European Psychiatry - Volume 33 - March 2016

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24th European Congress of Psychiatry / European Psychiatry 33S (2016) S72–S115 S83
Introduction Loneliness is a common emotional distress expe-
rience and there is increasing evidence of associations with
unhealthy lifestyle and adverse health-related factors. Little is
known about age and sex as potential effect modifiers, and about
the prevalence of loneliness.
Objective/aims To assess the associations of loneliness with
behavioral, physical and mental health factors, taking sex and age
into account and to examine the prevalence of loneliness in indi-
viduals aged 15+ years.
Methods Data from 20,007 participants of the cross-sectional
population-based Swiss Health Survey 2012 were analyzed. The
association of loneliness with lifestyle and health-related factors
were assessed with logistic regression analyses. Wald tests were
used to test for age and sex differences.
Results Loneliness was reported by 64.1% of individuals, and was
associated with smoking (OR 1.13, 95% CI 1.05–1.23), physical
inactivity (1.20, 1.10–1.31), non-adherence to the 5-a-day recom-
mendation for fruit and vegetable consumption (1.21, 1.07–1.37),
and more visits to a physician within the last year (1.29,
1.17–1.42). Loneliness was also associated with high cholesterol
levels (1.31, 1.18–1.45), diabetes (1.40, 1.16–1.67), self-reported
chronic diseases (1.41, 1.30–1.54), impaired self-perceived health
(1.94, 1.74–2.16), moderate and high psychological distress (3.74,
3.37–4.16), and depression (2.78, 2.22–3.48). Age modulated the
associations in BMI, smoking, visiting a physician within the past
year, and self-perceived health. Sex did generally not modulate the
associations.
Conclusion Loneliness is associated with unhealthy lifestyle, and
poorer physical and mental health. Associations were modulated
by age, but not sex. Further longitudinal studies are needed to elu-
cidate the causal relationships of these associations.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
Genetics and molecular neurobiology
FC30
Potential blood gene expression
markers for postpartum psychosis
M. Fuste
King’s College London, psychosis Studies, London, United Kingdom
Background Postpartum psychosis (PP) is the most severe psy-
chiatric disorder associated with childbirth. Previous evidence has
shown gene expression alterations in immune profile in women
with PP when compared with healthy postpartum women. How-
ever, no study has ever evaluatedwomen at riskwho do not develop
the disorder.
We conducted an exploratory analysis of a gene expression profile
that could distinguish women with PP episode (PPE) from women
at risk who do not develop PP (NPPE) after delivery.
Methods The sample was characterised by 24 women at risk of
PP of which n = 12 with PPE and n = 12 with NPPE and 21 healthy
women in the same postpartumperiod. FollowingMicroarray anal-
ysis, we assessed gene expression signature across the 3 groups
using ANOVA. We then studied Pathway analysis of genes differ-
ently expressed in PPE and PPE exploring canonical pathways and
upstream regulators using Ingenuity Pathway Analysis software.
Results Following an exploratory gene expression analysis we
identified 719 genes that are differently expressed across PPE and
NPPE. The PPE presented upregulation of several genes involved in
the inflammatory pathway and increased gene expression levels
of GRIA4, AKT3, SP4 and NRG1 genes, which have been previously
described in psychotic disorders. Moreover, 5 differently expressed
canonical pathways were identified including ones relevant to
development, mitochondrial formation and immune system.
Conclusion These preliminary results reveal the presence of
an immuno-neuro-endocrine dysregulation in postpartum psy-
chosis, with an upregulation of the immune system specific to
those women at risk who actually develop postpartum psychosis
episodes.
Disclosure of interest The author has not supplied his declaration
of competing interest.
FC31
A meta-analysis of gene
(5-HTT) × environment interactions in
eating pathology using secondary data
analyses
V. Rozenblat , D. Ng , M. Fuller-Tyszkiewicz , K. Akkermann ,
D. Collier , R. Engels , F. Fernandez-Aranda , J. Harro ,
A. Karwautz , J. Homberg , K. Klump , S. Racine , C. Larson ,
H. Steiger , J. Richardson , S. Stoltenberg , T. van Strien ,
G. Wagner , J. Treasure , I. Krug ∗
1 University of Melbourne, Psychological Sciences, Melbourne,
Australia
2 Deakin University, Psychology, Melbourne, Australia
3 University of Tartu, Psychological, Tartu, Estonia
4 King’s College London, Social Genetic and Developmental Psychiatry
SGDP, London, United Kingdom
5 Radboud University, Behavioural Science Institute, Nijmegen,
Netherlands
6 University of Barcelona, Bellvitge Hospital, Barcelona, Spain
7 University of Tartu, Psychology, Tartu, Estonia
8 Medical University of Vienna, Psychiatry, Vienna, Austria
9 Radbough University, Behavioural Sciences, Nijmegen, Netherlands
10 Michigan State University, Psychology, Michigan, USA
11 Ohio University, Psychology, Ohio, USA
12 University of Wisconsin-Milwaukee, Psychology, Wisconsin, USA
13 McGill, Psychology, Montreal, Canada
14 McGill University, Psychiatry, Montreal, Canada
15 University of Nebraska Lincoln, Psychology, Nebraska, USA
16 Radboud University, Behavioural Science Institute, Nijmegn,
Netherlands
17 King’s College London, Psychological Medicine, London, United
Kingdom
18 University of Melbourne, Psychology, Melbourne, Australia
∗ Corresponding author.
Background Gene × environment (G × E) interactions in eating
pathology have been increasingly investigated, however studies
have been limited by sample size due to the difficulty of obtaining
genetic data.
Objective To synthesize existing G ×E research in the eating dis-
orders (ED) field and provide a clear picture of the current state of
knowledge with analyses of larger samples.
Method Complete data from seven studies investigating com-
munity (n = 1750, 64.5% female) and clinical ( n = 426, 100% female)
populations, identified via systematic review, were included. Data
were combined to perform five analyses: 5-HTTLPR ×Traumatic
Life Events (0–17 events) to predict ED status (n = 909), 5-
HTTLPR× Sexual and Physical Abuse (n = 1097) to predict bulimic
symptoms, 5-HTLPR× Depression to predict bulimic symptoms
(n = 1256), and 5-HTTLPR ×Impulsivity to predict disordered eating
(n = 1149).
Results The low function (s) allele of 5-HTTLPR interacted with
number of traumatic life events (P < .01) and sexual and physical
abuse (P< .05) to predict increased likelihood of an ED in females
but not males No other G ×E interactions were significant,