Evidence Report/Technology Assessment: Number 116
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Introduction / Key Questions / Methods / Results / Discussion / Availability of Full Report / References
Authors: Schachter HM, Kourad K, Merali Z, Lumb A, Tran K, Miguelez M, et al..
The purpose of this study was to conduct a
systematic review of the scientific-medical literature to identify, appraise,
and synthesize the human evidence for the effects of omega-3 fatty acids on
mental health. The review was requested
and funded by the Office of Dietary Supplements, National Institutes of Health. It was undertaken as part of a consortium
involving three Evidence-based Practice Centers (EPCs), which investigated the
value of omega-3 fatty acid supplementation across eleven health/disease
areas. The three EPCs are Southern
California-RAND, Tufts-New England
and, the University of Ottawa. To ensure consistency of
approach, the three EPCs collaborated on selected methodologic elements,
including literature search strategies, rating of evidence, and data table
While the intention was to evaluate the
spectrum of psychiatric disorders or conditions (i.e., behavior
or symptoms which, while their consequences could be serious, do not warrant
receipt of a formal psychiatric diagnosis), certain foci were beyond the scope
of the review (go to Methods). At the same
time, a mental health disorder or condition did not require extant animal or
basic science data or models to justify the investigation of their
evidence. Nevertheless, justification
for the study of two disorders exists in the literature.
mechanism by which diet may affect health, including depression or
cardiovascular disease, has been thought to involve low levels of omega-3 fatty
acid content in biomarkers (e.g., red blood cells [RBCs]).1,2 An omega-3 fatty acid deficiency hypothesis
of depression has been put forward, which has helped justify treatment with
omega-3 fatty acid supplementation.3 The membrane phospholipid hypothesis of schizophrenia has been proposed
in an attempt to develop a model explaining its etiology.4
It describes the presumed biochemical dynamics underpinning a
neurodevelopmental theory. Some of the
evidence used to support this perspective suggests the existence of phospholipid
and PUFA metabolic abnormalities in schizophrenia.4-6 It has been posited that modifications to
diet could mitigate or even aggravate an underlying abnormality of phospholipid
the present review was not conducted to test these hypotheses. Rather, the rationale for this two-year
project investigating the possible health benefits of omega-3 fatty acids was
to systematically review the evidence to aid in the development of a research
agenda. Nevertheless, these emerging
models regarding depression and schizophrenia do suggest plausible bases for
the use of omega-3 fatty acids to treat or prevent these psychiatric
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Four basic questions were investigated with
respect to each psychiatric disorder or condition for which evidence meeting
eligibility criteria could be identified.
To illustrate, the questions pertaining to depression were:
- Are omega-3 fatty acids
efficacious as (primary or supplemental) treatment for depression?
- Is omega-3 fatty acid intake,
including diet and/or supplementation, associated with the onset, continuation
or recurrence of depression? (i.e., primary or secondary prevention)
- Is the onset, continuation or
recurrence of depression associated with omega-3 or omega-6/omega-3 fatty acid
content of biomarkers? (i.e., primary or secondary prevention)
- What is the evidence that, in
review-relevant studies concerning mental health, adverse events (e.g., side
effects) or contraindications are associated with the intake of omega-3 fatty
Where data permitted, the impact of effect
modifiers (e.g., covariates) was investigated with respect to the following
- Population (e.g., primary
diagnosis; disorder severity; smoker status; alcohol consumption).
- Intervention/exposure (e.g., source,
type, dose or serving size, and method to deliver the omega-3 fatty acids;
intervention length; dietary omega-6/omega-3 fatty acid content).
- Comparator/control (e.g., type of
placebo material; a "gold standard" medication).
- Cointerventions (e.g., concurrent
psychotropic medication; other supplement use).
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A Technical Expert Panel (TEP) consisting of
nine members was convened to provide advisory support to the project, including
refining the questions and highlighting key variables requiring consideration
in the evidence synthesis.
Several electronic databases were searched:
MEDLINE®, Embase®, the Cochrane Library including the Cochrane Central Register
of Controlled Trials, PsycInfo, and CAB Health.
Searches were not restricted by language of publication, publication
type, or study design, except with respect to the MeSH term "dietary fats,"
which was limited by study design to increase its specificity. Search elements included: scientific terms,
with acronyms, as well as generic and trade names relating to the exposure and
its sources (e.g., eicosapentaenoic acid [EPA]; omega-3 fatty acids; MaxEPA®); and,
relevant population terms (e.g., depression).
Additional published or unpublished literature was sought through manual
searches of reference lists of included studies and key review articles, and
from the files of content experts. A
final set of 1,212 unique references was identified and posted to an internet-based software system for review.
Studies were considered relevant if they
described live human populations of any age, which exhibited the psychiatric
status consistent with one of the above-noted research questions concerning
treatment or prevention (i.e., with or without [a known elevated risk to
develop] a psychiatric diagnosis or condition) in addition to any or no
comorbidity, and investigated at least one pertinent clinical outcome (e.g.,
symptom improvement; incidence of a disorder).
As markers of omega-3 fatty acid metabolism, the following fatty acid
compositions or concentrations, from any source (e.g., plasma phospholipids),
were considered relevant as possible predictors of the onset, continuation or
recurrence of psychiatric disorders or conditions: EPA, DHA, AA/EPA, AA/DHA,
AA/EPA+DHA. Studies exclusively
evaluating the role of other biomarkers (e.g., cytokine production, eicosanoid
levels) were not included. Excluded
populations were those with degenerative (e.g., Alzheimer's) and peroxisomal
(e.g., Zellweger's) disorders since each was addressed in SC-RAND's year-2
review of the evidence concerning omega-3 fatty acids in neurology.
Treatment studies, as well as those
investigating the possible association between omega-3 fatty acid intake and
the onset, continuation or recurrence of psychiatric disorders or conditions,
had to investigate foods or supplements known to contain omega-3 fatty acids of
any type (e.g., EPA), from any source (e.g., walnuts), any serving size or
dose, delivered in any fashion (e.g., capsules, PUFA-rich diet), and for any length
of time. In all studies, some method had
to have been employed to suggest the presence of omega-3 fatty acid content in
the exposure, if not its actual amount (e.g., g/d). Studies investigating "PUFAs" or " LC PUFAs,"
or even types of diet one might presume would contain marine or land sources of
omega-3 fatty acids (e.g., "Mediterranean diet") at minimum had to highlight at
least one source of the omega-3 fatty acid content (e.g., oily fish
servings). No restrictions were placed
on the types or doses of pre- or on-study cointerventions (e.g., psychotropic
medication, omega-6 fatty acid intake).
Controlled studies employing any control were
required to address questions of intervention efficacy (or effectiveness), with
randomized controlled trials (RCTs) being the gold standard method to
investigate these questions.7 Any type of research design other than
noncomparative case series or case studies was deemed appropriate for questions
concerning the possible association between the intake of omega-3 fatty acids
and the onset, continuation or recurrence of psychiatric disorders or
conditions. A special interpretative
emphasis was placed on results from prevention RCTs and other controlled
prospective designs. Controlled studies
involving any control were required to address the questions of the possible
association between the fatty acid content of biomarkers and the onset,
continuation or recurrence of psychiatric disorders or conditions. A special interpretative emphasis was placed
on results from controlled prospective designs.
These decisions were made with the assistance of our TEP.
initial levels of screening for relevance, and two reviewers per level, were
employed (directed at bibliographic records, then full articles). A third dual-assessor relevance screening
identified and thereby excluded uncontrolled studies with respect to
questions of intervention efficacy or the possible protective role of lipid
biomarker content. Calibration exercises preceded each step of
the screening process. Excluded studies
were noted as to the reason for their ineligibility using a modified QUOROM
Disagreements were resolved by forced consensus and, if necessary, third
Following a calibration exercise, seven
reviewers independently abstracted the contents of each included study using an
electronic Data Abstraction form. A
second reviewer verified these data.
Data included the characteristics of the report (e.g., publication
status), study (e.g., research design),
population (e.g., diagnosis), intervention/exposure (e.g., omega-3 fatty acid
type), comparator group(s), cointerventions (e.g., medications), withdrawals or
dropouts, and outcomes (i.e., symptom improvement; biomarker status;
After calibration exercises, each study's
quality (internal validity) and applicability (external validity) were formally
assessed. Dual-review appraised RCTs'
quality while only single-assessor evaluations could be conducted for other
research designs. For the RCTs, disagreements were resolved by
forced consensus and, if necessary, third party intervention. RCTs' reporting of randomization,
double blinding, withdrawals and dropouts, and the concealment of allocation,
were evaluated using Jadad's9 and Schulz's validated
instruments.10 The validated Newcastle-Ottawa Scale (NOS)
assessed case-control and cohort study designs,11 while all other designs were
evaluated using modifications of the NOS,11 Jadad's instrument,9 or items from Downs and
Black's validated 27-item tool.12 Applicability was defined as the extent to
which a given study's sample population was representative of a "typical" North
American population. The method of
diagnosis and the omega-6/omega-3 fatty acid ratio in the background diet were
the key variables defining the reference population of North Americans identified
with a psychiatric disorder. The omega-6/omega-3
fatty acid ratio in the background diet defined the reference population of
North Americans who did not exhibit a psychiatric disorder.
A summary table provided a question-specific
overview of included studies' relevant data presented in greater detail in
evidence tables. A question-specific
summary matrix situated each study in terms of its quality and applicability
ratings. Question-specific qualitative
syntheses of the evidence were derived.
A dearth of studies best suited to address a particular kind of question
(i.e., RCTs; prospective and controlled observational studies), as well as
limitations on, or the strong clinical heterogeneity of, available studies
(e.g., divergent intervention-comparator contrasts; use of complex
interventions where it was impossible to tease out the possible specific
benefit of omega-3 fatty acids; failure to control for key confounders), made
it impossible to perform meta-analysis for any question other than the
supplemental treatment for schizophrenia.
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Of 1,212 records entered into the initial
screening for relevance, 955 were excluded.
All but 7 of the remaining 257 reports were then retrieved, and
subjected to a more detailed relevance assessment.13-21 A
second relevance screening then excluded 137 reports. A third screening excluded 27 reports of
uncontrolled studies. In total, 86
reports, describing 79 unique studies, were deemed relevant for the systematic
review, with six studies each described by more than one report. To simplify matters, only one report per
study is referred to in this summary.
Yet, data from all of a study's documents were included in qualitative
and quantitative syntheses. Some studies
addressed more than one question.
Of the included studies, only one failed to be
described by at least one published report.22 Of the 16 relevant studies identified by
manual search, only this abstract was disseminated in a format other than a
journal publication.22 All but one of the included reports (all
published), which required translation from Chinese,23 were written in English.
Overall, depression (n=22 studies) and
schizophrenia (n=28) were the most frequently studied disorders. Only the 10 studies investigating
attention-deficit/hyperactivity disorder (AD/HD) enrolled pediatric
populations. Many of the studies
exhibited poor quality or weak applicability to North American
populations. Synopses of evidence are
presented according to seven cross-cutting topics:
number of study reports explicitly stated that no exposure-related adverse
events had been observed.24-32 Ten
RCTs described at least one mild adverse event associated with an omega-3 fatty
acid intervention/exposure.2,33-41 Results from these studies suggest that the
exposures were well tolerated. In spite
of a small number of discontinuations presumed to have been instigated by an
adverse event, it is unlikely that moderate or severe side effects were ever
observed in relation to an omega-3 fatty acid exposure. Reported difficulties tended to be mild and
transient, often involving gastrointestinal upset or nausea. Occasionally, adverse events were linked to
the intake of oily substances, rather than to the omega-3 fatty acid contents
in the oils. Aside from the mild adverse
effects associated with Stoll, et al.'s very high dose of 9.6 g/d EPA+DHA (i.e.,
three patients had to decrease the number of capsules swallowed per day, yet
none were required to discontinue),38 no other patterns were
discerned regarding the impact of dose, type (e.g., DHA, EPA) or source (e.g.,
marine, plant) of omega-3 fatty acids on safety. In one study, a child with AD/HD
in the active treatment group had to leave the study due to problems swallowing
the capsules.41 Few
of the events described in two trials by Hamazaki, et al., which enrolled
healthy volunteers, suggested that the adverse effects had been directly
related to the exposure.39,40
One RCT examined omega-3 fatty acids as primary
treatment for depression.34 It
found no benefit for 2 g/d DHA as primary treatment despite an increase in the
absolute RBC levels of DHA in the active treatment group.34
Reasons for this null result could include the use of too small a dose,
too short an intervention period, the "wrong" omega-3 fatty acid, broken
blinding, low power, or failure to modify the on-study background intake of
omega-6 fatty acids.
Notwithstanding the noncomparability of
interventions, comparators and populations (i.e., with32,42,43 or without a formal diagnosis of AD/HD;41 with32 or without significant
comorbidity41,43), the complex definitions of
the intervention where it was impossible to tease out the possible specific
benefit of omega-3 fatty acids,41 evidence for selection bias,43 or the failure to specify
study enrollees' specific diagnostic subtype of AD/HD (e.g., Inattentive),44 the results of the three RCTs32,41,42 and the comparative before-after study43 addressing the question about
the primary treatment of AD/HD were inconsistent. Thus, no definitive conclusions can be drawn
about the value of omega-3 fatty acids as primary treatment for AD/HD.
One RCT examined E-EPA as primary treatment for
borderline personality disorder and observed significant clinical
effects, as the E-EPA group had, at study end, significantly lower mean scores
on both clinical outcomes compared with the placebo group.31 Despite its strong applicability to the North
American population, this is a small study requiring replication.
While the results of Peet, et al.'s trial37 indicate placebo-controlled
benefits accruing to omega-3 fatty acids as primary treatment for schizophrenia,
this was a small albeit methodologically adequate pilot trial with little
applicability to a North American population.
More work is required before we can determine omega-3 fatty acids'
promise in this context.
Peet, et al.'s dose-ranging RCT of ethyl eicosapentaenoate (E-EPA) as supplemental
treatment for depression found that only 1 g/d for 12 weeks had a
significant impact on various clinical outcomes.2 Two
RCTs of shorter duration also showed significant benefits associated with 2 g/d
E-EPA and 6.6 g/d of EPA+DHA, respectively;27,33 the
significant clinical effect reported by Su, et al. was associated with a
significant increase in RBC EPA exclusively in the active treatment group.33
However, we decided to forego meta-analysis due to study differences on
the basis of the intervention (i.e., type, dose, followup length) and
comparator (i.e., placebo source). Also,
unlike the other two trials, Peet, et al.'s did not formally identify patients
with a depressive disorder.2 This
may account for their finding that 1 g/d E-EPA had a beneficial effect on
depressive symptomatology.2 A
low dose might not have helped the treatment-resistant depressive disorders
investigated in the other RCTs. Yet,
this likely cannot explain why Peet, et al.'s higher doses (2 g/d, 4 g/d) did
not likewise ameliorate depressive symptoms, or why more responders (i.e., 50%
improvement) were found in the placebo group than in the 2 g/d E-EPA
group. Su, et al.'s trial may have been
confounded by uncontrolled combinations of medication.33 The
question of omega-3 fatty acids as supplemental treatment for depression
requires additional investigation.
Two studies, one RCT38 and one defined merely as
"controlled,"45 evaluated the supplemental
treatment of bipolar disorder.
Only the RCT report gave us an opportunity to assess its study
parameters and results.38 While it had to be stopped prematurely, their
very high dose of 9.6 g/d EPA+DHA produced a significantly longer period of
remission in the active treatment group compared with controls. This study's limitations (i.e., loss of power
due to its stoppage; broken blind) require its replication. Therefore, the evidence base is too limited
to allow us to conclude anything about the value of omega-3 fatty acids as
supplemental therapy for bipolar disorder.
Likewise, one underpowered and flawed crossover RCT, which failed to
show that E-EPA is effective as supplemental treatment for obsessive-compulsive
disorder, is insufficient to permit drawing a definitive conclusion.25
Inconsistencies in the results produced by
three RCTs, the occasional use of a complex intervention making it impossible
to tease out the possible specific benefit of omega-3 fatty acids,46 the confirmation by
parents—but not by professionals—of an AD/HD diagnosis,46 interventions that did not
last long enough,30,42,46 and failures to weight-adjust doses of omega-3
fatty acids prevent us from identifying clear conclusions about their value as
supplemental treatment for AD/HD.30,42,46
Three of four good quality placebo-controlled
RCTs investigating the supplemental treatment of schizophrenia26,35-37 reported significant clinical effects in favor
of EPA using total PANSS scores,26,36,37 although Peet, et al.'s study observed this
effect only for those receiving clozapine as primary treatment.36 Emsley, et al.'s RCT also found that the
reduction in PANSS total scores associated with E-EPA supplementation was
greater in patients taking clozapine.
However, the latter's placebo-controlled difference only approached
being statistically significant.26 Results of our meta-analysis of two studies'
PANSS total data revealed that dose influenced outcome. A significant placebo-controlled effect was
identified for 2g/d EPA yet not for doses of at least 3g/d EPA.36,37 However, these results might have been
different had we been able to analyze data by type of psychotropic medication,
had both studies used either the purified or unpurified form of EPA as well as
the same placebo oils, had their intervention periods lasted longer, or had
both trials employed capsules to deliver the omega-3 fatty acids. While the findings are suggestive, they
remain inconclusive given that the data subjected to meta-analysis were derived
from two small trials exhibiting certain limitations.
Primary Prevention (i.e., Onset) Via Omega-3 Fatty Acid Intake
Inconsistent results, in addition to too few
studies exhibiting sound methodologies or research designs that are ideally
suited to investigate this question (e.g., prospective, controlled, with
subject-level data), suggest that it is too early to conclude whether or not
the intake of omega-3 fatty acids protects against the onset of depressive
disorders or symptomatology.1,24,28,47-55 The same issues prevent us from concluding
whether or not the intake of omega-3 fatty acids protects against the onset of suicidal
ideation or behavior.51,55 Given the inability of any cross-national
ecological analysis to provide meaningful subject-level data, and the failure
to control for key confounders (i.e., socioeconomic status, urban/rural ratio,
educational level, marital status, alcohol consumption, smoker status or family
history), we cannot conclude anything about the value of seafood consumption as
protection against the onset of bipolar disorder.56
Two RCTs failed to clarify the protective value
of omega-3 fatty acid intake with respect to the onset of symptoms, not
disorders, of anxiety.28,47 However, these small studies do not
constitute optimal tests of this potential.
Based on one cross-sectional study, which controlled for age, income,
smoking, alcohol consumption and eating patterns, mental health difficulties
were more prevalent in those consuming no fish.57 However, this design precludes inferring a
causal link between fish consumption and the onset of mental health difficulties.
Four RCTs,28,39,40,58 three of which enrolled healthy volunteers,
one single population cross-sectional survey59 and one cross-national
ecological analysis60 studied the possible
association between omega-3 fatty acid intake and the onset of tendencies or
behavior with the potential to harm others.
Overall, their findings are too inconsistent and involve too few
research designs permitting the drawing of causal inferences or too many
different definitions of the exposure, population or outcome to permit us to
draw a consistent, individual/patient-level conclusion regarding the value of
omega-3 fatty acid intake to protect against tendencies or behavior with the
potential to harm others.
Research designs were not identified which—due
to their prospective and controlled nature—are most appropriate for addressing
the question of the possible relationship between intake of omega-3 fatty acids
(e.g., via breastfeeding) and the onset of schizophrenia. Five case-control designs,22,61-64 one single prospective cohort65 and three cross-national
ecological analyses50,56,66 were found.
The only prospective study was not controlled, and its followup was very
short.65 Moreover, failures to control for confounders
were common (e.g., maternal feeding patterns, sex of children, maternal age,
socioeconomic status, early mother-infant contact). Thus, nothing definitive can be asserted
about a reliable association between omega-3 fatty acid intake and the onset of
Secondary Prevention (i.e., Continuation, Recurrence) Via Omega-3 Fatty
One small, multiple-group cross-sectional study
revealing that, relative to healthy controls, AD/HD children consumed
significantly lesser amounts of LA and ALA is insufficient to permit us to
conclude anything definitive regarding the potential of these PUFAs to alter
the course, or continuation, of AD/HD.23 Likewise, a single RCT demonstrating that a
complex intervention including omega-3 fatty acids—whose independent effect
could not be ascertained—provided young adult prisoners with some protection
against committing new offences29 is insufficient to determine
its capacity to prevent the recurrence of tendencies or behavior with the
potential to harm others (i.e., antisocial behavior).29
Primary Prevention (i.e., Onset) Via Lipid Biomarker Content
Inconsistent results as well as too few studies
exhibiting sound methodologies (e.g., protection against selection bias;
control for smoking, alcohol use, and psychotropic medication) or research
designs (e.g., prospective, controlled) that are ideally suited to investigate
this question suggest that it is too early to conclude whether or not omega-3
fatty or omega-6/omega-3 acid content in biomarkers protects against the onset
of depressive disorders or symptomatology. One RCT24 and seven multiple-group
cross-sectional studies1,67-72 were included.
The inconsistency in findings across two
multiple-group cross-sectional studies,73,74 which is potentially attributable to the fact
that the studies obtained their PUFA samples from different biomarker sources,
in addition to the recognition that this type of research design is less than
an ideal test of the research question, and the observation that the studies
failed to control for different key confounders together indicate that nothing
definitive can be concluded about the ability of specific lipid biomarker
content to protect against the onset of bipolar disorder. Irrespective of the limited agreement in
observing that both ALA and total omega-6 fatty acid levels in plasma
phospholipids were significantly lower in anorexic patients compared with
controls, the use of cross-sectional designs in two small studies prevent the
drawing of causal inferences regarding the role of lipid biomarker content in
the onset of anorexia nervosa.75,76 Inconsistent findings from three
multiple-group cross-sectional studies whose designs are of limited use in
investigating the research question,77-79 the failures to control for dietary intake,77 to formally rule out the
presence of psychopathology in the control subjects, or to employ formal
diagnostic criteria (i.e., DSM-III) to identify their hyperactive subjects78 made it impossible to draw
causal inferences about the role of omega-3 or omega-6/omega-3 fatty acid
content in biomarkers to prevent the onset of AD/HD.
Three multiple-group cross-sectional studies
examined the possible association of the onset of tendencies or behavior
with the potential to harm others with the omega-3 or omega-6/omega-3 fatty
acid content of biomarkers.80-82 Inconsistent results, small sample sizes, and
the exclusive use of cross-sectional designs preclude deriving clear inferences
regarding etiology. Two multiple-group
cross-sectional studies investigated the possible association of the onset of alcoholism
with the omega-3 or omega-6/omega-3 fatty acid content of biomarkers.83,84 However, conflicting results and the use of
cross-sectional designs do not allow us to draw conclusions regarding this
possible etiology of alcoholism.
While medication status may have had somewhat
of an influence on between-group differences in RBC or plasma phospholipid
fatty acid content when the comparison group was healthy controls, because
these data were obtained exclusively from twelve, multiple-group
cross-sectional studies74,85-95 or two single prospective cohort studies with
methodologic flaws,96,97 no meaningful possibility exists to permit
drawing causal inferences regarding patterns of lipid biomarker content and the
onset of schizophrenia. The same
criticism relating to cross-sectional designs applies to the single study
examining biomarkers data with respect to the onset of autism.98
Secondary Prevention (i.e., Continuation, Recurrence) Via Lipid Biomarker
This question could not be evaluated since
studies meeting eligibility criteria were not identified.
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A notable safety profile (i.e., beyond
occasional and mild discomfort) for any type or dose of omega-3 fatty acid
supplementation was not observed.
Overall, other than for the topics of schizophrenia and depression, few
studies were identified.
Only with respect to the supplemental treatment
of schizophrenia is the evidence even somewhat suggestive of omega-3 fatty
acids' potential as short-term intervention.
However, these meta-analytic results exclusively pertaining to 2 g/d EPA
require replication using design and methods refinements. Additional research might reveal the
short-term or long-term therapeutic value of omega-3 fatty acids.
One study demonstrating a significant
placebo-controlled clinical effect related to 1 g/d E-EPA given, over 12 weeks,
to 17 patients with depressive symptoms—rather than depressive disorders—cannot
be taken to support the view of the utility of this exposure as a supplemental
treatment for depressive symptomatology or disorders. Nothing can yet be concluded concerning the
clinical utility of omega-3 fatty acids as supplemental treatment for any other
psychiatric disorder or condition, or as a primary treatment for all
psychiatric disorders or conditions examined in our review. Primary treatment studies were rare.
Much more research, implementing design and
methods improvements, is needed before we can begin to ascertain the possible
utility of (foods or supplements containing) omega-3 fatty acids as primary
prevention for psychiatric disorders or conditions. Studies of omega-3 fatty acids' primary
protective potential in mental health could be "piggybacked" onto longitudinal
studies of their impact on general health and development.
Overall, almost nothing is known about the
therapeutic or preventive potential of each source, type, dose or combination
of omega-3 fatty acids. Likewise,
limitations within the evidence base prevented us from identifying the influence
of key covariables (e.g., smoking, alcohol use, psychotropic medication) on the
relationship between omega-3 fatty acid content and clinical outcomes.
Because of limited study designs, little is
known about the relationship between PUFA biomarker profiles and the onset of
any psychiatric disorder or condition.
Studies examining the possible association between the intake of omega-3
fatty acids, or the PUFA content of biomarkers, and the continuation or recurrence
of psychiatric disorders or conditions were virtually nonexistent.
If future research is going to produce data
that are unequivocally applicable to North Americans, it will likely need to
enroll either North American populations or populations exhibiting a high
omega-6/omega-3 fatty acid intake ratio similar to what has been observed in
the diet of North Americans.
Furthermore, if a reasonable view is that omega-3 fatty acids may play a
role in mental health, then given the observed or proposed inter-relationships
among omega-3 and omega-6 fatty acid contents both in the human diet and
metabolism, it may behoove researchers to investigate the possible therapeutic
or preventive value of the dietary omega-6/omega-3 fatty acid intake
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Availability of Full Report
The full evidence report from which this summary was taken was prepared for the Agency for Healthcare Research and Quality (AHRQ) by the University of Ottawa Evidence-based
Practice Center under Contract No. 290-02-0021. Requesters should ask for Evidence Report/Technology Assessment No. 116, Effects of Omega-3 Fatty Acids on Mental
The Evidence Report is also online on the National Library of Medicine Bookshelf, or can also be downloaded as a PDF File (3.6 MB). Plugin Software Help.
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