Skip to main content
. Author manuscript; available in PMC: 2011 Mar 18.
Published in final edited form as: Front Biosci (Schol Ed). 2011 Jan 1;3:298–330. doi: 10.2741/s153

Table 3.

Influence of bioactive lipids on cognition: Clinical studies of psychosis

Study Study aims and design Sample Variables Results
G. P.
Amminger
et al.
(115)
Effect of n-3 PUFAs on
rate of progression to
first-episode psychotic
disorder in young
individuals with
subclinical psychosis.

Randomized, double-
blind, placebo-controlled
trial conducted from 2004
to 2007
81 individuals (13 – 25 yrs) at ultra-
high risk for psychotic disorder
IV:
Random assignment (stratified by
depression symptom score) to 12-week
treatment trial of:
(1) n-3 PUFA (1.2 g/day marine fish oil:
700 mg/day EPA, 480 mg/day DHA,
220 mg/day Other n-3 PUFAs including
α-linolenic acid)
vs.
(2) placebo (coconut oil)

DV:
(1) Conversion to psychotic disorder
determined by assessments conducted
weekly (first 4 wks), and then at 8 and
12 wks, and 6 and 12 mos.

(2) n-6 to n-3 ratio at baseline and 12-
wks (fasting erythrocyte FA
composition).
A. Cumulative rates of
conversion to psychotic
disorder at 12 mos.:
(1) 4.9% in n-3 PUFA group
(2) 27.5% in placebo group.

B. Compared to placebo, n-3
PUFAs improved functioning
and reduced positive, negative,
and general symptoms.

C. For n-3 PUFA group,
magnitude of change in n-6 to
n-3 ratio from baseline to 12
wks was significantly
associated with improvement
in functioning between
baseline and 12 wks.
G. E.
Berger et
al. (116)
Effect of n-3 FA
augmentation on efficacy
and tolerability of
treatment with
antipsychotic drugs in
patients with first-episode
psychosis (FEP).

Randomized, double-
blind, placebo-controlled
trial conducted from 2000
to 2003
80 FEP patients, which included 53
(76.8%) patients meeting criteria for
non-affective psychosis
IV:
12-weeks augmentation protocol:
(1) 2 g/d ethyl-eicosapentaenoic acid
(E-EPA)
vs.
(2) placebo oil
Both E-EPA and placebo were added on
to flexible doses of atypical
antipsychotics (risperidone, olanzapine,
or quetiapine). Additional medications
allowed: benzodiazepines,
chlorpromazine, zuclopenthixol,
zolpidem, SSRIs.

DV:
Clinical assessments conducted at 5
time points (baseline and weeks 3, 6, 9,
12):
(1) Symptom change scores and time to
first response
(2) Tolerability measures and
cumulative antipsychotic dose
A. No difference between E-
EPA and placebo groups for
symptom change scores at 12
weeks.

B. Time to first response was
shorter in patients diagnosed
with non-affective psychosis
and receiving E-EPA.

C. Patients receiving E-EPA
required lower doses of
antipsychotic medications
between weeks 4 and 6,
compared to patients receiving
placebo.

D. Patients receiving E-EPA
showed fewer extrapyramidal
side effects during the initial 9
wks, compared to patients
receiving placebo.
R.
Condray
et al. (43)
Association between RBC
membrane FAs and
cognition in
schizophrenia patients.

Repeated measures
design, double-blind
placebo-replacement.
37 chronic schizophrenia patients (mean
age = 38 yrs) tested during haloperidol
maintenance therapy (n=30) and
placebo replacement (n=21). (Different
n’s for medicated and placebo phases
due to electrophysiological artifact.)
DV:
(1) RBC membrane FAs (venous blood
draw after overnight fast)

(2) Cognition:
Electrophysiological measure of
semantic memory (N400 component of
event-related brain potential: N400-
Unrelated minus N400-Related words)
A. Semantic memory was
associated with AA and total
PUFAs for patients during
unmedicated (placebo) phase:
↑ N400 semantic priming
↓ AA and Total PUFAs

B. Semantic memory was not
significantly associated with
PUFAs for patients during
haloperidol maintenance
therapy.

Abbreviations for Table 3: ↑, increase; ↓, decrease; AA, Arachidonic acid; DHA, Docosahexaenoic acid; DV, Dependent variable; EPA, Eicosapentaenoic acid; FA, Fatty Acid; IV, Independent variable; PUFA, Polyunsaturated fatty acid; RBC, Red Blood Cell.