Obesity Research & Clinical Practice (2013) 7, e173—e181

ORIGINAL ARTICLE

Dietary supplementation with long chain omega-

3 polyunsaturated fatty acids and weight loss in
obese adults
Irene A. Munro, Manohar L. Garg ∗

Nutraceuticals Research Group, School of Biomedical Sciences and Pharmacy, The University of Newcastle,
Callaghan NSW 2308 Australia

Received 29 April 2011; accepted 9 November 2011

KEYWORDS Summary
Weight loss; Background: Obesity is associated with elevated levels of inflammation and
Obesity; metabolic abnormalities, with increased risk of developing insulin resistance, type
Omega 3 fatty acids 2 diabetes, stroke and CVD. Nutrients that can assist in weight loss may also reduce
the risk of obesity related co-morbidities.
Aim: The aim of this study was to investigate whether LCn-3PUFA, combined with a
reduced energy diet, facilitated weight loss and improvements in blood lipids and
inflammatory mediators.
Design: A double blind randomised controlled trial with two parallel groups. Both
groups followed a low energy diet for 12 weeks, one group consumed 6 × 1 g
capsules/d monounsaturated oil (Placebo) (n = 18), the other 6 × 1 g capsules/d LCn-
3PUFA (fish oil) (n = 17). Fasting blood samples, anthropometric measurements and
3-day food diaries were collected at baseline and post intervention.
Results: There was a two-fold increase in plasma levels of EPA and DHA in the fish
oil group (p < 0.001). There were no significant difference within and between the
placebo and the fish oil groups for weight reduction (3.37% and 4.35% respectively),
fat mass reduction (8.95% and 9.76% respectively), or changes in inflammatory
biomarkers and blood lipids apart from triglycerides, reduced by 27% in fish oil group
(p < 0.05). For fish oil group there were significant correlations between leptin and
weight loss (p = 0.01) and leptin and EPA and DHA (p < 0.05 for both).

∗ Corresponding author at: Nutraceuticals Research Group, 305C Medical Sciences Building, The University of Newcastle,

Callaghan, NSW 2308 Australia. Tel.: +61 2 4921 5647; fax: +61 2 4921 2028.
E-mail address: manohar.garg@newcastle.edu.au (M.L. Garg).

1871-403X/$ — see front matter. Crown Copyright © 2011 Published by Elsevier Ltd on behalf of Asian Oceanian Association for the Study of Obesity. All rights reserved.
doi:10.1016/j.orcp.2011.11.001
e174 I.A. Munro, M.L. Garg

Conclusion: Dietary LCn-3PUFA supplementation during a weight loss program does not
appear to assist weight loss. Poor dietary compliance may be a contributing factor in
accurate assessment of the role of these fatty acids in weight loss.
Crown Copyright © 2011 Published by Elsevier Ltd on behalf of Asian Oceanian Asso-
ciation for the Study of Obesity. All rights reserved.

Introduction The purpose of this study was to investigate the

effect of LCn-3PUFAs on weight loss in obese adults
The original concept of obesity was as an adipose by comparing two groups who were following the
tissue storage depot for energy in excess of require- same energy controlled weight loss diet, with one
ments. It is now well established that adipose group consuming fish oil and the other placebo
tissue is also an active endocrine organ associated capsules.
with low-grade systemic inflammation through the
expression of proinflammatory mediators such as
tumour necrosis factor-␣ (TNF-␣), interleukin-6 (IL- Methods
6) [1], C-reactive protein (CRP) [2] and leptin [3]
all of which have been linked to increased risk Participants
of CVD [4]. Adipose tissue also secretes the anti-
inflammatory mediator, adiponectin, which has Both male and female participants, aged
direct positive effects on vascular function [5]. 18—60 years and with a BMI between 30 and
In addition to body size, the location of body 40 kg/m2 , were recruited from the university
fat can be a critical indicator of disease risk. Vis- campus and the general public in Newcastle,
ceral adiposity, measured by waist circumference Australia to take part in a weight loss study. People
(WC) >102 cm (males) and >88 cm (females), is one with diagnosed diabetes mellitus, a chronic inflam-
of a group of established risk factors for several matory condition, already following an energy
metabolic diseases [6] which, in addition to CVD, restricted diet, allergic to fish, taking fish oil
include insulin resistance, type 2 diabetes melli- capsules or consuming two or more oily fish meals
tus (T2DM), hypertension and dyslipidemia [7]. The per week were excluded from the study, as were
other contributing risk factors in the group are women who were pregnant or lactating. This study
impaired fasting plasma glucose [5], raised levels of was conducted according to the guidelines laid
triglycerides and of low-density lipoprotein choles- down in the Declaration of Helsinki and approved
terol (LDL-C) and reduced levels of high-density by the Human Research Ethics Committee of
lipoprotein cholesterol (HDL-C) [8]. Waist-to-hip the University of Newcastle, Australia. Written,
ratio (WHR) is also used to measure the distribu- informed consent was obtained from participants
tion of body fat and cardio-metabolic risks, and a prior to commencement. The trial was registered
high reading is considered to be a better predictor with the Australian New Zealand Clinical Trials
of CVD than a large waist circumference alone [9]. Registry (ACTRN12610000659000).
Loss of adipose tissue through weight loss results
in a decrease in circulating levels of proinflam- Study design
matory biomarkers [10] and decreased metabolic
abnormalities [11]. There is no shortage of dietary This was a double blind randomised controlled
interventions for weight loss but dietary adherence trial. Simple randomisation using computer gen-
can be difficult [12] and weight loss is diffi- erated random numbers was used to allocate
cult to achieve and maintain [13]. It has been participants to one of two parallel groups. For
suggested that supplementation with long chain 12 weeks one group consumed 6 × 1 g capsules
omega-3 polyunsaturated fatty acids (LCn-3PUFA) of placebo per day (placebo group), containing
will reduce metabolic risk factors and reduce sunola oil (monounsaturated oil), and the other
inflammation [14,15]. It has also been shown that group consumed 6 × 1 g capsules of fish oil per day
supplementing the diet with LCn-3PUFA of marine (fish oil group). Each fish oil capsule contained
origin reduces body weight in mice [16,17]. tuna oil comprising 360 mg LCn-3PUFA with 270 mg
Omega-3 fatty acid supplementation and weight loss e175

docosahexaenoic acid (DHA) and 70 mg eicosapen- hip ratio was calculated as waist girth in centime-
taenoic acid (EPA) (HiDHA® NuMega Ingredients tres (cm) divided by the hip girth (cm). Fat mass
Pty Ltd., Australia). Two capsules were consumed (FM), fat-free mass (FFM) and muscle mass (MM)
with each meal, that is breakfast, lunch and din- were measured using single-frequency bioelectrical
ner providing 1.62 g DHA and 0.42 g EPA per day. impedance (Maltron International, Rayleigh, Essex,
All capsules contained peppermint to mask the UK). Under identical conditions, these anthropo-
flavour. Both groups of participants followed an metric measurements were repeated at the end of
energy reduced, portion controlled healthy eating the weight loss phase.
weight loss diet (HEWLD) comprising a daily intake
of 5000 kJ for females to 6000 kJ for males. For
Biochemical analyses
the first four weeks participants attended weekly
so that they could receive nutrition education Blood sample collection
and counselling, with the sessions focusing on the Fasting (≥10 h) blood samples were collected into
energy density of foods, understanding and using tubes, EDTA, Lithium Heparin and Sodium Fluoride,
food labels, appropriate portion sizes and the num- by venipuncture at baseline and again at the end of
ber of portions to be consumed daily from the the weight loss phase. The samples were prepared
different food groups. This information was used by centrifuging (Heraeus Biofuge Stratos) for 10 min
to build a healthy diet using the guidelines from at 3000 × g at 4 ◦ C. Plasma samples from the EDTA
the Australian Guide to Healthy Eating (AGHE) [18] tubes were collected and stored at −80 ◦ C awaiting
for the participants to follow. At these meetings, further analysis. The Lithium Heparin and Sodium
participants were weighed so that progress could Fluoride tubes were taken to Hunter Area Pathology
be monitored and their supplements replenished. Services (Newcastle) for plasma analysis for blood
Thereafter participants attended monthly to weigh lipids and blood glucose, respectively.
in and collect their supplements.

Dietary assessment Plasma fatty acid analysis

Prior to commencing the weight loss program, The plasma lipids were analysed for fatty acid
dietary intake was assessed with a 3-day food diary composition using an acetyl chloride methylation
to determine every-day nutrient and energy intake. procedure, a modification of the method of Lepage
Participants used the weights given on food prod- and Roy [19]. Fatty acid methyl esters were quan-
ucts and handy measures of cups and spoons to tified using a GC (Hewlett Packard 6890, Hewlett
record food intake which was analysed using the Packard, Palo Alto, CA, USA) and identified by com-
dietary software program, Foodworks Professional paring peak retention times with the retention
2009, version 6 (Xyris Software (Australia) Pty Ltd.) times of synthetic standards of known fatty acid
and the mean values were calculated. In the final composition (Nu Check Prep, Elysian, MN, USA).
two weeks of the weight loss program participants
again completed a 3-day food diary to measure Analysis of inflammatory markers
changes in dietary intake.
High sensitivity (hs) enzyme-linked immunosorbent
Anthropometric assessment assay (ELISA) kits (R&D Systems, Minneapolis, MN,
USA) were used to determine levels of hs-TNF-␣ and
On the first day of the weight loss trial, anthropo- hs-IL-6. Minimal detectable concentration of the
metric measurements were taken in the morning kits was 0.106 pg/ml and 0.039 pg/ml respectively
after a ≥10-h overnight fast and no alcohol with an intra- and inter-assay coefficients of varia-
consumption, with participants dressed in light tion (CV) of <9%. Analysis of hs-CRP was conducted
clothing and without shoes. Standing height was using an immunoturbidimetric method (Hunter Area
measured to the nearest 0.1 cm using a stadiome- Pathology Service, Newcastle, NSW, Australia) with
ter. Body weight was measured to the nearest 0.1 kg a minimal detection level of 0.15 mg/l. Plasma
using a calibrated balance beam scale (PCS Mea- leptin levels were quantified with a commercial
surement, NSW, Australia). BMI was calculated in double-antibody enzyme immunometric assay (EIA)
kilograms (kg) per meter squared from weight and (Cayman Chemical Company, Ann Arbor, MI, USA)
height. WC was measured at the mid-point between with a detection limit of 1.0 ng/mL and inter-
the lowest rib and the top of the hipbone; the and intra-assay CVs of less than 9%. Adiponectin
hip measurement was taken at the fullest point levels were determined using an ELISA kit (SPI-
of the hip, as viewed from the side. The waist: bio, Montigney le Bretonneux, France). Intra- and
e176 I.A. Munro, M.L. Garg

inter-assay CVs were 6.4% and 7.3% respectively

25.31
86.93
19.39
1.47a
0.86a
0.94a
2237
with a detection range of 0.1—10.0 ␮g/mL.

±
±
±
±
±
±
±
Statistical analyses

−1254
−10.70
−47.66
−11.76
3.74
1.23
2.57

Data are presented as mean values and standard
deviations, with p ≤ 0.05 indicating significance.
ANOVA was used to test group mean differences
within groups and changes from baseline were

33.68
60.11
17.53
1.91b
1.20b
0.90b
1834
determined using paired samples t-test. Pearson
product—normal correlations (r) were used to show

±
±
±
±
±
±
±
relationships. All statistical analyses were carried

6673
90.03
173.27
48.82
8.07
2.29
4.60
out with SPSS software (version 17.0, SPSS Inc.,

Baseline values and changes or percent changes from baseline for daily energy and nutrient intake and LCn3-PUFA.

PI
Chicago, IL, USA).

Results

34.99
94.86
23.65
0.94b
0.40b
0.67b
Fish oil (n = 15)

2832
Forty-three participants commenced the study,

±
±
±
±
±
±
±
7928
100.73
220.93
60.58
4.33
1.06
2.03
seven withdrew and one was excluded at com-
mencement of study when initial blood results

BL
identified him as being diabetic. At the end of the
study two participants from the fish oil group were
excluded. One did not comply with the consumption
of the fish oil capsules as evidenced by an 8% return

23.39
63.32
20.83
0.75a
0.33a
0.43a
2044

Mean values ± standard deviations. In each row superscripts with a common letter differ, p < 0.001
of unused capsules and the very modest increase in
plasma LCn-3PUFA. The other participant did not

±
±
±
±
±
±
±
comply with the energy-reduced diet as evidenced
−1123
−0.50
−47.94
−7.00
0.61
0.17
0.36
by a weight gain of 2 kg and a 3-day food diary


at the end of the study showing a consumption of

9000 kJ/d. Of the 33 participants who completed
the study, 18 were in the placebo group (6 males,
12 females) and 15 were in the fish oil group (FO)
20.20
47.38
25.13
1819

1.21
0.40
0.64
(5 males, 10 females). Two extreme outliers were
excluded from the analysis of the inflammatory
±
±
±
±
±
±
±
biomarker adiponectin (1 from placebo and 1 from
7069
92.26
158.33
55.87
4.82
1.09
2.37

FO group) and two from hs-CRP (both placebo).

PI

Diet and supplementation

Placebo (n = 18)

Dietary intake was calculated from 3-day food

25.71
67.73
31.00
2457

0.89
0.30
0.62

diaries completed prior to commencement of the

study and again at 12 weeks. There were no signif-
±
±
±
±
±
±
±
8170
94.73
197.35
73.69
4.21
0.92
2.00

icant differences in daily dietary intake between

the two groups at either time-point. Table 1 shows
BL

mean daily energy and nutrient intake at baseline

and the mean daily intake difference from base-
line for both groups. There were slightly greater
reductions in protein, CHO and fat intake by FO
(22:6n-3) DHA (%)
(20:5n-3) EPA (%)

than placebo and the mean reduction in energy

LCn3-PUFA (%)

intake by FO was greater (−10.9%) compared to

Energy (kJ)
Protein (g)

placebo (−6.7%) but the differences were not sig-

CHO (g)
Table 1

Fat (g)

nificant. Baseline EPA and DHA levels were very

similar for FO and placebo. After 12 weeks of sup-
plementation with fish oil capsules, there was a
Omega-3 fatty acid supplementation and weight loss e177

>2-fold increase in plasma levels of both EPA and

DHA in FO. This difference from baseline was highly

3.90***
1.32***
3.27***

4.04**
3.71**
1.41

0.01
significant (p < 0.001) as was the difference in EPA
and DHA levels between the two groups (p < 0.001)

±
±
±
±
±
±
±
post intervention (Table 1).

−4.19
−1.40
−3.80
−0.36
−3.77
−2.93
−0.02

Anthropometric measurements

Baseline anthropometric characteristics and

changes from baseline are shown in Table 2. Over

11.07
2.49
7.32
8.94
7.83
6.97
0.07
12 weeks body weight reduced by 3.37% (−3.17 kg)
and 4.35% (−4.19 kg) for placebo and FO, respec-

±
±
±
±
±
±
±
tively. There was a reduction in FM of 8.95%

90.74
31.15
35.87
54.88
97.97
116.40
0.84
(−3.43 kg) and increase in FFM of 0.67% (0.29 kg)

PI
for placebo. For FO there was a reduction in both
FM of 9.76% (−3.8 kg) and FFM of 0.51% (−0.36 kg).
The differences from baseline within groups were
significant for weight, FM, BMI (p < 0.001 for all in

11.70
11.53
both groups). Differences between groups were

Fish oil (n = 15)

2.07
6.88
9.51
6.89
6.93
0.08
not significant. The baseline waist circumference
was above the acceptable range <102 cm for males

±
±
±
±
±
±
±
±
39.94
94.92
32.55
39.67
55.27
101.73
119.33
0.86
and <88 cm for females for almost all participants,
with one male (FO) and two females (placebo)

BL
below the recommended cut-off point. After
weight loss eight participants had reduced their
waist circumference to below the cut-off point, 4
Baseline values and changes from baseline for anthropometric measurements.

3.09***
0.99***
3.51***

2.46***
placebo and 4 FO. Within groups the reduction in

3.93*
1.77

0.02
waist circumference was significant (p < 0.01 and
p < 0.05 for FO and placebo, respectively) but the ±
±
±
±
±
±
±
−3.17
−1.11
−3.43
0.29
−2.25
−2.53
0.01
differences between the two groups was not.


Blood biomarkers

The changes in blood lipids from baseline to the

end of the intervention are summarised in Table 3.
16.12

10.02
11.65
10.43
3.70
8.06

0.08

Apart from a significant 27% (−0.53 mmol/l) reduc-

tion in triglycerides (p < 0.05) in FO, which was
±
±
±
±
±
±
±

significantly greater than the 1.09% (−0.25 mmol/l)

90.78
31.42
35.55
54.69
100.86
117.14
0.86

reduction in placebo (p < 0.05), there were no other

PI

significant differences for blood lipids from base-

line within and between groups. While changes
from baseline were modest, some were positive for
health, for example, increased HDL-C in FO and
Placebo (n = 18)

11.27
16.39

10.43
12.11
3.58
7.49

9.78
0.08

reduced TC in placebo, while others were nega-

tive, for example, increased TC and LDL-C in FO
Mean values ± standard deviations.
±
±
±
±
±
±
±
±

and reduced HDL-C and increased LDL-C in placebo.

41.11
93.95
32.53
38.98
54.40
103.11
119.67
0.86

Changes to inflammatory biomarkers, both within

BL

groups and between FO and placebo, were also

modest and non-significant due to the large vari-
ance in the results. The results are shown in Table 3.
Correlations between changes in anthropometric
*** p < 0.001.

measurements, blood biomarkers and LCn-3PUFA

BMI (kg/m2 )
Weight (kg)

* p < 0.05.
** p < 0.01.
Waist:hip

were computed. For both groups there were pos-

Hip (cm)
WC (cm)
FFM (kg)
Table 2

FM (kg)

itive and significant correlations between weight

Age

loss and changes to BMI and FM (p < 0.001 for both),

also changes to waist (p < 0.001 for FO and p < 0.01
e178 I.A. Munro, M.L. Garg

for placebo). For FO there were also positive and

0.50***
10.57
0.83*
0.78
0.22
0.49
0.54

4.62

1.20
1.71
significant correlations between leptin and changes
to weight, FM, EPA and DHA (p < 0.05 for all),

±
±
±
±
±
±
±
±
±
±
suggesting a possible interaction with LCn-3UFA,

−0.53
0.11
0.04
0.13
0.14
−0.91
−0.23
−0.76
−0.23
0.11
weight loss and leptin. However, there was no cor-

relation with LCn-3PUFA and weight loss.

20.60
0.46
0.84
0.25
0.88
0.58

6.37
1.28
0.67
4.22
Discussion
±
±
±
±
±
±
±
±
±
±
Although studies with animals have shown that
0.80
5.02
1.25
3.25
4.95
35.36
13.04
0.96
1.73
3.68
dietary intake of LCn-3PUFA may reduce body
PI

weight in obese animals, and may reduce body

fat accumulation, particularly visceral fat in ani-
mals fed a high fat diet [20], the effectiveness of
Fish oil (n = 15)

supplementation with LCn-3PUFA as an adjunct to

19.92
1.00
0.91
0.27
0.79
0.39

4.93
1.62
1.19
4.36

weight loss in humans is less certain. It has been

suggested that LCn-3PUFA may reduce body fat in
±
±
±
±
±
±
±
±
±
±

humans by suppressing the appetite and increasing

1.32
4.91
1.21
3.12
4.81
36.27
13.27
1.72
1.96
3.57

fat oxidation and energy expenditure [20] but stud-

BL

ies with humans have provided conflicting results.

The hypothesis of this study was that supplement-
ing an energy restricted diet with LCn-3PUFA may
12.00

have a complementary effect on weight loss.

0.59
0.56
0.18
0.47
0.50

5.86
0.80
1.82
2.53

In this study we observed a significant increase in

EPA and DHA from baseline in FO and a significantly
±
±
±
±
±
±
±
±
±
±
−0.25
−0.10
−0.03
0.06
0.31
1.50
1.17
−0.33
0.07
−0.18

greater level of EPA and DHA in FO compared to

placebo. Despite the increase in LCn-3PUFA in FO,


over the 12 weeks the differences in loss of weight

Baseline values and changes from baseline for blood biomarkers.

and FM between the two groups were marginal

and not significant, suggesting that LCn-3PUFA may
19.38

not contribute to loss of weight or FM in humans.

0.40
0.73
0.27
0.66
0.57

7.33
1.11
3.89
4.21

Similar results have been reported in comparable

±
±
±
±
±
±
±
±
±
±

studies involving supplementation with LCn-3PUFA

1.07
4.74
1.12
3.13
5.02
35.82
13.36
1.01
2.98
4.15

on weight loss. One study involving overweight,

PI

insulin-resistant females, used a very low energy

diet for weight loss with a treatment group receiv-
a Data available n = 31 (placebo: n = 17; fish oil: n = 14).
b Data available n = 31 (placebo: n = 16; fish oil: n = 15).

ing supplementation of 2.9 g DHA + 1.3 g EPA each

day. No significant difference in loss of weight
Placebo (n = 18)

13.47

or FM was observed between the treatment and

0.71
0.93
0.24
0.81
0.51

6.41
1.13
2.34
3.59

control groups [21]. In another two similar stud-

±
±
±
±
±
±
±
±
±
±

ies individuals followed energy controlled, but not

1.33
4.84
1.16
3.07
4.71
34.32
12.18
1.34
2.92
4.34

restricted diets. In both studies, supplementation

BL

with LCn-3PUFA in the proportion of 1 g EPA + 0.7 g

Mean values ± standard deviations.

DHA/day for the treatment group, influenced a sig-

nificantly greater decrease in FM in the treatment
group compared to the control group but no sig-
Adiponection (␮g/ml)a

nificant differences in weight loss between the two

groups [22,23]. Using oily fish to provide 3.65 g LCn-
Glucose (mmol/l)

hs-TNF-␣ (pg/ml)

hs-CRP (␮g/ml)b
HDL-C (mmol/l)
LDL-C (mmol/l)

3PUFA/d, a study reported no significant difference

hs-IL-6 (pg/ml)
Leptin (ng/ml)
Trigs (mmol/l)
TC (mmol/l)

in weight loss between participants who followed

*** p < 0.001
* p < 0.05.

an energy restricted diet alone and an energy

Table 3

restricted diet + fish. There was also no change

in weight in a diet of usual energy intake + fish
[24]. Another study with an energy restricted diet
Omega-3 fatty acid supplementation and weight loss e179

plus lean fish or fatty fish or LCn-3PUFA capsules, Balk et al. suggests that LCn-3PUFA increases LDL-
reported that the diets did not differ in their effect C [35]. Our findings for TC and LDL-C agree with
on weight loss for females, but weight loss in those reported by Harris (1989) with no significant
males was significantly greater in all three treat- changes in FO or between FO and placebo. It is
ment groups when compared with the control group possible that the modest increase in TC observed
[25]. It is proposed that this difference between in FO could reflect the amount of saturated fat
males and females could be attributed to a dif- in the diet of individuals. Obesity is associated
ferent response to marine foods by gender or to a with decreased plasma levels of HDL-C. A modest
different effect of the intervention diet on weight increase of HDL-C is associated with weight loss
loss for males and females [25]. [37,38] and an increase of 5—10% is associated with
A possible reason for the different outcomes consumption of LCn-3PUFA [35]. While our results
from these studies could be the different amounts showed such an increase in HDL-C concentrations,
of LCn-3PUFA supplementation and the relative that is 5% (0.04 mmol/) for FO, the variance in the
proportions of EPA to DHA. It is noteworthy that results could have been influenced by individual dif-
the controversy about the weight loss potential ferences in weight lost.
of omega-3 fatty acids is limited to the human Weight loss is known to influence a decrease
studies while animal studies have consistently in circulating inflammatory markers [10] and LCn-
demonstrated body weight reduction following 3PUFA have been shown to have anti-inflammatory
administration of omega-3 fatty acids in the diet. properties [39—41]. In keeping with the modest
These differences could be attributed to dietary weight loss in this study, plasma leptin levels
compliance in humans versus animals. It is easier reduced by a small amount in FO but despite a simi-
to manage dietary compliance when working with lar weight loss in placebo, leptin levels in that group
animals compared to working with humans, par- increased. Although the differences were not signif-
ticularly when faced with feelings of hunger on icant, there was a significant, positive correlation
an energy restricted diet. Self-reporting of dietary between leptin and weight loss (p = 0.01) and lep-
compliance can be misleading both through under- tin and EPA and DHA (p < 0.05 for both) in FO. This
reporting and over-reporting dietary intake [26,27]. would appear to indicate that the reduction of lep-
Moreover, the effect of LCn-3PUFA on weight reduc- tin in FO could also be attributed to LCn-3PUFA. In a
tion, if any, is likely to be small, with gradual study involving overweight men and women serum
changes over time. Therefore, it is likely that vari- leptin levels were significantly reduced in a weight
able compliance (both diet and physical activity), loss plus fish meal diet but not in a weight loss diet
coupled with short duration of the intervention or usual energy plus fish diet, showing that this
period may negate any small and gradual beneficial reduction occurred from an interaction between
effects of dietary supplementation with LCn-3PUFA n-3 fatty acids and weight loss [41]. In our study
on weight loss. there was a modest increase in adiponectin levels
Not only have studies with mice found that in placebo but a reduction in FO, which suggests
dietary supplementation with LCn-3PUFA reduces that weight loss and not LCn-3PUFA influenced the
body weight and fat mass but it has been shown to increase. These results appear to be in keeping with
prevent weight gain [16,17]. Also, feeding fish oil- a study investigating the effect of LCn-3PUFA con-
enriched diets to rodents, compared to other types sumption on adiponectin in overweight and obese
of dietary oils, has been shown to prevent abdomi- men and women that found that weight loss influ-
nal fat accumulation [28—30]. Perhaps LCn-3PUFAs enced an increase on adiponectin concentrations
are more effective in preventing weight gain rather not LCn-3PUFA [42].
than assisting weight loss. In this context, stud- In our study there was an overall mean increase
ies with humans have shown that when compared of hs-CRP and an overall mean decrease of TNF-
to healthy-weight individuals, significantly lower ␣ and IL-6 by FO, but changes were very small
concentrations of n-3 PUFA have been observed in and not significantly different to placebo. Findings
obese females and/or males [31—33]. for the effect of LCn-3PUFA on CRP are not con-
It is well established that weight loss has a posi- sistent. A study involving healthy postmenopausal
tive influence on blood lipids. LCn-3PUFAs are also women found that there was a reduction in
known to be effective in lowering triglyceride lev- serum hs-CRP with supplementation of 7 g/d LCn-
els [34,35] which were the findings in our study with 3PUFA but not with 14 g/d [43]. Another study
a significant decrease in triglycerides from base- involving healthy males and females, found that
line for FO. It has been suggested that TC is not there was no significant reduction in serum hs-
affected by LCn-3PUFA [35,36]. Harris also contends CRP with daily supplementation of 2 g or 6.6 g
that LDL-C are not affected by LCn-3PUFA [36] while LCn-3PUFA [44].
e180 I.A. Munro, M.L. Garg

Conclusion inflammatory markers and PAI-I antigen in obese men dur-

ing the fasting and postprandial state. Eur J Clin Invest
2004;34:766—73.
While studies with animals have consistently shown [12] Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer
that LCn-3PUFA influences weight loss, studies in EJ. Comparison of the Atkins, Ornish, Weight Watchers, and
humans have produced conflicting results. Reasons Zone diets for weight loss and heart disease risk reduction:
for this might include the different amounts of LCn- a randomized trial. JAMA 2005;293:43—53.
[13] Hill JO, Thompson H, Wyatt H. Weight maintenance: what’s
3PUFA consumed by humans in the various studies
missing? J Am Diet Assoc 2005;105(Suppl. 1):S63—6.
and the relative proportion of EPA to DHA. A major [14] Calder PC, Grimble RF. Polyunsaturated fatty acids, inflam-
factor could be the uncertainty of dietary compli- mation and immunity. Eur J Clin Nutr 2002;56(Suppl.
ance which can be controlled in animals but not as 3):S14—9.
easily in humans. Future studies on LCn-3PUFA and [15] Calder PC. Dietary modification of inflammation with lipids.
Proc Nutr Soc 2002;61:345—58.
weight loss should consider more effective manage-
[16] Nakatani T, Kim HJ, Kaburagi Y, Yasuda K, Ezaki O. A low
ment strategies to encourage dietary compliance. fish oil inhibits SREBP-1 proteolytic cascade, while a high-
fish-oil feeding decreases SREBP-1 mRNA in mice liver:
relationship to anti-obesity. J Lipid Res 2003;44:369—79.
Conflict of interest [17] Ruzickova J, Rossmeisl M, Prazak T, Flachs P, Sponarova J,
Veck M, et al. Omega-3 PUFA of marine origin limit diet-
The authors have no conflict of interest to disclose. induced obesity in mice by reducing cellularity of adipose
tissue. Lipids 2004;39:1177—85.
[18] Kellet E, Smith AE, Schmerlaib Y. The Australian guide to
Acknowledgement healthy eating. Canberra: Gov Dpt Health and Ageing; 1998.
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lipids in a one step reaction. J Lipid Res 1986;27:114—20.
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