About 13 percent of older individuals have symptoms of depression, and other researchers have speculated that vitamin D may be linked to depression. Underlying causes of vitamin D deficiency such as less sun exposure as a result of decreased outdoor activity, different housing or clothing habits and decreased vitamin intake may be secondary to depression, but depression may also be the consequence of poor vitamin D status. Moreover, poor vitamin D status causes an increase in serum parathyroid hormone levels. Overactive parathyroid glands are frequently accompanied by symptoms of depression that disappear after treatment of the condition. We recently measured blood levels of vitamin D and parathyroid hormone and assessed symptoms of depression among 1,282 community residents age 65 to 95 and found a strong decrease in vitamin D level and increase in parathyroid hormone level (Hoogendijk et al., Arch Gen Psychiat 2008;65(5):508-512). This finding may be important to patients because both low blood vitamin D levels and high parathyroid hormone levels can be treated with higher dietary intake of vitamin D or calcium and increased sunlight exposure. Moreover light treatment has been used successfully to treat seasonal affective disorder. Taking these two lines of studies together, sunlight may have an antidepressant effect via the eye-biological clock tract and via the skin-vitamin D-tract. Interestingly, the biological clock is located in the hypothalamus, where vitamin D receptor is most abundant.

The objective of the present study was to examine the cross-sectional relation between serum 25-hydoxyvitamin D (25(OH)D) levels and depression in obese subjects, and to assess the effect of vitamin D supplementation on depressive symptoms. 441 subjects (body mass index 28 - 47 kg/m2, 159 men and 282 women, aged 21 - 70 years) were recruited by advertisements or from the out-patient clinic at the University Hospital of North Norway, and in a double blind controlled trial randomized to 20.000 or 40.000 IU vitamin D per week versus placebo for 1 year.

Subjects with serum 25(OH)D levels < 40 nmol/L scored significantly higher (more depressive traits) than those with serum 25(OH)D levels ≥ 40 nmol/L on the Beck Depression Inventory (BDI) total (6.0 (0 - 23) versus 4.5 (0 - 28) (median and range)) and the BDI subscale 1 - 13 (2.0 (0 - 15) versus 1.0 (0 - 29.5)) (P < 0.05). In the two groups given vitamin D, but not in the placebo group, there was a significant improvement in BDI scores after one year. There was a significant decrease in serum parathyroid hormone in the two vitamin D groups, without a concomitant increase in serum calcium.

It appears to be a relation between serum levels of 25(OH)D and symptoms of depression. Supplementation with high doses of vitamin D seems to ameliorate these symptoms, indicating a possible causal relationship.

Our group has pioneered research indicating that Developmental vitamin D (DVD) deficiency (a candidate risk factor for schizophrenia) alters both brain development and function. We have convergent evidence indicating a disturbance in dopamine signalling in this model. 1stly the superior colliculus (the proto-basal ganglia) is the initial site where the vitamin D receptor is expressed in foetal brain; 2ndly we show a reduction in Catechol-O-methyl transferase (a major metabolic enzyme for dopamine) in these foetal brains; 3rdly dopamine metabolites in the DVD deplete neonatal brain reflect this enzymatic change. When we allow these animals to mature under vitamin D normal conditions we repeatedly observe alterations in both spontaneous and psychomimetic enhanced locomotion. Consistent with the theme of persistent changes in dopamine signalling in this model we now present new data showing that dopamine transporter density and/or affinity are altered in DVD deplete female offspring whilst DA 1 receptor density and dopamine cell number are reduced in DVD deplete male offspring (all P< 0.05 n>8).

Our most recent studies indicate that Nurr-1, a nuclear transcription regulator important in both bone and dopamine neuron development and survival may be a molecular mediator of these processes. Nurr-1 is upregulated by parathyroid hormone (PTH). PTH levels are 2-3 fold greater in vitamin D deficient Dams across gestation. Most importantly we have just shown that Nurr-1 is dose-dependently upregulated by parathyroid hormone (PTH) in a neuroblastoma cell line.

Experience-dependent changes in synaptic connectivity are thought to play a vital role not only in memory formation, but also in long-term adaptive responses involved in mood regulation, reward behavior, and pain control. The neurotrophin, brain-derived neurotrophic factor (BDNF), which has recently been implicated in memory formation and aspects of major depression, is also an important regulator of long-term synaptic plasticity in the adult mammalian brain. We have investigated BDNF function in the dentate gyrus, a brain region implicated in depression and the action of antidepressant drugs. Local infusion of BDNF into the dentate gyrus generated a long-term potentiation (LTP) of synaptic efficacy at medial perforant path-granule cell synapses. This LTP is associated with expression of the immediate early gene, Arc, in postsynaptic granule cells and transport of Arc mRNA to synaptic regions on dendrites. Using local infusion of antisense oligodeoxynucleotides to block Arc synthesis, we show that Arc is required for the induction and time-dependent consolidation of BDNF-induced LTP. The sustained synthesis of Arc during a critical time-window is required for local expansion of the actin cytoskeletal network in dendritic spines. These results identify Arc as a critical mediator of BDNF in long-term synaptic plasticity in the adult brain. Microarray expression profiling has further revealed a panel of genes that, like Arc, are strongly upregulated following acute BDNF infusion or chronic treatment with the antidepressant fluoxetine.

Recent investigations have implicated brain-derived neurotrophic factor (BDNF) in pathogenesis and treatment of psychiatric disorders. Studies in patients with major depression have demonstrated significant decline of serum BDNF concentration that correlated to the severity of depressive symptoms and restored to normal values after chronic treatment with antidepressants (Gervasoni et al., 2005). The involvement of BDNF in anxiety disorders has been less clear. Preliminary studies in patients with panic disorder did not find any changes in serum BDNF levels (Kobayashi et al., 2005) or associations with its gene polymorphisms (Lam et al., 2005). These findings are at odds with data from animal studies consistently confirming the involvement of BDNF in the regulation of anxiety-like behaviours. For example, decreased BDNF levels in the amygdala had provoked anxiety-like behaviors in rats (Pandey et al., 2006), whereas BDNF mRNA levels in this region significantly increased in response to higher stress (Aguilar-Valles et al., 2005). Moreover, Govindarajan et al. (2006) have shown that transgenic over-expression of BDNF may facilitate anxiety-like behavior, magnitude of which was positively related to BDNF levels in the dorsal hippocampus in another study using the elevated plus maze (Yee et al., 2007). Considering these conflicting data between animal and human studies we assumed that using experimental challenge in healthy subjects could shed more light on the role of BDNF in anxio- and panicogenesis. Our recent findings suggested a general involvement of BDNF in the regulation of anxiety rather than a specific role of BDNF in disposition to panic attacks.

Neural cell adhesion (NCAM) plays important roles in the structural and functional plasticity in the CNS. Recent years much attention was put on the role brain plasticity in relation to depressive state. Mice deficient in NCAM molecule demonstrated signs of depression-like behavior in the tail suspension- and sucrose consumption tests. Analysis of hippocampal neurogenesis in NCAM deficient mice revealed a reduced survival of the newborn cells and their differentiation into calbindin-positive granule neurons. NCAM-deficient mice have also demonstrated reduction of CREB phosphorylation in the basolateral nucleus of amygdala, pre- and frontal cortex and CA3 regions of hippocampus. Since BDNF signaling system plays a significant role in the mechanisms of depression and in the effects of antidepressants, we measured the levels of BDNF and the level of phosphorylation of TrkB receptor in the brain of NCAM-/- mice. Experiments demonstrated a reduced BDNF signaling in the brains of NCAM-/- ice as a reduced level of phosphorylated Trk B receptor evidenced it. The depression-like signs in NCAM-/- mice were reversed by the NCAM-mimetic peptide FGL. In addition, repeated FGL administration enhanced survival of the newly generated cells in the dentate gyrus of NCAM-/- mice. Our data suggest that reduced brain plasticity due to deficiency in NCAM plays a role in the development of depressive state and NCAM mimetic peptide FGL might represent a new class of drugs with antidepressant activity.

Recent publications by the Institute of Medicine have unearthed several fundamental flaws in clinical trial methodology that, if corrected by the next generation of clinical investigators, can transform the field of mental health intervention research. Using a clinician-friendly approach, this workshop will succinctly review the essential elements of optimal design and implementation of a randomized controlled clinical study and the strategies to enhance signal detection. These include minimizing bias in the estimate of treatment effect while maintaining a nominal level of type I error (i.e., false positive results) and maintaining sufficient statistical power (i.e. reducing the likelihood of false negative results). Particular attention will be paid to reducing the problems of attrition and the hazards of multiplicity. Methods to examine moderators of the treatment effect will also be explored. Examples from psychopharmacologic, psychotherapy, and vocational rehabilitation trials for the treatment of posttraumatic stress disorder, depression, and panic disorder will be provided to illustrate these issues. Techniques to reduce the study's costs, risks, and participant burden will be described. Following the didactic session, the participants are encouraged to bring forth their own questions regarding clinical trial design for a 45-minute interactive discussion with the presenters. The objectives of the workshop are to improve the participants’ understanding of the goals of clinical trial design and methods to achieve those goals in order to improve their own research techniques, grantsmanship, and abilities to more accurately judge the results of studies presented in the literature.

Recent publications by the Institute of Medicine have unearthed several fundamental flaws in clinical trial methodology that, if corrected by the next generation of clinical investigators, can transform the field of mental health intervention research. Using a clinician-friendly approach, Dr. Davis will succinctly review the essential elements of optimal design and implementation of a randomized controlled clinical study. These elements include the need for a hypothesis that has clinical relevance based on sound theoretical reasoning, reasonable and generalizable inclusion and exclusion criteria, feasibility of an enrollment goal and study time-line, and appropriate choice of a comparator intervention and primary outcome. Techniques to reduce the study's costs, risks, and participant burden will be described. Examples from psychopharmacologic, psychotherapy, and vocational rehabilitation trials for the treatment of posttraumatic stress disorder will be discussed. Following the didactic session by the two presenters, the participants will be encouraged to bring forth their own questions regarding clinical trial design for a 45-minute interactive discussion with the presenters. The objectives of the workshop are to improve the participants’ understanding of the goals of clinical trial design and methods to achieve those goals in order to improve their own research techniques, grantsmanship, and abilities to more accurately judge the results of studies presented in the literature.

Dr. Leon will present the biostatistical considerations that contribute to a clinical trial design and the strategies to enhance signal detection. These include minimizing bias in the estimate of treatment effect while maintaining a nominal level of type I error (i.e., false positive results) and maintaining sufficient statistical power (i.e. reducing the likelihood of false negative results). Particular attention will be paid to reducing the problems of attrition and the hazards of multiplicity. Methods to examine moderators of the treatment effect will also be explored. Examples from psychopharmacologic and psychotherapy trials for the treatment of depression and panic disorder will be provided to illustrate these issues. Following the didactic session, the participants will be encouraged to bring forth their own questions regarding clinical trial design for a 45-minute interactive discussion with the presenters. The objectives of the workshop are to improve the participants’ understanding of the goals of clinical trial design and methods to achieve those goals in order to improve their own research techniques, grantsmanship, and abilities to more accurately judge the results of studies presented in the literature.

We discuss about psychiatric and psychological expertise exams and about the assessment of competence in the elderly and ethical aspect of care and research in elderly demented or not demented people and about involuntary commitment of incompetent patients.

We also refer to the complications and difficulties when trying to apply the civil commitments compulsive hospital admission measure, foreseen in the law for mental health, when the dementia diagnostic falls within this age group. Historically, involuntary commitment of incompetent patients took in the consideration the best interest of the patient, but also the well-being of the family and the potential risk for others.

After a short review of legislation and of conditions of hospitalization concerning involuntary commitment of the mentally ill people during our history before and after 1989, we'll analyze the activity on involuntary commitment in a Forensic Psychiatry Hospital in district Bihor, in last five years from a 30 years experience working in the field. Standards and practice in our country regarding the involuntary commitment have been changed more that three times after the second War and has been improved in 2002, when there appeared the new Mental Health Law, emphasizing protection of patients’ rights. There are legal and ethical limits to involuntary hospitalisation, because involuntary treatment and hospitalisation restricts a person's liberty. There should be a lot of things to do to improve the quality standards: improvement of elementary care needs, improvement of their quality of life.

The number of older people in prison has quadrupled in the UK in recent years, such that older prisoners now make up 2.6% of the total prison population, despite the fact that the number of offences committed by older adults has remained static. Older prisoners have high levels of psychiatric and physical morbidity, and forensic psychiatric services are receiving increasing numbers of referrals of older adults. In the past, few of these referrals resulted in admissions to secure psychiatric beds, however, reflecting a reluctance by forensic psychiatrists to admit older adults, who were perceived as being at risk from younger patients. Over the past 10 years, however, specialist secure inpatient units have been established in the UK for the assessment and management of older mentally disordered offenders. This seminar will explore the research evidence and clinical experience relating to this group of patients.

The patient with a narcissistic personality disorder may be among the most difficult patients in the clinician's caseload to treat. They may take more time in therapy, more of the theraapist's energy, and overwhelm the therapist's ability to dea;l with the countertransference. Given their self-serving and demanding style, they are more frequently "sent" to therapy than electing to come for treatment. Thus the morivation for therapy and for change is severely limited. The patient's ability to establish a working therapeutic bond is also limited by the very nature of their disorder. Given all of this they can be treated. The active, directive, structred, and problem oriented facets of Cognitive Behavior Therapy make this model an ideal treatment modality. Helping the patient to examine what is in their best personal interest, the therapy proceeds by examining the patienbt's thoughts, feelings, and behaviors.

The present study explored the moderator role of depression in the relationship of self esteem and the direction of social comparison in the context of marital relationships among married couples. The relationship between the direction of social comparison and depression was also explored. The sample consisted of 100 married individuals (50 Married Couples) having diverse educational and occupational background and form all the three socio economic background. The sample was taken from different cities of Pakistan. The couples were requested to complete Beck Depression Inventory (BDI) and Index of Self Esteem (ISE) along with another scale, Social Comparison in Marital Relationship Measure (SCMRM). SCMRM was developed by the researcher to explore the couples’ inclination of comparing their spouses with others around them on different dimension of marital relationship satisfaction. The standardized method was used for the development of SCMRM. The study provided evidence of significant negative relationship of depression with social comparison in marital relationship and with self esteem. The findings also supported the hypothesis that depression will play a role of moderator in the relationship between direction of social comparison in marital relationship and self esteem. Beck's (1967) cognitive model of depression suggested that depressives’ systematic bias against the self is reflected in their tendency to compare themselves with better off others. Thus our results confirm the cognitive depressive model which proposed that depressives engage in dysfunctional social comparison (upward).

The founders of Positive Psychology promoted the study of the "positive end" of human functioning such as happiness, strengths, virtues etc". One of the major findings of a decade of research on the positive side of human behavior, cognitions and emotions is that the positive aspects are qualitatively different from the negative aspects on a number of dimensions (e.g., negative emotions occur automatically whereas one has to be active in order to produce positive emotions). Hence, we propose a new approach to psychotherapy that is based on current conceptualization of positive psychology: Applied Positive Psychology Therapy (APPT). It is a meta theory for a therapeutic approach based n positive psychology principles. More specifically, APPT is based on the following assumptions:

1. 1. The long range goals of most human beings are to feel good and be psychologically satisfied.

2. 2. Failures to materialize these goals are not a function of deep seated pathologies but lack of skills or knowledge how to materialize these goals.

3. 3. The goal of therapy is not to cure clients from their pathologies (i.e., the "causes" of their anxieties, phobia, or aggression) but to train them in self-control skills and other skills that would enable them to achieve psychological well being in the most effective way and in harmony with their long range goals.

Contrasting with the invalidation social phobia with an early beginning may have, research on cognitive-behavioural conceptualization and treatment in children and adolescents with social phobia is scarce.

In our presentation, we will propose a new treatment protocol for adolescents with social phobia, based on the most widely accepted conceptualization model of social phobia in adulthood - Clark & Wells, 1995 - taking into consideration idiosyncrasies in this age group, and also incorporating a positive and acceptant attitude towards themselves and their symptoms, and a curiosity attitude in the changing process. The aim is not only to overcome their social phobia but also to enable the adolescents with a positive view of themselves and of their strengths to empower them to overcome other difficulties and to promote their self-determination, in order to pursue their life-long projects and values.

The lecture describes a school-based aggression reduction learning intervention. The intervention program aimed to impart children with learned resourcefulness repertoire for reducing aggressive behavior. Based on the self-control intervention model developed by Ronen and Rosenbaum (2001), and in light of positive psychology theory the intervention focused on increasing children's coping, teach them to work toward positive goals such as increasing social relationships, and help themselves change.

447 ninth grade students participated in this study. 167 students participated in the intervention groups and 280 students from the same schools who received no intervention and served as a control group.

The outcomes point to the efficacy of the model in reducing aggression. The rate of aggression in the intervention group decreased significantly in compare with their base-line grade and in compare with the control group. Also hostile thought and negative emotion did not change - the child could control those and not behave in an aggressive way. Analysis showed that the changed in reducing aggression results from the increase in self-control skills.