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Dietary Omega-3 Fatty Acids and Depression in a
Community Sample
F.N. JACKA, J.A. PASCO, M.J. HENRY, M.A. KOTOWICZ, G.C. NICHOLSON and M. BERK*
Department of Clinical and Biomedical Sciences: Barwon Health, The University of Melbourne, P.O. Box 281, Geelong 3220, Vic., Australia
(Received 7 January 2004; Revised 25 February 2004; In final form 12 April 2004)
To evaluate the association between omega-3 poly-
unsaturated essential fatty acids and depression, data
regarding prevalence rates of self-reported depression
and median daily dietary intakes of these fatty acids
were obtained from an age-stratified, population-based
sample of women (n5755; 2397 year) in the Barwon
Statistical Division of south-eastern Australia. A self-
report questionnaire based on Diagnostic and Statistical
Manual-IV criteria was utilised to determine 12-month
prevalence rates of depression in this sample, and data
from biennial food frequency questionnaires examining
seafood and fish oil consumption over a 6-year period
were examined. Differences in median dietary intakes of
omega-3 fatty acids between the depressed and non-
depressed cohorts were analysed and results were
adjusted for age, weight and smoking status. No
significant differences in median intakes were identified
between the two groups of women (median, interquartile
range; depressed 50. 09 g/day, 0.04– 0.18 versus non-
depressed 50.11 g/day, 0.05– 0.22, p50.3), although
overall average intakes of omega-3 fatty acids were
lower than recommended and rates of depression within
this sample higher than expected, based on previous
data. Further research that takes into account ratios of
omega-6 to omega-3 polyunsaturated essential fatty
acids, as well as other dietary sources of omega-3 fatty
acids, is warranted.
Keywords: Depression; Diet; Fatty acid; Fish; Omega-3; Mood
INTRODUCTION
Essential polyunsaturated fatty acids (PUFAs) are
major components of neuronal cell membranes
(Maidment, 2000) and play a vital role in neuronal
function. Linoleic acid (LA) and alpha-linolenic acid
(ALA) are essential long-chain PUFAs that are
synthesised endogenously to create the omega-6
PUFAs, arachidonic acid (AA) and docosapentaenoic
acid (DPA), and the omega-3 PUFAs, eicosapenta-
enoic acid (EPA) and docosahexaenoic acid (DHA),
respectively. These essential fatty acids, particularly
DHA, are the predominant structural fatty acids in
the grey matter of the brain (Horrocks and Yeo, 1999).
Abnormalities of PUFA composition in neuronal cell
membranes can affect receptor function, neurotrans-
mitter reuptake and signal transmission (Tiemeier
et al., 2003) and may therefore contribute to
psychiatric disorders.
Astrocytes, a type of glial cell, play a primary role in
converting omega-3 PUFA precursors to DHA in the
brain and delivering this essential fatty acid to
neurons (Moore et al., 1991; Moore, 1993). There is
considerable evidence that increases in dietary EPA
and DHA intake through the consumption of seafood
and fish oil supplements increase the supply of
preformed DHA to the brain (Connor and Neuringer,
1988; Connor et al., 1996), and this preformed DHA is
a more effective source of DHA for astrocytes than
equivalent omega-3 PUFA precursors such as ALA
found in vegetable sources (Williard et al., 2001).
Recent research has suggested that the omega-3
PUFAs EPA and DHA play a role in depression.
Epidemiological studies have revealed an inverse
relationship between national fish consumption and
the annual prevalence of major depression and post-
partum depression (Hibbeln, 1998; 2002). A study
examining levels of fish consumption, depression
and suicidal tendencies among a random commu-
nity sample of 3004 Finnish people demonstrated
significantly lower levels of depression and suicidal
tendencies among frequent fish consumers, even
ISSN 1028-415X print/ISSN 1476-8305 online q2004 Taylor & Francis Ltd
DOI: 10.1080/10284150410001710438
*Corresponding author. Tel.: þ61-3-5226-7764. Fax: þ61-3-5222-2420. E-mail: mikebe@barwonhealth.org.au
Nutritional Neuroscience,Volume 7 Number 2 (April 2004), pp. 101–106
after controlling for demographic, health and
lifestyle factors (Tanskanen et al., 2001). However, a
more recent large-scale, population-based study of
29,133 men in Finland revealed no association
between dietary intakes of fish and omega-3 PUFAs
and depressed mood, major depressive episodes, or
suicide (Hakkarainen et al., 2004).
Examinations of essential PUFA levels in blood
samples from clinical populations have produced
mixed findings. Several investigators have reported
lower levels of omega-3 PUFAs in depressed patients
(Adams et al., 1996; Maes et al., 1996; Edwards et al.,
1998; Peet et al., 1998; Tiemeier et al., 2003), as well as
increased omega-6/omega-3 ratios in depressed
patients (Adams et al., 1996; Tiemeier et al., 2003).
Conversely, a significantly higher proportion of EPA
and DHA has been reported in one study of subjects
with endogenous depression compared to controls
(Ellis and Sanders, 1977).
Two recent clinical trials comparing the efficacy of
omega-3 PUFAs with placebo as a treatment for major
depressive disorder revealed significant improve-
ments in depressive symptoms with treatment. Su
et al. (2003) conducted an 8-week, double-blind,
placebo-controlled trial of omega-3 PUFAs, compris-
ing both EPA and DHA, in 28 patients diagnosed with
major depressive disorder. They found that a dosage
of 9.6 g/day was effective in significantly reducing
depression scores in the omega-3 PUFA group from
the fourth week after treatment. Similarly, Peet and
Horrobin (2002) reported that a dosage of 1 g/day of
EPA alone for 12 weeks in a sample of 70 clinically
depressed patients was efficacious in significantly
improving depressive symptoms. However, a
double-blind, placebo-controlled trial of DHA alone
(2 g/day for 6 weeks) in 36 clinically depressed
patients demonstrated no significant improvements
in the treatment group compared to controls
(Marangell et al., 2003).
Omega-3 PUFAs have also been examined as a
treatment option for bipolar disorder. In two
double-blind, placebo-controlled trials of omega-3
PUFAs, one pilot study administered combined
EPA and DHA to 30 bipolar patients, demonstrat-
ing significant symptom reduction and longer
periods of remission compared to controls (Stoll
et al., 1999), while a larger study, trialing EPA alone,
demonstrated no significant differences in symp-
toms or functioning in 121 bipolar and rapid
cycling patients from baseline to 4 months (Keck
et al., 2002).
This study sought to examine the association
between omega-3 PUFA dietary intake, as measured
by seafood and fish and cod liver oil supplement
consumption, and the occurrence of self-reported
depression in a random community sample of
women from the south-eastern region of Australia.
It was hypothesised that there would be a difference
between the depressed and non-depressed groups
in terms of their average omega-3 PUFA dietary
intake.
MATERIALS AND METHODS
Participants
This study examined data collected from women
participating in the Geelong Osteoporosis Study, an
age-stratified, community sample of women ran-
domly selected from Commonwealth electoral rolls
in the Barwon Statistical Division (south-eastern
Australia) between 1994 and 1997 (Henry et al.,
2000). The initial study group totalled 1494
women, with a reduction due to attrition of 219
women at the 6-year follow-up. The sample
spanned the full adult age range (median ¼57
years, range ¼23 97). The Barwon Health Research
and Ethics Advisory Committee approved the study
and written, informed consent was obtained from
all participants.
Depression Assessment
Symptoms of past and present depression were
ascertained by a self-report questionnaire based on
DSM-IV criteria (American Psychiatric Association,
1994) and measured symptoms from the year
between July 2000 and July 2001. A categorical
diagnosis of clinically significant depression was
made on the basis of DSM-IV criteria for major
depressive disorder, i.e. either depressed mood or
loss of interest or pleasure consistently over a 2-week
period, with at least four accompanying symptoms
of depression. All those participants eligible for the
6-year follow-up ðn¼1275Þwere sent the depression
questionnaire, with a total of 758 women returning
the questionnaire (60%). Three responses were
incomplete and therefore excluded, resulting in 755
women participating in this aspect of the study.
Percentages of those determined as depressed were
calculated and the participants divided into
depressed and non-depressed subgroups. Internal
reliability analysis of the depression questionnaire
yielded a standardised Cronbach’s alpha coefficient
of 0.895.
Omega-3 Fatty Acid Intake Assessment
Participants completed a food frequency question-
naire at baseline, 2-, 4- and 6-year follow-ups. Weekly
consumption of seafood including salmon, tuna,
white fish, mackerel, prawns and sardines at
each 2-year measurement were ascertained. Regular
supplement intake was also recorded. Intakes at each
2-year measurement were compared to determine the
stability of the dietary data. There were no significant
F.N. JACKA et al.102
differences between dietary intakes at baseline
compared to the 2-year follow-up, or between
4- and 6-year follow-ups, although there was a
difference of 0.02 g/day between 2- and 4-year
follow-ups and this difference was statistically
significant. A mean daily omega-3 intake was
therefore calculated, utilising the data from each
biennial measurement, based on the known average
level of omega-3 contained in a regular portion of
each seafood serve. Regular supplemental intake of
fish or cod liver oil was examined and an average
daily intake calculated and added to the dietary data.
These average daily intakes were regarded as being
representative of each individual’s normal dietary
consumption of seafood and fish oil supplements
over the long-term.
Estimates of omega-3 PUFA levels in each seafood
serve and supplement were derived from product
information (Table I). Six-year follow-up dietary and
supplement data was only included for those
subjects who completed the questionnaire prior to
or concurrent with completion of the depression
questionnaire. The remaining participants had the
closest 2-year visit data included in the omega-3
analysis. The median time lag between the last
dietary questionnaire and the depression measure-
ment was 1.3 years (IQR ¼0.7 1.9 years). Medians
and interquartile ranges of age and weight were also
calculated and current smoking status (yes/no)
determined.
Statistical Analysis
Analyses were performed using the Minitab statis-
tical package (Version 12). A Mann Whitney test for
non-parametric data was used to test for significant
differences between omega-3 PUFA intake in the
depressed and non-depressed cohorts. A Kruskal
Wallis test was used to test for differences in omega-3
PUFA intakes across 10-year age groups.
Further analyses of omega-3 PUFA intake adjust-
ing for age, smoking and weight were undertaken by
splitting the data into appropriate subgroups and
Mann Whitney tests performed. Chi-square ana-
lyses tested for differences in depression rates
between age and weight groupings and smokers/
non-smokers. The significance level for all tests was
a
¼0:05:
RESULTS
Characteristics for the whole group, and for the
depressed and non-depressed subgroups are given
in Table II.
In this sample, 97 women (12.85%) were
identified as depressed. Figures were standardised
to the Barwon Statistical Division (1996) yielding a
standardised rate of 15%. Analysis of age group-
ings revealed that participants in the 20 29 (15%)
and the 40 49 (23%) year age groups were more
depressed and those in the 70 þ(3.7%) age
groups less depressed than expected if there was
an even distribution across age groups (
x
2¼33:9;
p,0:001). The depressed subjects were younger
and weighed more than the non-depressed, and a
higher proportion of the depressed group were
smokers.
The distribution of omega-3 PUFAs was positively
skewed. The overall average omega-3 PUFA intake
was low with 48 participants (6.4%) of the sample
recording a zero intake and a further 680 people
(90.1%) recording a mean intake of less than
0.5 g/day. Only 27 participants recorded an intake
of .0.5 g/day. An analysis of omega-3 PUFA intakes
across 10-year age groups revealed that those in the
2039-year age groups had lower intakes, whereas
those in the 60 –79-year age groups had higher intakes
than the group median ðp,0:001Þ(Fig. 1).
TABLE I Omega-3 fatty acid levels contained in standard
servings
Food/supplement Standard serve
Total omega-3
(g)
Sardines (canned) 5 Sardines (75 g) 1.25
Salmon (canned) 1/2 cup (105 g) 1.3
Tuna (canned) 1/2 cup (100 g) 0.2
King prawns (cooked) 6 prawns (95 g) 0.2
Scallops 5 or 6 (95 g) 0.3
White fish 1 medium fillet (120 g) 0.4
Herring/Mackerel 1/2 cup (105 g) 1.5
Cod liver oil 1 tblspn (12 ml) 5.4
Cod liver oil 1 tspn (4 ml) 1.8
Cod liver oil 1 capsule (1 g) 0.27
Cod liver oil 1 capsule (0.3 g) 0.1
Fish oil 1 capsule (1 g) 0.3
Sources: Blackmores Ltd., Meadow Lea Foods Ltd.
TABLE II Characteristics for the whole group, and for the depressed and non-depressed subgroups
All (n=755) Depressed (n=97) Not depressed (n=658) p
Age (years) 57 (4272) 48 (3558.5) 59 (43–73) ,0.001
Weight (kg) 66.5 (58.5– 76) 69 (60.784.1) 66.1 (58.475.2) ,0.05
Smokers (%) 11.7 (88) 17.9 (17) 10.9 (71) #0.05
Omega-3 (g/day) 0.11 (0.050.22) 0.09 (0.04–0.18) 0.11 (0.05– 0.22) 0.3
Values are given as median (interquartile range) or percentage (n).
OMEGA-3 FATTY ACIDS AND DEPRESSION 103
No difference in omega-3 PUFA intake was
detected between the depressed and non-depressed
groups ðp¼0:3Þ:After dividing the group into
quartiles by weight, the difference in omega-3 PUFA
intake between the two cohorts remained non-
significant (all p.0:05), as was the case after
splitting across 10-year age groups (all p$0:05)
and dividing the sample into smoking and non-
smoking groups (p¼0:43;non-smokers; p¼0:62;
smokers).
DISCUSSION
The findings from this population-based study do
not support the hypothesis that omega-3 PUFA
intake, as measured by regular seafood and fish and
cod liver oil supplement consumption, was associ-
ated with self-reported depression in this commu-
nity sample of women.
Our findings are in contrast to some of the
previous epidemiological data and aspects of
the study warrant discussion. First, the overall
dietary intake of omega-3 PUFAs in the study
population was low. The World Health Organisation
recommends that omega-3 PUFAs comprise
between 1 and 2% of energy intake (World Health
Organisation, 2003) and The National Institute of
Medicine states a recommended dietary allowance
(RDA) of 1.1 g/day omega-3 PUFAs for women
(Food and Nutrition Board, National Institute of
Medicine, 2002). Previous studies demonstrating
improvements in depressive symptoms following
treatment with EPA, E-EPA or a combination of EPA
and DHA indicated that dosages of between 1 and
9.6 g/day, over and above dietary intake, were
effective (Peet and Horrobin, 2002; Nemets et al.,
2002; Su et al., 2003). Similarly, a dosage of 9.6 g/day
of combined EPA and DHA was effective in
the positive trial of omega-3 PUFAs in patients
diagnosed with bipolar disorder (Stoll et al., 1999).
In the present study, only 3.7% of the participants
were recorded as having a mean intake above
0.05 g/day. It is possible that a wider range of
intakes with higher concentrations would have
allowed for a more accurate detection of differences
between the groups.
Measurement of omega-3 PUFA intake was
limited in that only seafood and fish oil consumption
was ascertained. Adams et al. (1996) found that
estimated long-term dietary consumption of fish and
other marine food by participants in their study did
not correlate significantly with plasma and erythro-
cyte levels of EPA. As omega-6 and -3 fatty acids
cannot be formed in the body and must, therefore, be
taken in through the diet (Maidment, 2000), their
findings suggest that seafood was not the major
influence of EPA levels in that study. Omega-3
PUFAs are also contained in oils such as canola and
flaxseed (linseed) and, to a limited extent, in leafy
green vegetables and some nuts and seeds. A more
comprehensive dietary questionnaire would have
allowed for a more accurate measurement of true
levels of omega-3 PUFAs in the diet.
Additionally, the question of omega-6 to omega-3
PUFA ratios was not addressed in this investigation.
Some studies have proposed that higher omega-6 to
omega-3 ratios are related to depression (Adams
et al., 1996; Maes et al., 1996), and the World Health
Organisation recommends a ratio of not higher than
5:1 (Food and Agriculture Organisation (FAO) and
Health Organisation (WHO), 1995). Omega-6 PUFAs
are found predominantly in vegetable oils such as
margarines (Tiemeier et al., 2003) and the ratio of
omega-6 to omega-3 PUFAs is considered to be of
importance as these PUFAs compete for the same
enzymes and have different biological roles (FAO,
1995). This ratio may be a critical aspect of
the proposed relationship between dietary factors
and depression.
FIGURE 1 Distribution of omega-3 PUFA intake by 10-year age groupings.
F.N. JACKA et al.104
The limitations of utilising the DSM-IV criteria
for major depressive disorder as a self-report
diagnostic instrument, rather than as a clinical
diagnostic interview, must also be acknowledged.
The 12-month prevalence rates in this investigation
were higher than those reported in previous
epidemiological studies. The National Comorbidity
Survey Replication (Kessler et al., 2003) reported a
12-month prevalence rate of 6.6% in a comprehen-
sive survey of 9090 adults in the United States, and
an Australian national survey of 10,641 people
reported a 30-day prevalence rate of 5.2% in females
in mid-life, and an overall rate of 3.2% (Wilhelm et al.,
2003). Although the DSM-IV criteria are well
validated, the validity of utilising these criteria in
the form of a self-report questionnaire has not been
established. The much higher rate of self-reported
depression in this study (15%) could be a function of
the lack of specificity in the diagnostic tool utilised,
or it may reflect true rates of depression in this
community. It may also be a function of sampling
bias as only 60% of the eligible population responded
to the depression questionnaire. Although analyses
of differences between those who responded to
the depression questionnaire compared to non-
responders did not reveal any significant differences
in age, weight or height, it is possible that the
response rate amongst those with depression was
higher than amongst those who were not depressed.
It is also possible that those identified as depressed
according to their self-reported symptoms would
not have been diagnosed as such by a validated
clinical interview. In other words, it may be that
the differences between the two groups in terms
of their levels of depressive symptoms was
potentially not pronounced enough to adequately
differentiate between them. Further investigation of
rates of clinical depression in this sample using a
validated clinical diagnostic interview is warranted
and planned.
Although this study had several limitations, its
strengths were the un-selected, community-based
study population and the representativeness of this
population in relation to the rest of Australia.
Comparisons between the Barwon Statistical
Division characteristics and the Australian female
population indicate that the similarities between the
characteristics in age, country of birth, education,
marital status, employment and income profiles
afford a firm base for extrapolating this data to
national levels (Henry et al., 2000). The recognition of
the generally low dietary intakes of omega-3 fatty
acids in this sample is cause for concern in itself.
DHA is essential for brain functioning and
the development of the brain and retina in infants
(Innis, 1994), and plays an important role in the
maintenance of normal neural functions in adults.
DHA may also prevent or ameliorate hypertension,
arthritis, atherosclerosis, asthma, adult-onset dia-
betes mellitus, myocardial infarction, thrombosis
and some cancers (Horrocks and Yeo, 1999; Connor,
2000). Results from this study suggest that a
considerable proportion of Australian women may
be at risk for omega-3 deficiencies.
The findings of this study are also in concordance
with those reported in the recent large-scale
community study of men in Finland demonstrating
no association between dietary intakes of omega-3
PUFAs and fish and depressed mood, major
depressive episodes, or suicide (Hakkarainen et al.,
2004). The total average dietary intake of omega-3
PUFAs in that study exceeded ours (2.2g/day), and
were above the RDA, giving rise to two possibilities.
It could suggest that even though our study may have
lacked power due to a smaller sample size and low
average daily intakes, our results were representative
of the true association between dietary intakes of
these PUFAs and depression in this community,
particularly as their study found no association
between the two variables even in those in the
lowest decile for omega-3 PUFA intake. Another
interpretation, however, is that the consistently low
(below the RDA) omega-3 PUFA intakes in our
sample precipitated depression in those predisposed
to developing it, and this would be consistent
with the higher than expected levels of depression
observed.
In conclusion, no significant differences in omega-3
PUFA intakes were identified between those
categorised as depressed and those not-depressed in
this community sample of women. However, omega-
3 PUFA intakes were below the recommended levels,
and prevalence rates of depression were higher than
expectedbasedonpreviousAustraliandata.
Future investigations that utilise more detailed
dietary analyses that take into account other sources
of EPA and DHA, as well as data on omega-6
PUFA intakes, may afford more insight into the
possible aetiological role of essential fatty acids in
depression.
Acknowledgements
We gratefully acknowledge the support of the
Geelong Regional Medical Research Foundation
and The Victorian Health Promotion Foundation.
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