Psychische Erkrankungen in der Lebensspanne ... - DGPPN

Topic 9 G Komorbidität von psychischen und somatischen Störungen, Psychosomatik // Comorbidity of psychic and somatic disorders, psychosomatics
Diskussion / Ergebnisse: In den Interviews zeigte sich, dass das
Gefühl, von der Transplantation profitiert zu haben, aber auch die
Beziehung zum Organ / Spender sowie bestimmte Merkmale der
Arzt-Patientenbeziehung das Complianceverhalten massgeblich
beeinflussen. Anhand der Fragebogen-Untersuchung liess sich u. a.
empirisch belegen, dass ein signifikanter Zusammenhang zwischen
einer problematischen Organintegration und Non-Compliance besteht.
Auf Grund dieser Studienergebnisse werden verschiedene
psychotherapeutischen Interventionen diskutiert, die insgesamt
auf eine psychische Integration der Transplantationserfahrungen
abzielen.
Donnerstag, 26. 11. 2009, 17.15 - 18.45 Uhr, Saal VIP 1
S-079 Symposium
The Selfish-Brain-Theory. The link between depression and
vascular disorders
Vorsitz: U. Schweiger (Lübeck), I. Heuser (Berlin)
001
New Aspects of the Selfish-Brain-Theory
Achim Peters (Universität zu Lübeck, Medizinische Klinik I)
Obesity and type 2 diabetes have become the major health problems
in many industrialized countries. A few theoretical frameworks
have been set up to derive the possible determinative cause
of obesity. One concept views that food availability determines food
intake, i. e. that obesity is the result of an external energy “push”
into the body. Another one views that the energy milieu within the
human organism determines food intake, i. e. that obesity is due to
an excessive “pull” from inside the organism. Here we present the
unconventional concept that a healthy organism is maintained by a
„competent brain-pull“ which serves systemic homeostasis, and
that the underlying cause of obesity is “incompetent brain-pull”, i. e.
that the brain is unable to properly demand glucose from the body.
We describe the energy fluxes from the environment, through the
body, towards the brain with a mathematical “supply chain” model
and test whether its predictions fit medical and experimental data
sets from our and other research groups. In this way, we show databased
support of our hypothesis, which states that under conditions
of food abundance incompetent brain-pull will lead to build-ups in
the supply chain culminating in obesity and type 2 diabetes. In the
same way, we demonstrate support of the related hypothesis, which
states that under conditions of food deprivation a competent brainpull
mechanism is indispensable for the continuance of the brain‘s
high energy level. In conclusion, we took the viewpoint of integrative
physiology and provided evidence for the necessity of brainpull
mechanisms for the benefit of health. Along these lines, our
work supports recent molecular findings from the field of neuroenergetics
and continues the work on the “Selfish Brain” theory
dealing with the maintenance of the cerebral and peripheral energy
homeostasis.
002
Cytokines and Allocation System in Depressive Disorder
Ulrich Schweiger (Universität zu Lübeck, Psychiatrie und Psychotherapie)
W. Greggersen, S. Rudolf
Introduction: Adipokines may link altered body composition and
increased risk for developing diabetes mellitus and cardiovascular
disease in patients with major depressive disorders (MDD).
Method: Twenty-three patients with typical and 8 patients with
240
atypical major depression (20 women, 11 men) underwent a hyper- /
hypoglycemic stepwise glucose clamp. Eight healthy women and
16 healthy men served as the comparison group (CG).
Discussion / Results: Mean glucose disposal rates (GDR) were
lower in patients with atypical MDD and typical MDD than in the
CG (2.4 ± 0.7 vs. 3.2 ± 0.9 vs. 4.1 ± 1.2 ml / h / kg, p< .001). Patients
with atypical MDD showed a higher mean concentration of leptin
(14.0 ± 8.6 ng / ml) than patients with typical MDD (3.6 ± 3.3 ng /
ml) and the CG (2.5 ± 2.0 ng / ml). MANCOVA with the covariate
BMI showed a significant group effect for leptin (F= 7.0; p= .002)
but not for visfatin or resistin. GDR correlated with leptin (r= -.40;
p= 0.003) and visfatin (r= -.50; p