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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.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.033

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.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.034

FC31

A meta-analysis of gene

(5-HTT)

×

environment interactions in

eating pathology using secondary data

analyses

V. Rozenblat

1

, D. Ng

1

, M. Fuller-Tyszkiewicz

2

, K. Akkermann

3

,

D. Collier

4

, R. Engels

5

, F. Fernandez-Aranda

6

, J. Harro

7

,

A. Karwautz

8

, J. Homberg

9

, K. Klump

10

, S. Racine

11

, C. Larson

12

,

H. Steiger

13

, J. Richardson

14

, S. Stoltenberg

15

, T. van Strien

16

,

G. Wagner

8

, J. Treasure

17

, I. Krug

18 ,

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

( Fig. 1 ).

No other G

×

E interactions were significant,