blood
samples
taming
for lipid
sodium
EDTA,
analyses placed
fuged
at 600
X g for 10 mm
were
frozen
at -20
analyses
for
carried Nutley,
out together NJ) with
Mannheim, containing syth, end
phase. for
VLDL
PEG
6000
triglyceride
period
and
was prepared
by
so that
rotor
were
once
from
plasma
(Beckman
using
Kil-
once
ofthe
Alto,
(LDL) cholesterol of the Friedewald
a modification
was equa-
(22).
Apolipoproteins
were
using dards
Boehringer (Hyland
trifugal For
analyzer determination
measured
antisera Diagnostics, (Cobas
(Boehringer) Malvern,
Bio, of LDL
ples ofplasma
from individuals
yielding
pools:
three
separated
from
control,
duplicate
by immunoturbidimetry and Hyland Ortho PA) on an automated
in each dietary
samples
and
Polyacrylamide slab gradient
gradient-gel gels (Gradient
Acrylamide HDL samples
gels
and
ofeach
(0.03
particles, mL)
were
and
plasma
2-16%
respectively. mixed
with
group
equal
sam-
were pooled
pool
used
Duplicate 0.01
mL
10 mm
and
assay
by
Klaus
method for clotting
Simplate
at the end
ofthe
Ifthe
difference
a third
bleeding
phases. mm, were
taken
on both the
there
was
bleeding > 30
taken
pressure
was
X
varied
according
the guidelines was ignored,
taken
was
between
model
been
sitting
DBP
five to six occasions
taken with
1 mm the
apart.
before
the
procedure.
intervention
All
was > 1
measurements bleeding
times
average
< 30 s
of the then
time.
The
subjects
were
two.
the
If
greater had
willing
an automated Critikon,
of the
ceased
were
two,
for
the
Belgium)
the
845XT,
Blood
and
2 consecutive
at which
with
(Roche).
is ±0. 1 gIL.
ofthe
and
quietly
to the diameter
Diagnostica
Fibro
at least
If these
demonstrated
measured
#{176}C) for
automated
is added
end
by was
measurements
time
noted.
given by the manufacturers. and a maximum offour
to separate
Downloaded from https://academic.oup.com/ajcn/article-abstract/53/5/1210/4731818 by Denise Hannibal user on 03 June 2018
was
and
of bleeding and
had
subjects
The
a poly-
(-20 an
kit,
measured.
was
5 difference
frozen
Turnhout,
on
the two
was
nurse.
time
explained
Blood
subjects
time
as a measure
technique ticipate.
period
between
incisions
ter
sucrose!
baseline
then
separated
Accuracy
times
and
supernatant
using
Teknika,
bleeding
by one clinic parallel
apart,
(Organon
to measure
was the
of thrombin
is measured.
II templates
used
days
to occur
was
using
on the Cobas
amount
for
serum
thromboxane
(Fibri-Prest
France)
a fixed
50.3 g.
technique
Asnieres-Sur-Seine,
lipoprotein of 40%
a functional
(Dinamap
was performed with Sydney, Australia). were
x g for
In this
incubated
10 mm
plasma
at 8000
manometer
by a single
citrated
recentrifuged Von
(30
B3 (24).
and
were
of 1 .21 kg/L in the for 17 h at 1 50 000
electrophoresis Laboratories,
of 2.5-27%
LDL
size,
fish oil. Lipoproteins
centrifugation at a background density rotor (of a Beckman ultracentrifuge)
stancen-
B2 and 10 mm
Stago,
silica
The
by radioimmunoassay
fibrinogen,
by
was
stimulated
X g for
was
Roche) (23). and HDL particle fish,
by
blood
Maximal
to thromboxane
analysis
were
(Hewlett-Packard)
X g for
at 600
analysis.
was determined measuring
hy-
esters
a vitreous
waterbath.
at 300
were CA)
whole
centrifugation
at the
intervention Palo
For
methyl
column
agitating
centrifugation #{176}C) until
antibody
time
by ultracentrifugation
Instruments,
by (-20
modified
B)
(VLDL)
measured
at the end
separated frozen
acids
gas.
thromboxane,
#{176}C in a slowly
batch
cholesterol
Chemicals,
as carrier
measuring
1 h at 37
all
B-(apo
(BDH
hydrogen
butylated offatty
50 g anhydrous
ofthe
FFAP
chloroform-
esters
by using
id) cross-linked
oc-
at the
compliance.
with 0.005%
with
Analysis
again
dietary zL)
Methyl
by gas chromatography
For
cbonal
were
ofapolipoprotein
x g. Low-density-lipoprotein
at 1 50 000 calculated
study
methanol.
mm
production
centrisamples
Very-low-density-lipoprotein
VLDL
baseline
17 h in a 50.3
tion
with
Australia). and
ofthe
and
con-
concentrations
(HDL)
precipitation
lipoproteins
cholesterol
ice,
Plasma
of the
triglyceride
High-density-lipoprotein
after
Victoria,
on
the plasma.
completion
and
in tubes
in a centrifugal analyzer (Cobas-Bio, Roche, standard enzymatic test kits (Boehringer,
FRO).
was determined
collected
immediately
to isolate
#{176}C until
cholesterol
were
and
as antioxidant.
a
on two
and
1) containing
(BHT)
m X 0.53
fasted for 12 h and avoided each clinic visit. Alcohol intake,
(4:2:
(2202 by using
measured period
(100
in were
PA).
to determine
hydroxytoluene
performed
Subjects preceding
HC1/L
0-250 Gels
densitometer
were
plasma
Fine sulfosal-
acid.
quantified
baseline
from
a high-
Coomassie
and
acids
phase
extracted 1 mob
drogen
Measurements
fatty
from
in 10%
(Avondale,
ofthe
intervention
fixed
a laser
integrator
plasma
nm)
in 5% acetic
with
cal-
kit (Pharmacia
were
Sweden)
at the end
were
Gels
track)
3390a
once
of the
per
were
of thyro-
dehydrogenase
(3.55
calibration
Bromma,
radii
lactate
Elecof Tris
standards
nm),
destained
gel.
buffer
for 4 h in 0.4%
and
scans
LKB,
to the
Stokes’
albumin
Sweden).
1 h, stained
(two
Ultrascan,
Lipids
(6.10
serum
acid,
methanol-0.
Blood
femtin
bovine
for
directly
V. The
electrophoresis
3.5%
end
course
applied
in a nondenaturing
to coelectrophoresed
Uppsala,
casions,
and
17 h at 160
nm),
and
icylic
in
was included
during
reference
scanned 13)
=
was to compare
subjects
changes
(n
as a control
the objective
8.35,
by
respectively),
randomly
for
pH
Chemicals,
were
performed
culated
triglycerides,
This ensured that matched as closely
groups
was
by
blue
was
borate,
molecular-weight
12) or the fish-oil
=
group
number
followed
of the baseline groups on the
of plasma
pressure
during
1211
RISK
bromophenol
trophoresis
a liquid
fat intake,
At the end three dietary
mass index, and plasma cholesterol. values of these characteristics were
as possible
period,
ofconsuming
measurements
diastolic
age, body the mean
baseline
routine
dietary-intervention phase. subjects were stratified into
basis
CARDIOVASCULAR 0.01%
8-wk
which
the
FATTY
the
to par-
sphygmo-
Tampa,
5 mm.
Cuff
subject’s
arm
FL) sizes
af-
were
following
The first measurement measurements ofSBP and pressure
the intervention
was began
measured to familiarize
on
1212
COBIAC
Dietary
diets
were
requirements structed was
designed
and
dietary
to consume
given
to accommodate preferences.
30%
to enable
in addition
subjects
intake
to a daily
liquid
for
the
ratio
hydrate,
Table
of total
fatty energy,
sodium,
There which
was
all subjects
and
ham
plus
ture
of palm
powder; flavoring
the
5-wk
supplements.
tinuation
with
salmon
steak,
chicken
breast,
period
The
diet
for the control
diet.
The
(1 kg raw
that
contained
oil;
added
potassium;
test
the
three
a mixskim
milk
emulsifiers;
groups
and
consumed
subjects
fish group
weight/wk)
groups.
supplements. during
olive
and
three
the
period
lean
and
to carbo-
dietary
supplement oil,
of the baseline
Atlantic
a variety
fat,
the
from
baseline
cholesterol; sodium agents (Table 1).
During ferent
for
intake
supplied
safflower
Meat or fish meals each
protein,
dif-
was
a con-
was provided
and
Norwegian
sugar
The
fish-oil
a fish-oil bourne,
to match group
preparation, Australia),
a daily
average
tamed
no added
oil,
total
MaxEPA
carbohydrate
continued MaxEPA was of 4.6
intake
meats (105
supplied g EPA
cholesterol, (4.80
with
g/wk;
in the plus
a small
RP
The
added
flavoring agents. Table 2 shows the distribution the salmon, sardines, and fish-oil preparation centage of total fatty acids of edible portion).
a
4.4 16.8 5.6 4.3 22.6 3.4 1.4 1.5
of supplements
(daily
Mel-
to provide conand
0.8 6.1 4.2 3.6 17.4 of total
Protein (g) Fat (g) Carbohydrate (g) Energy(MJ) Sodium (mmol) Potassium (mmol) Cholesterol (mg) Polyunsaturated fatty acids (g) Monounsaturated fatty acids (g) Saturated fatty acids (g) EPA + DHA EPA:DHA
of fatty (expressed
Dietary
a
Fish comprised
I kg Atlantic
salmon
and acids in as per-
Controlf
42 27 12 1.94 14 24.7 183 6.9 8.5
41 27 12 1.90 16.3 23.5 17S 7.2 9.0 6.6
7.7
4.6 2:1
plus
-
150 g sardines
in sild oil
f Mixture oflipids
(I 5 g/d; RP Scherer,
chosen to approximate
to monounsaturated to saturated § EPA, eicosapentaenoic acid;
Melbourne,
Australia).
the ratio of polyunsaturated
fatty acids. DHA, docosahexaenoic
in edible
food
inventories
were
portion.
collected
days and on 3 consecutive for a further 1 wk during
days during the intervention
subjects were were checked
to monitor compliance.
Statistical
encouraged for dietary
on
the
specified
single
baseline period phase. In addition
daily
fat intake.
and the
Records
analyses
The values used for analysis were the average of 3 consecutive days’ measurements for plasma lipids, lipoprotein lipids (except VLDL), bleeding time, and blood pressure. Other variablesVLDL
fibrinogen,
three
and
acid.
Downloaded from https://academic.oup.com/ajcn/article-abstract/53/5/1210/4731818 by Denise Hannibal user on 03 June 2018
groups
lipids,
plasma
fatty
thromboxane-were
phase and A one-way by using
acids,
HDL
measured
particle
once
at the
once at the end of the dietary-interanalysis of variance compared
intraindividual
changes
from
the
baseline
to
end of intervention phase (5 wk). Schefle tests of contrast were performed where appropriate. A paired Student’s t test was used to determine the significance of changes from baseline to end of the
intervention
period.
SPSS/PC
with
(SF55,
Statistical Inc,
analyses
were
performed
Chicago).
Results The
baseline
subjects) There the two Total but
per week.
t 105 g MaxEPA/wk
present
0.2 1.0 20.5 0.8 2.1 11.6
records
end of baseline vention phase.
Fish oilt
41 28 12 1.89 16.3 23.5 175 7.2 8.9 6.9 4.5 1:2
fatty acids
-
olive
sodium,
average)
Fish*
8.3 0.3 0.1 0.3 10.4 8.1 0.6 12.1
-
size, 1 composition
-
-
Percent
9.4 19.3 11.2 3.1 12.4 1.6 0.8 4.2 0.1 1.7
-
6.9
apolipoproteins, TABLE Nutrient
6.2 17.9 9.5 2.1 20.8 1.8 1.1
-
Weighed but
Scherer,
of palm
some
14:0 16:0 16:1 18:0 18:1 18:2 18:3 18:4 20:0 20:1 20:2 20:3 20:4 20:5 22:1 22:5 22:6
flavoring.
supplement
amount
%*
with
baseline
supplement
DHA.
g cholesterol/L),
and
as during
Fish oil
sardines
in sild oil (150 g/wk). This provided a daily average of 4.5 g EPA plus DHA. The liquid supplement contained substantially less oil, some added cholesterol, no skim milk powder, and some added
salmon,
Sardines
fat
monounsaturated
potassium
the milk-based oil,
to
daily 3-wk
were
Salmon
total
containing
cholesterol,
and
a common
estimate
Atlantic
in-
supplements were designed to energy as fat and were matched
(P:M:S),
the average
was
Information
vegetable oils. and two smaller
polyunsaturated
acids
1 shows
and
supplement
energy
subject
as fat.
to monitor
of oils. These foods and liquid supply an average of 10% oftotal saturated
Each
of energy
intake and to avoid polyunsaturated was provided for five larger meals week
individual
AL
TABLE 2 Fatty acid composition of farmed Tasmanian Norwegian sardines in sild oil, and fish oil
interventions
All
ET
characteristics
experimental
cholesterol
the fish-oil and the nificant
groups decreased
to a lesser
triglycerides
of each
are shown in Tables were no significant
extent were
and
changes
equally
significantly
the fish groups.
three
in plasma
compared
in the
of the
groups
(31
3 and 4. with
in the control
fish-oil
group.
reduced The
fish-oil group, by 28%. Both these compared with the control-group
and
(Table
from
fish group
cholesterol
the control
baseline decreased
reductions reduction.
in group.
fish groups 3). Plasma in both by 20% were Both
sigthe
n-3 TABLE 3 Effects of fish, fish-oil,
FATTY
ACIDS
AND
CARDIOVASCULAR fish and
and control
diets on plasma
lipids,
lipoproteins,
the fish-oil
cholesterol
and apolipoproteins* Baseline
Intervention
Change
and
(5 1% and
did
show
not
6.99 ± 0.23 6.77 ± 0.21 6.82 ± 0.25 1.93 ± 0.24 2.03 ± 0.21 1.59±0.19
Fish Fish oil Control Lipoproteins
a
SEM.
± 0.10
-0.39 -0.57
± 0.lOf
+0.21
±0.12
± 0.23f
triglycerides
occurred
component
where
seen
fish
1.23 ± 0.08t 1.12 ± 0.07t 1.41 ± 0.33
+0.1 1 ± 0.03t +0.09 ± 0.04f -0.03 ± 0.02
± 0.09
0.27 ± 0.08t 0.25 ± 0.03t 0.42 ± 0.10
-0.28 -0.43 +0.02
0.68 ± 0.10 0.40 ± 0.10 5.07 ± 0.24 4.95 ± 0.22 4.76 ± 0.47
4.76 ± 0.22t 4.98 ± 0.15 4.30 ± 0.45t
-0.31 +0.03 -0.46
1.35 ± 0.18 1.43 ± 0.21 0.96 ± 0.20
0.78 ± 0.18t 0.67 ± 0.08t 1.12 ± 0.24
-0.57 -0.76 +0.16
the in the
respectively.
This
± 0.0Sf
significant (P with a reduction
± 0.1 lf
group,
and
± 0.04
ratios
of apo
± 0.09
16%
in the
± 0.12
significant
when
± 0.l4f
fish-oil
group
B were
not
was
± 0.23f
LDL particle unchanged
± SD)
control
(P
oftotal
HDL
particles
0.29 0.30 0.36
± 0.02
of particles
± 0.01
to 36.7
± 0.07
-0.08 -0.07 -0.04
± 0.02
The plasma from baseline
1.00 ± 0.04 0.99 ± 0.03 0.97 ± 0.07
0.95 ± 0.04 1.0 1 ± 0.03 0.93 ± 0.08
-0.05 +0.02 -0.04
± 0.06
daily addition of 1 5 g fish-oil produced the greatest change
3.22 ± 0.19 3.19±0.24 3.41 ± 0.21
3.83 ± 0.23t 3.59±0.26t 3.55 ± 0.29
19 ± S 13±4 4 ± 8
I .20 ± 0.06 1.18 ± 0.04 1.40±0.26
1 . 16 ± 0.06 1.08 ± 0.OSt 1.36±0.32
-2 ± 2 -8 ± 3 -3±3
± 0.02t ± 0.03t
± 0.03 ± 0.02
0.93 ± 0.03 0.88 ± 0.02 1.06 ± 0.09 =
HDL-C,
1 . 1 1 ± 0.04t 1.03 ± 0.03t 1 . 1 1 ± 1 .08t
12; for fish oil, n
=
high-density-lipoprotein
different from baseline fil Significantly different from control § Change given as percent change.
values, change:
n
P < 0.05. fP < 0.05,
lIP
=
was
of the
in the
extent.
The
A-I to apo
gel electrophoresis However, HDL altered
(P
± 6.9%
no significant
HDL2
EPA
EPA
the
s, or Table SBP
and
size
DHA
level
increase
in control
by both
fish
of particles 32.4 ± 5.6% < 0.01)
of (1
in subjects
proportion
(34.0
± 3.9%
fish
and
EPA
fish
compared
with
fell by (all
and
DBP
P
10.8%,
4.4
1 . I 1 ± 0.04t 1.09 ± 0.04t 1.26 ± 0.l7t
± 0.02
19%
groups
size as assessed by gradient by dietary supplementation.
I .20 ± 0.04 1 . 17 ± 0.04 1.35 ± 0.16
± 0.02
three
fish groups
0. 1). Changes
=
to apo A-I rose by
fish and
with
fish-oil
7% (Table
-
fell in all three groups, group, 22% in the fish
group
and
distribution
and fish-oil HDL2 size
± 0.02
the
and
by
groups,
in the
compared
fish
cholesterol
among
A-Il
were changes
significant.
particle-size
± 0.09
in the
fish-oil
fish-oil
A-I to apo
Both
groups
0.002). Apo A-Il also of 10% in the control
=
fell by 4% in the
± 0.15
of HDL
difference
0.5 1 mmol/L
3).
cholesterol
and
did in total
VLDL-triglycende
and
in all three
ratio fish
cholesterol
respectively.
(Table
cholesdecreases
reduction
in the
groups,
fell equally
3). Consequently
B
For fish, n
A-I
significantly
not
fish-oil
the
LDL
of 0.33
different
in LDL
3). The
entirely
at P < 0.05 rises in HDL
were significant Despite the apo
almost
group
3).
mirrored
(Table
reductions and
changes
By contrast
group
control
(Table
not significantly
the
fish groups
cholesterol.
in the fish-oil
in the
were
However, the
respecconcen-
the
cholesterol
cholesterol
and
in total
not change
ratios A-Il
Apo, apolipoprotein;
t Significantly
observed
± 0.13
1.12 ± 0.06 1.03 ± 0.05 1.44 ± 0.32 0.55
Control Apo B
HDL-C:apo Fish Fish oil Control
± 0.10
control
whereas
in VLDL
groups.
in HDL9%,
in VLDL-cholesterol
respectively),
in LDL
increase
( 10% and
baseline
reduction
63%,
three
in the
groups,
Fish Fish oil Control Apolipoproteins Apo A-I Fish Fish oil Control Apo A-Il Fish Fish oil
Control Apo A-I:apo Fish Fish oil Control
1.54 ± 0.21t 1.46 ± 0.07t 1.80±0.18
-0.41 -0.10 -0.41
(mmol/L)
HDL cholesterol Fish Fish oil Control VLDL cholesterol Fish Fish oil Control LDL cholesterol Fish Fish oil Control VLDL triglyceride
Fish Fish oil Control Apolipoprotein Apo A-I:apo Fish Fish oil
6.58 ± 0.22t 6.67 ± 0.18 6.41 ± 0.21t
the
a significant
from
a change
changes
among terol
showed
a significant
tration The Lipids (mmol/L) Cholesterol Fish Fish oil Control Triglycerides
groups
concentrations
tively)
1213
RISK
the The
in fibrinogen, fell by 5.7%, increased control decreases
by 38 group; in SBP
from baseline to end of the interbut were not significantly different DBP
dropped
from
baseline
in the
1214
COBIAC
TABLE Effects
blood
4
Discussion
of fish, fish-oil, pressurea
and control
diets
on hemostatic
Baseline Fibrinogen
variables
Intervention
and
As expected the greatest effect was on plasma triglycerides nitude of the falls in triglycerides
Change
2.65
Control(n=6)
1.96±0.14
±
0.15
2.49 ± 0.12 2.73 ± 0.18 2.14±0.10
2.35 ± 0.20
-0.15
± O.12t
+0.38
± 0.19
+0.18±0.17
Thromboxane (ig/L)
107.3
Fish Fish oil
Control time
6.9
95.8
± 5.1
85.0 ± 13.3
90.0
± 9.1
68.6±
85.7±
±
10.9
-1 1.6 ± 6.3t +5.2 ± 10.0 +17.1 ±8.5
11.6
(s)
Fish
348.7
±
Fish oil
365.2
± 23.3
20.1
Control Systolic blood
327.2
± 29.4
386.4
± 28.1
+37.7
± 19.4t
364.3 294.6
± 21.4
-0.9
± 14.4
± 26.1
-32.6
Diastolic
2.3
127.5
±
127.9
± 3.5
127.2
± 4.7
122.4 ± 1.8f
-5.1
± 1.7
123.6 ± 2.4t 123.5 ± 2.3
-4.3
±
-3.7
±
2.0 3.0
0.5
Hg) ±
1.7
79.5
±
l.8f
-2.8
±
80.1 77.5
± 1.7
78.9
±
1.4
-1.2
±
1.4
3.3
75.0
±
2.9f
-2.5
±
0.9
SEM.
s+
t Significantly
t
82.3
±
Significantly
different different
from from
control baseline
change, value,
the
and the fish groups but there the groups (Table 4).
between There groups
was
no significant
did experience
change
rich
P < 0.05. P < 0.05.
an average
to end of the intervention
difference
dose
DHA
in some studies DHA appeared
of fish
oil tended
However,
ofO.5
kg from
of our
compared but
increase
plus
is consistent
with
other
oil given,
EPA and DHA were to have the greater
simultaneous
changes
equipotent inhibitory
in dietary
sat-
to raise
LDL
cholesterol
whereas
the DHA-rich
fish did not. However, the effect of the fish was no greater than the background drift shown by the control group. The interpre-
was no significant in weight.
g EPA
urated fatty acids, and the underlying lipid disorder (3). It is generally agreed that fish oils are beneficial in hypertriglyceridemia but less useful for individuals with combined hyperlipidemia in whom LDL cholesterol may increase with fish oil (3). A recent report by Childs et al (20) showed that fish oil rich in DHA lowered LDL-cholesterol concentrations whereas fish oil rich in EPA did not. This is consistent with our findings in which EPA-
tation
control
of 4.5
(3, 15). Mechanisms for the fall in plasma triglycerides a reduction in hepatic VLDL lipoprotein lipid synthesis
effect on triglyceride secretion by hepatocytes (26). Changes in plasma cholesterol as a result of fish-oil supplementation have been more variable and appear to be related to
blood
(mm
intake
studies include
(3, 15). Although (25), in others
pressure
Fish Fish oil Control
daily
± 17.8
pressure
(mm Hg) Fish Fish oil Control
of consuming 4.5 g n-3 fatty and VLDL lipids. The mag(both plasma and VLDL triglycerides) were similar with fish and fish oil, suggesting that the fish oil may have reduced triglycerides to a greater extent. Reductions in plasma and VLDL triglycerides with either fish or fish oil have been widely reported. The decrease in VLDL triglyceride in the range of 42-52% seen in this study with a acids
(gIL)
Fish (n = 12) Fish oil (n = 13)
Bleeding
ET AL
not
nonspecific
baseline
the overall outcome
must
with
the type
all three
phase.
data
fish
fish
of fatty
changes
effects with
take oils acid;
such
on LDL
the EPA-rich
two that
factors were
second,
as regression
cholesterol
into
account:
matched the control
first,
we
for the
amount
group
defined
to the mean. Nevertheless, do suggest a less desirable
fish oil than
with
the DHA-rich
fish.
TABLE S Plasma fatty acidsa Control
Fish
Baseline
Intervention
Baseline
Fi sh oil Intervention
Baseline
Intervention
%
14:0 16:0 16:1 18:0 18:1 18:2n-6 l8:3n-3 20:3n-6 20:4n-6 20:Sn-3 22:Sn-3 22:6n-3
1.3±0.1 23.5 ± 0.7 2.8 ± 0.2 8.3 ± 0.3 20.9 ± 0.5 30.3 ± 1.1 0.6 ± 0.1 2.0 ± 0.2 7.3 ± 0.6 1.0±0.1 0.7 ± 0.1 1.4 ± 0.1
1.3±0.2 23.7 ± 0.8 2.9 ± 0.2 8.3 ± 0.3 21.2 ± 0.6 29.4 ± 1.0 0.7 ± 0.1 1.9 ± 0.2 7.9 ± 0.8 0.8±0.1 0.8 ± 0.1 1.2 ± 0.1
1.4±0.1 24.1 ± 0.6 3.1 ± 0.2 8.0 ± 0.3 21.9 ± 0.5 29.0 ± 1.1 0.7 ± 0.1 2.3 ± 0.2 6.2 ± 0.4 1.0±0.2 0.7 ± 0.1 1.5 ± 0.1
a±SEM
t Significantly f Significantly
different different
from baseline, P < 0.05. from control, P < 0.04.
§ Significantly
different
from
fish, P