- Email: [email protected]
E.05.02 European Psychiatric Association (EPA) guidance on suicide treatment and prevention
S156
E.05. The EPA Guidance Project: improving quality in European mental health care
References [1] Volkow ND, Wang GJ, Fowler JS, Telang F. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. 2008. Philos Trans R Soc Lond B Biol Sci. 363, 3191–3200. [2] Wang G-J, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, Netusil N, Fowler JS. 2001. Brain dopamine and obesity. Lancet. 357, 354–357. [3] Leshner AI. 1997. Addiction is a brain disease, and it matters. Science. 278, 45−47.
E.03.02 Obesity and the brain: how convincing is the addiction model? H. Ziauddeen1 ° , I.S. Farooqi2 , P.C. Fletcher1 1 University of Cambridge, Department of Psychiatry, Cambridge, United Kingdom; 2 University of Cambridge, Institute of Metabolic Science, Cambridge, United Kingdom The concept of food addiction, and its role in the obesity epidemic, now has a widely established and growing currency both in the scientific literature and the lay media. According to the more stringent version of this model, certain kinds of overeating e.g. binge eating, represent a phenotype that resembles drug addiction. Accordingly the case has been made that food addiction is characterized by neurobiological changes similar to those seen in drug addiction. We have previously argued that the neuroscientific literature supporting both the phenotypic model and its putative neurobiological concomitants is scant and at present there is little convincing empirical evidence for this model [1]. However we also acknowledge the need for a more comprehensive examination of the concept [2] to either validate it or disprove it, both from the clinical and scientific point of view and given the potential role it may play in the formulation of public health policy. Here we review the existing evidence for food addiction with a particular focus on the neuroscientific examination of the model in humans, which does not thus far support a food addiction model. We also examine how the drug addiction literature can inform the elaboration and more rigorous investigation of the model both in terms of the clinical phenotype and the underlying neurobiology. Finally we consider the implications of the food addiction model on the formulation of treatments and public health policy, with a particular focus on the associated risks of a premature acceptance of the model on these issues [3]. References [1] Ziauddeen H, Farooqi IS, Fletcher PC. Obesity and the brain: how convincing is the addiction model? Nat Rev Neurosci. 2012 Mar 31; 13(4): 279−86. [2] Ziauddeen H, Farooqi IS, Fletcher PC. Food addiction: is there a baby in the bathwater? Nat Rev Neurosci. 2012 Jul 1; 13(7): 1. [3] Ziauddeen H, Fletcher PC. Is food addiction a valid and useful concept? Obesity Reviews. 2013; 14(1): 19−28. Disclosure statement: My Translational Medicine and Therapeutics PhD fellowship was jointly funded by the Wellcome Trust and GlaxoSmithKline. This work was carried out during the fellowship but was not connected in any way to my collaboration with GSK.
E.05. The EPA Guidance Project: improving quality in European mental health care E.05.02 European Psychiatric Association (EPA) guidance on suicide treatment and prevention D. Wasserman1 , V. Carli1 ° 1 Karolinska Insitutet, National Centre for Suicide Research and Prevention of Mental Ill-Health (NASP), Stockholm, Sweden Background: Suicide is a major public health problem in the WHO European Region accounting for over 150,000 deaths per year. Acute intervention for suicidal crises should start immediately in order to keep the patient alive. An underlying psychiatric disorder is present in up to 90% of people who completed suicide. Diagnosis: Comorbidity with depression, anxiety, substance abuse and personality disorders is high. In order to achieve successful prevention of suicidality, adequate diagnostic procedures and appropriate treatment for the underlying disorder are essential. Treatment: Existing evidence supports the efficacy of pharmacological treatment and cognitive behavioural therapy (CBT) in preventing suicidal behaviour. Studies show that antidepressant treatment decreases the risk for suicidality among depressed patients. However, the risk of suicidal behaviour in depressed patients treated with antidepressants exists during the first 10−14 days of treatment, which requires careful monitoring. Shortterm supplementary medication with anxiolytics and hypnotics in the case of anxiety and insomnia is recommended. Treatment with antidepressants of children and adolescents should only be given under supervision of a specialist. Long-term treatment with lithium has been shown to be effective in preventing both suicide and attempted suicide in patients with unipolar and bipolar depression. Treatment with clozapine is effective in reducing suicidal behaviour in patients with schizophrenia. Safety: A secure home, public and hospital environment, without access to suicidal means is a necessary strategy in suicide prevention. Prescription of medication and discharge of the patient from hospital should be carefully evaluated against the involved risks. E.05.03 EPA Guidance and the future of European psychiatry W. Gaebel1 ° 1 Heinrich-Heine Universit¨at, Klinik und Poliklinik f¨ur Psychiatrie und Psychotherapie, LVR-Klinikum D¨usseldorf, D¨usseldorf, Germany The European Guidance project provides a series of guidance documents on topics related to the quality of mental healthcare service structures and the prevention of mental disorders, for which evidence- and consensus-based guidelines are currently lacking. The “EPA Guidance on the quality of mental health services” as one of its components provides recommendations on structures and processes of mental healthcare services in European countries [1]. In a first step, a systematic literature research was conducted in order to detect all relevant evidence. The quality of evidence was graded by a three-part evidence grading system. In a second step, on the basis of the generated evidence, recommendations were developed and subjected to peer review within the work group, the Steering Committee of the EPA
E.05. The EPA Guidance Project: improving quality in European mental health care
References [1] Volkow ND, Wang GJ, Fowler JS, Telang F. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. 2008. Philos Trans R Soc Lond B Biol Sci. 363, 3191–3200. [2] Wang G-J, Volkow ND, Logan J, Pappas NR, Wong CT, Zhu W, Netusil N, Fowler JS. 2001. Brain dopamine and obesity. Lancet. 357, 354–357. [3] Leshner AI. 1997. Addiction is a brain disease, and it matters. Science. 278, 45−47.
E.03.02 Obesity and the brain: how convincing is the addiction model? H. Ziauddeen1 ° , I.S. Farooqi2 , P.C. Fletcher1 1 University of Cambridge, Department of Psychiatry, Cambridge, United Kingdom; 2 University of Cambridge, Institute of Metabolic Science, Cambridge, United Kingdom The concept of food addiction, and its role in the obesity epidemic, now has a widely established and growing currency both in the scientific literature and the lay media. According to the more stringent version of this model, certain kinds of overeating e.g. binge eating, represent a phenotype that resembles drug addiction. Accordingly the case has been made that food addiction is characterized by neurobiological changes similar to those seen in drug addiction. We have previously argued that the neuroscientific literature supporting both the phenotypic model and its putative neurobiological concomitants is scant and at present there is little convincing empirical evidence for this model [1]. However we also acknowledge the need for a more comprehensive examination of the concept [2] to either validate it or disprove it, both from the clinical and scientific point of view and given the potential role it may play in the formulation of public health policy. Here we review the existing evidence for food addiction with a particular focus on the neuroscientific examination of the model in humans, which does not thus far support a food addiction model. We also examine how the drug addiction literature can inform the elaboration and more rigorous investigation of the model both in terms of the clinical phenotype and the underlying neurobiology. Finally we consider the implications of the food addiction model on the formulation of treatments and public health policy, with a particular focus on the associated risks of a premature acceptance of the model on these issues [3]. References [1] Ziauddeen H, Farooqi IS, Fletcher PC. Obesity and the brain: how convincing is the addiction model? Nat Rev Neurosci. 2012 Mar 31; 13(4): 279−86. [2] Ziauddeen H, Farooqi IS, Fletcher PC. Food addiction: is there a baby in the bathwater? Nat Rev Neurosci. 2012 Jul 1; 13(7): 1. [3] Ziauddeen H, Fletcher PC. Is food addiction a valid and useful concept? Obesity Reviews. 2013; 14(1): 19−28. Disclosure statement: My Translational Medicine and Therapeutics PhD fellowship was jointly funded by the Wellcome Trust and GlaxoSmithKline. This work was carried out during the fellowship but was not connected in any way to my collaboration with GSK.
E.05. The EPA Guidance Project: improving quality in European mental health care E.05.02 European Psychiatric Association (EPA) guidance on suicide treatment and prevention D. Wasserman1 , V. Carli1 ° 1 Karolinska Insitutet, National Centre for Suicide Research and Prevention of Mental Ill-Health (NASP), Stockholm, Sweden Background: Suicide is a major public health problem in the WHO European Region accounting for over 150,000 deaths per year. Acute intervention for suicidal crises should start immediately in order to keep the patient alive. An underlying psychiatric disorder is present in up to 90% of people who completed suicide. Diagnosis: Comorbidity with depression, anxiety, substance abuse and personality disorders is high. In order to achieve successful prevention of suicidality, adequate diagnostic procedures and appropriate treatment for the underlying disorder are essential. Treatment: Existing evidence supports the efficacy of pharmacological treatment and cognitive behavioural therapy (CBT) in preventing suicidal behaviour. Studies show that antidepressant treatment decreases the risk for suicidality among depressed patients. However, the risk of suicidal behaviour in depressed patients treated with antidepressants exists during the first 10−14 days of treatment, which requires careful monitoring. Shortterm supplementary medication with anxiolytics and hypnotics in the case of anxiety and insomnia is recommended. Treatment with antidepressants of children and adolescents should only be given under supervision of a specialist. Long-term treatment with lithium has been shown to be effective in preventing both suicide and attempted suicide in patients with unipolar and bipolar depression. Treatment with clozapine is effective in reducing suicidal behaviour in patients with schizophrenia. Safety: A secure home, public and hospital environment, without access to suicidal means is a necessary strategy in suicide prevention. Prescription of medication and discharge of the patient from hospital should be carefully evaluated against the involved risks. E.05.03 EPA Guidance and the future of European psychiatry W. Gaebel1 ° 1 Heinrich-Heine Universit¨at, Klinik und Poliklinik f¨ur Psychiatrie und Psychotherapie, LVR-Klinikum D¨usseldorf, D¨usseldorf, Germany The European Guidance project provides a series of guidance documents on topics related to the quality of mental healthcare service structures and the prevention of mental disorders, for which evidence- and consensus-based guidelines are currently lacking. The “EPA Guidance on the quality of mental health services” as one of its components provides recommendations on structures and processes of mental healthcare services in European countries [1]. In a first step, a systematic literature research was conducted in order to detect all relevant evidence. The quality of evidence was graded by a three-part evidence grading system. In a second step, on the basis of the generated evidence, recommendations were developed and subjected to peer review within the work group, the Steering Committee of the EPA