By L. Tangach. Cazenovia College. 2018.
It is well known that the gluco- ing characteristics of networks of neurons throughout corticoid and mineralocorticoid hormones buy pristiq 100mg mastercard symptoms whiplash, released the life cycle buy generic pristiq 100 mg medicine and health, while antidepressant treatments act to from the adrenal glands during stress, contribute to reverse such injurious effects. These findings suggest that the evidence that links up-regulation of these pathways behavioural effects of chronic antidepressants may and antidepressant activity comes from behavioural be mediated by the stimulation of neurogenesis in the models (Duman et al. Lithium, one of the most effective anti- mortem studies of depressed patients with or with- depressant potentiating agents, also increases out antidepressive treatment it was shown that there neurogenesis in the dentate gyrus (Chen et al. Other studies demonstrate that chronic clinical response to antidepressant treatment antidepressant treatment increases the rate of neu- (Russo-Neustadt et al. In addition, two studies (Neves-Pereira One of the most robust biological markers in et al. Several data decreased in depression, as indicated by a decreased show the importance of fibroblast growth factors maximal binding capacity (Bmax). These stimulate cell growth in many areas of the body, findings correspond to a decrease of maximal bind- and are involved in the growth of multiple tissues ing capacity of imipramine to brain tissue. A meta- and in growth that takes place at various stages of analysis by Ellis and Salmond (1994) has shown that life. They have potent effects during embryonic, imipramine binding to platelets is indeed a robust foetal and child development, and can modify the biological marker of depression. These studies have employed a number of trol subjects and was verified by quantitative real- different methods. The con- nection of hypertriglyceridemia and depression Lipids involves insulin resistance, as the ingestion of high The search for biochemical markers of depression glycemic food releases insulin which immobilizes has been particularly intense. Several studies have the modulation of essential fatty acid metabolism, searched for lipids as biological markers of depres- negatively impacting the production of prostaglan- sion. Examination accumulating evidence suggests that low or lowered of red cell membrane fatty acid profiling is reflec- cholesterol may be associated with increases of tive of long-term insufficiencies and imbalances in suicides and accidents. Plasma fatty acids reflect brain chemistry affect the lipid environment of the dietary intake of a few days duration rather than brain and modulate neurotransmitter action and metabolic conversion observed in fatty acids incor- function of neuronal proteins. Lipid and electrolyte abnormalities have istic patterns that may be addressed with lipid a marked impact on neuronal disturbance and manipulation with targeted fatty acids through ultimately, mood and behaviour. Brain function depends on of depression is often characteristic in the blood the organic metal constituents of the central ner- chemistry as low levels of cholesterol, iron, potas- vous system as well as lipids but the convergence of sium, albumin and nitrogen markers and elevation these systems occurs in the case of depression for of triglycerides. It has been People with low cholesterol scored significantly proposed that the Omega 6 to Omega 3 ratio higher on the Hamilton depression scale. Recent triglyceridemia-driven metabolic cause of depres- evidence has suggested an important role for lipids sion has also been demonstrated in controlled in the aetiology and treatment of depression (Ross clinical trials, showing that triglyceride lowering et al. Deficiencies of mechanisms involving the phospholipase A2 magnesium can provoke a wide range of psychiatric cyclooxygenase pathway, an important signalling symptoms related to depression, ranging from system, involved in the action of several neurotrans- apathy to psychosis (Rasmussen et al. Methylnicotinate-in- search on manic patients, on the other hand, has duced erythema was reduced in subjects with revealed elevated vanadium in the hair, significantly unipolar depression compared to controls at 5 min higher levels than those measured in both a control after application and it returned to normal after 15 group and a group of recovered manic patients min. Studies involving a large sample of psychiatric patients found that a large part of those tested had high levels of the milk protein b-casomorphin-7 in Nitrogen their blood and urine and defective enzymatic Macronutrients such as consumption of high quality processes for digesting milk protein. As mercury levels are re- indicated in the patients blood chemistry will duced the protein binding is reduced and improve- attenuate nitrogen retention. It is interesting to remember that the inhalation of mercury to proteins include the blockade of of nitrous oxide (laughing gas) may evoke the sulphur oxidation processes and neurotransmitters emotion of pleasure with the increase in nitrogen, (Stefanovic et al. Lithium protects synthases have not yielded any conclusive evidence brain cells against excess glutamate and calcium for their involvement in the pathogenesis of major (Rossi et al. In a inhibits macrophage and neutrophil defense against small sample of 15 subjects with major depression, candida by affecting Th1 and Th2 cytokine effects decreased plasma nitric oxide metabolite levels and (Perlingeiro and Queiroz 1994; Mathieson 1995; platelet endothelial nitric oxide synthase activity Hua et al. This enzyme Acute and chronically ill patients frequently become synthesizes noradrenaline, and low noradrenaline severely depressed and lose their will to live when can cause fatigue and depression. Mercury mole- serum potassium levels drop to below the low end cules can block all copper-catalysed dithiolane of the laboratory reference range. They also suggest that the dietary intake and Vitamins: folic acid psychopharmacological action of methionine, the Several cross-sectional studies have focused on the precursor of S-adenosylmethionine, should be stu- low blood folate levels of depressed patients. The limited is a cofactor in 1-carbon metabolism, during which available evidence suggests folate may have a it promotes the remethylation of homocysteine (a potential role as a supplement to other treatments cytotoxic sulfur-containing amino acid, that can for depression. Dietary folate is required for normal for those with folate deficiency (Taylor et al. Genetic and clinical data suggest roles for in those folate-deficient patients whose symptoms folate and homocysteine in the pathogenesis of were not related to folate deficiency. In returned to normal with folate treatment in the a large Finnish study, depressed patients in the patients exhibiting folate-responsive neuropsychia- general population with energy-adjusted folate in- tric signs. The data indicated a close association take below the median had a higher risk of getting a between folate-responsive neuropsychiatric symp- discharge diagnosis of depression during the follow- toms and changes in serotonin metabolism in the up period than those who had a folate intake above central nervous system (Botez et al. A low dietary intake of folate may be a larly, in another study, a subgroup of severely risk factor for severe depression (Tolmunen et al. These peripheral folate levels may be expected in patients observations provided further evidence of the links who commit violent suicide. In this respect, the between folate, biopterin and monoamine metabo- red-cell and serum folate levels in nine persons who lism in depression (Bottiglieri et al. Folate later committed suicide were compared with those deficiency, or inborn errors of folate metabolism, in age- and sex-matched control groups. However, cause reduced turnover of serotonin, and perhaps no significant difference between the groups was dopamine, in the central nervous system. Although one of been concluded that the mechanism by which the first biological treatments of a major psychiatric deficiency of 5-methyltetrahydrofolate causes re- disorder was the dietary treatment of pellagra, the duced 5-hydroxytryptamine and dopamine turnover use of diet and dietary components in the study of is unlikely to be mediated by S-adenosylmethionine psychopathology has not aroused much interest in (Surtees et al. Folic acid deficiency depression has been a low plasma and red cell causes a lowering of brain serotonin in rats, and of folate, which has also been linked to poor response cerebrospinal fluid 5-hydroxyindoleacetic acid in to antidepressants (Coppen and Bailey 2000).
Today pristiq 100mg with visa treatment xanthoma, a clinical understanding of male eja- culatory and orgasm disturbances is no longer possible without a basic under- standing of the neurophysiology order pristiq 50 mg on line 5 medications, neuropharmacology, and neuroanatomy of serotonergic neurons in the brain. Therefore, I will start off by giving you a general explanation and overview of serotonergic neurotransmission, serotoner- gic receptors and how animal sexual behavior determines our understanding of sexual psychopharmacology. After this basic pharmacological introduction, I will describe the ejaculatory disturbances in rank order of frequency in the general population. As most research in recent years has been focused on prema- ture ejaculation, it is inevitable that this disorder receives more attention than the other ejaculatory disorders. At the same time, the internal sphincter of the urinary bladder is closed, thereby prevent- ing retrograde passage of the semen into the bladder. Emission and bladder neck closure are mediated through the thoracolumbar sympathetic system. It is suggested that the sensation of ejaculatory inevitability parallels the emission phase. Male Ejaculation and Orgasmic Disorders 219 muscles of the urethra and contractions of the striated muscles of the pelvic oor (mainly bulbospongiosus muscles). Orgasm There is limited knowledge about the physiological mechanisms and neurobiol- ogy underlying the sensation of orgasm. The intense feelings of pleasure and desire accompanying orgasm are mediated by the brain. Serotonergic neurons originate in the raphe nuclei and adjacent reticular formation in the brainstem. A rostral part with cell-bodies in the midbrain and rostral pons projecting to the forebrain and a caudal part with cell-bodies predominantly in the medulla oblongata with projections to the spinal cord. In the forebrain and spinal cord, the serotoner- gic neurons contact other serotonergic neurons. The location of connection is the synaps, in which the neurotransmitter serotonin provides information from one neuron to another. After its fabrication in the cell-body, serotonin runs through the serotonergic neuron to the presynaptic membrane, through which it is released into the synaps. In the synaps, serotonin proceeds to receptors at the opposite neuron (postsynaptic receptors) and after it has contacted these receptors serotonin runs back to the presynaptic membrane. The process of serotonin release and its action on postsynaptic receptors is called serotonergic neurotransmission. There is normally a sort of equilibrium in the serotonergic neurotrans- mission system due to remarkable mechanisms. However, serotonergic neurotransmission becomes seriously disturbed by the action of serotonergic antidepressants. As a consequence, serotonin concentration increases outside the cell-body and in the synapses. This increased serotoneric neurotransmission exerts a stronger effect on all post- synaptic receptors. Male Ejaculation and Orgasmic Disorders 221 Neuroanatomy In recent years, much progress has been made in neuroanatomical research of eja- culatory processes. Most knowledge about the functional neuroanatomy of ejacu- lation is derived from male rat studies. On the other hand, brain areas activated as a result of the occurrence of one or more ejaculations have been observed in several mammals (9). The func- tional signicance of this ejaculation-subcircuit is still poorly understood but it might well be that these areas play a role in satiety and thus mediate the post- ejaculatory interval. Truitt and Coolen (13) highlighted the role of the lumbar spinal cord in the processing of ejaculation. These and other animal studies have clearly shown the existence of a neural circuitry for ejaculation in mammals. Positron Emission Tomography-Scan Studies in Humans Although male rat studies are of utmost importance for a better understanding of the neurobiology of ejaculation, brain imaging studies in humans are the tools which provide a better understanding of how the human brain mediates ejacula- tion and orgasm. Brain imaging studies will probably lead to a deeper insight into which parts of the brain mediate ejaculation and which parts are involved in the mechanism of orgasm, how these neural areas are linked to each other, and which parts are disturbed in the different ejaculatory and orgasm disturbances. Eleven healthy male volunteers were brought to ejaculation by manual stimulation of their female partner. Male Ejaculation and Orgasmic Disorders 223 all the activations of these various cortical areas is not yet clear. Further studies need to clarify whether associated sensations of orgasm are mediated by these cortical areas. Unexpectedly, a very strong activation was found in parts of the cerebellum, the meaning of it remaining unclear. Decreased blood ow, and thus less activity was found in the amygdala during sexual arousal, erection, and ejaculation. This may perhaps indicate that the brain looses a state of anxiety or fear during sexual activity. Hypothalamic involvement, as has been demonstrated in animal sexual behavior, has not been found in these male volun- teers. During the last century, prema- ture ejaculation has been considered from both a medical and a psychological view, often resulting in contrasting psychotherapeutic and drug treatment approaches. For a better understanding of the current debate regarding its etiol- ogy and treatment, it is important to consider the history of how clinicians thought about and treated premature ejaculation. History Waldinger (5,15) distinguishes four periods in the approach to and treatment of premature ejaculation. The First Period (18871917): Early Ejaculation In 1887, Gross (16) described the rst case of early ejaculation in medical litera- ture. Although publications were rare, it is worth noting that during the rst 30 years of its existence in the medical literature, early ejaculation was viewed as an abnormal phenomenon but not signicantly as a psychological disturbance.
Pre-Sleep Conditions: Patients with insomnia may de- ety pristiq 100 mg on line abro oil treatment, frustration generic pristiq 100mg online treatment zoster ophthalmicus, sadness) may contribute to insomnia and should velop behaviors that have the unintended consequence of per- also be evaluated. Daytime Activities and Daytime Function: Daytime strategies to combat the sleep problem, such as spending more activities and behaviors may provide clues to potential causes time in bed in an effort to catch up on sleep. Sleep-Wake Schedule: In evaluating sleep-related sleepiness should prompt a search for other potential sleep symptoms, the clinician must consider not only the patients disorders. However, these exams may Pulmonary Theophylline, albuterol provide important information regarding comorbid conditions Alcohol and differential diagnosis. A physical exam should specifcally evaluate risk factors for sleep apnea (obesity, increased neck Mood disturbances and cognitive diffculties. Complaints circumference, upper airway restrictions) and comorbid medi- of irritability, loss of interest, mild depression and anxi- cal conditions that include but are not limited to disorders of ety are common among insomnia patients. The daytime activities and exercise may in turn contribute to choice of assessment tools should be based on the patients pre- insomnia. Likewise, (1) A general medical/psychiatric/medication questionnaire poor sleep may exacerbate symptomatology of comorbid (to identify comorbid disorders and medication use) conditions. Sleep complaints may herald the onset of mood (2) The Epworth Sleepiness Scale or other sleepiness assess- disorders or exacerbation of comorbid conditions. Primary baseline measures obtained from a sleep and potentially on family, friends, coworkers and caretakers. Genetics: With the exception of fatal familial insomnia, a Objective Assessment Tools: Laboratory testing, polysom- rare disorder, no specifc genetic associations have been identi- nography and actigraphy are not routinely indicated in the eval- fed for insomnia. A familial tendency for insomnia has been uation of insomnia, but may be appropriate in individuals who observed, but the relative contributions of genetic trait vulner- present with specifc symptoms or signs of comorbid medical ability and learned maladaptive behaviors are unknown. For example, changing to a less stimulating antidepres- rhythm sleep disorders; sant or changing the timing of a medication may improve sleep Insomnia due to medical or psychiatric disorders or to or daytime symptoms. It should be Before consideration of treatment choices, the patient and noted that comorbid insomnias and multiple insomnia diagno- physician should discuss primary and secondary treatment goals ses may coexist and require separate identifcation and treat- based on the primary complaint and baseline measures such as ment. After discussing treatment options tailored to address the primary complaint, a specifc follow-up Indications for Treatment plan and time frame should be outlined with the patient, regard- less of the treatment choice. It is essential ment, often using specifc questionnaires for specifc insomnia to recognize and treat comorbid conditions that commonly oc- problems (Table 8). If the clinician is unfamiliar with these tests, cur with insomnia, and to identify and modify behaviors and administration and monitoring of these measures may require medications or substances that impair sleep. By defnition, and behavioral interventions show short and long term effcacy Journal of Clinical Sleep Medicine, Vol. When using this diagram, the clinician should be aware that the presence of one diagnosis does not exclude other diagnoses in the same or another tier, as multiple diagnoses may coexist. Psychological and behavioral interventions and phar- with psychological and behavioral therapies. Regardless of treatment choice, frequent outcome agement of both primary and comorbid insomnias. In addition, periodic clinical reassessment following While most effcacy studies have focused on primary insomnia completion of treatment is recommended as the relapse rate for patients, more recent data demonstrate comparable outcomes in chronic insomnia is high. In co- psychological and Behavioral Therapies morbid insomnias, treatment begins by addressing the comorbid condition. This may include treatment of major depressive dis- Current models suggest that physiological and cognitive hy- order, optimal management of pain or other medical conditions, perarousal contribute to the evolution and chronicity of insom- elimination of activating medications or dopaminergic therapy nia. In addition, patients typically develop problematic behaviors for movement disorder. In the past, it was widely assumed that such as remaining in bed awake for long periods of time, often treatment of these comorbid disorders would eliminate the in- resulting in increased efforts to sleep, heightened frustration and somnia. Negative learned responses may These perpetuating factors commonly include worry about in- Journal of Clinical Sleep Medicine, Vol. The sleep disturbance has a relatively short duration (days-weeks) and is expected to resolve when the stressor resolves. Psychophysiological Insomnia The essential features of this disorder are heightened arousal and learned sleep-preventing as- sociations. Individuals typically have increased concern about sleep diffculties and their consequences, leading to a vicious cycle of arousal, poor sleep, and frustration. Paradoxical Insomnia The essential feature of this disorder is a complaint of severe or nearly total insomnia that greatly exceeds objective evidence of sleep disturbance and is not commensurate with the re- ported degree of daytime defcit. To some extent, misperception of the severity of sleep disturbance may characterize all insomnia disorders. Idiopathic Insomnia The essential feature of this disorder is a persistent complaint of insomnia with insidious on- set during infancy or early childhood and no or few extended periods of sustained remission. Idiopathic insomnia is not associated with specifc precipitating or perpetuating factors. Insomnia Due to Mental Disorder The essential feature of this disorder is the occurrence of insomnia that occurs exclusively during the course of a mental disorder, and is judged to be caused by that disorder. The insom- nia is of suffcient severity to cause distress or to require separate treatment. This diagnosis is not used to explain insomnia that has a course independent of the associated mental disorder, as is not routinely made in individuals with the usual severity of sleep symptoms for an associated mental disorder. Inadequate Sleep Hygiene The essential feature of this disorder is insomnia associated with voluntary sleep practices or activities that are inconsistent with good sleep quality and daytime alertness.
Patients should be aware that weight loss toreducedphysicalactivityandhenceweightgain 100 mg pristiq mastercard medications on nclex rn,which induces a reduction in energy expenditure and there- continues until the sixth decade cheap pristiq 50 mg overnight delivery symptoms multiple myeloma. Techniques pattern of food intake have all been implicated in the used include the following: development of obesity. Both the appetite and the sensa- r Behaviour modication including examining the tionofsatiety(fullness)areimplicated. Centraladiposity background of the individual, the eating behaviour (waist-to-hipratiomeasurements>0. Diets include hormones and nutrients: balanced low-calorie diets, low-fat diets and low- r Leptin production correlates with body fat mass; a carbohydrate diets, which are ketogenic possibly in- leptin receptor has been identied in the ventromedial ducing calcium loss and tend to be high in saturated region of the hypothalamus. Mono- 1 Sibutramine is a noradrenaline and serotonin re- amines, including noradrenaline and serotonin, also uptake inhibitor and promotes a feeling of satiety. The remaining 20% of energy expenditure is due scribed for patients aged 1875 years who have lost to physical activity and exercise. Blood pressure, cardiovascular risk factors and viewed at 4 and 6 months to conrm that weight diabetes should all be reviewed. Surgery is considered only if a r Children with kwashiorkor develop oedema, conceal- patient has been receiving intensive management in a ing the loss of fat and soft tissues, the hair may be specialised hospital or obesity clinic, is over 18 and all discoloured and an enlarged liver may be found. Previously jejunoileal and gastric bypass proce- Complications dures were performed, which despite being effective Malnutrition greatly increases the susceptibility to infec- were associated with signicant side effects. In children it has been shown to affect brain growth banded gastroplasty either by laparoscopic surgery or and development. Often oral rehydration is safest, fol- and mortality from diabetic-related illness and cardio- lowed by nutritional replacement therapy. Nutritional replacement is gradually increased Malnutrition (including kwashiorkor until 200 kcal/kg/day. Aetiology Many countries in the developing world are on the verge Aetiology/pathophysiology of malnutrition. Drought, crop failure, severe illness and Lipids are found in dietary fat and are an important en- war often precipitate malnutrition in epidemics. The two main lipids are triglycerides and choles- Pathophysiology terol, which are found in dietary fat and may also be It is unclear why insufcient energy and protein in- synthesised in the liver and adipose tissue (see Fig. The oedema seen in kwashiorkor results from in- eride, cholesterol and apoproteins). These are then creased permeability of capillaries and low colloid on- transported to the liver where the triglyceride is re- cotic pressure (low serum albumin). Oncotic pressure moved and the remaining cholesterol-containing par- is produced by the large molecules within the blood ticle is also taken up by the liver. The end product, deplete r Adults and children with marasmus have loss of mus- of triglyceride, is termed an intermediate-density cleandsubcutaneousfatwithwrinkledoverlyingskin. Hyperlipidaemias are classied as primary and sec- Clinical features ondary (see Table 13. The clinical signs of hypercholesterolaemia are pre- Primary hyperlipidaemia is a group of inherited condi- mature corneal arcus, xanthelasmata and tendon xan- tions subdivided into those that cause hypertriglyceri- thomata. Acute pancreatitis and eruptive xanthomata daemia, hypercholesterolaemia and combined hyperlip- are features of hypertriglyceridaemia. Bitots spots, which are ecks caused by heaped up desquamated cells occur and progress to corneal xerosis, and eventually corneal clouding ul- Management ceration and scaring. Patients are at risk of secondary The management of hyperlipidaemia is based on an as- infection. Management r General measures include weight loss, lipid-lowering r Prevention of eye disease with adequate diet and diets, reduction of alcohol intake, stopping smoking supplementation in patients with disorders of fat and increasing exercise. In pregnant women, vitamin A but not r Control of hypertension is important preferably carotene is teratogenic. Corneal transplant may be required 1 Cholesterol-lowering drugs include resins, which for irreversible corneal ulceration. Deciency of vitamin A, a fat-soluble vitamin, is a major cause of blindness in many areas of the world. Occasionally it can be seen in disorders of fat malabsorption, such as cystic brosis, cholestatic Pathophysiology liver disease and inammatory bowel disease. Thiamine is an essential factor for the maintenance of the peripheral nervous system and the heart. It is also involved in glycolytic pathways, mediating carbohydrate Pathophysiology metabolism. Vitamin A is required for maintenance of mucosal sur- faces, the formation of epithelium and production of Clinical features mucus. Dry beriberi is an endemic form of polyneuritis re- Retinal function is dependent on retinol, a constituent sulting from a diet consisting of polished rice decient of the retinal pigment rhodopsin. Wet beriberi is the high output heart failure caused by thiamine deciency resulting in Management oedema. Supplementation with nicotinic acid and treatment of other coexisting deciencies. Erythrocyte transketolase activity and blood pyruvate Vitamin B6 (pyridoxine) deciency are increased. Denition Deciency of pyridoxine is rarely a primary disorder, but Management it does occur as a secondary disorder.
Imaging studies have shown that the frontal lobe of the brain becomes less active when a person is depressed cheap pristiq 50mg on line medicine reminder app. Depression is also associated with changes in how the pituitary gland and hypothalamus respond to hormone stimulation 50 mg pristiq fast delivery treatment zollinger ellison syndrome. Diagnosis To be diagnosed with depression, a person must have experienced a major depressive episode that has lasted longer than two weeks. The symptoms of a major depressive episode include: Loss of interest or loss of pleasure in all activities Change in appetite or weight Sleep disturbances Feeling agitated or feeling slowed down Fatigue Feelings of low self-worth, guilt or shortcomings Difficulty concentrating or making decisions Suicidal thoughts or intentions Treatments Although depression can be a devastating illness, it often responds to treatment. My interest in this important topic, which has direct consequences on the lives of an individual and his or her family, friends and co-workers, led me to start an initiative entitled Depression in the Workplace. This disease has the ability to lower an individuals capability of functioning in the workplace and in some cases renders employees incapable of performing their jobs and function in their daily lives (cognitive effects of depression). Angelika Werthmann Member of the European Parliament from Austria for the Alliance of Liberals and Democrats The launch of this recommendations paper is an important milestone towards raising awareness of depression and its consequences for the individual and society in particular due to its effects in the workplace. The recommendations paper is a frst step towards increasing the knowledge of psychosocial risks and addressing the stigma associated with mental health problems, which often leads employees to hide their conditions from their colleagues and employer. In my work with the Womens Rights and Gender Equality Committee, I have made it a priority to address the consequences of depression in women, both in relation to specifc mental health risks for women in the workplace and depression in other phases of womens lives such as depression following childbirth. Emer Costello Member of the European Parliament from Ireland for the Group of the Progressive Alliance of Socialists and Democrats As a Member of the European Parliament, I have become increasingly aware and concerned about the consequences of depression in the workplace in Ireland and across Europe. Rising unemployment, job insecurity and more stressful working conditions have led to an increase in depression and depression-related suicides. I have been following and am enormously impressed by the work of the Irish organisation Aware, which seeks to help patients and their families overcome depression. I am strongly committed to ensuring that depression receives the attention it deserves, at both European and at Member State level, and am grateful for the opportunity to contribute to addressing this major societal challenge. Jutta Steinruck Member of the European Parliament from Germany for the Group of the Progressive Alliance of Socialists and Democrats As a Member of the Employment and Social Affairs Committee in the European Parliament, I am pleased about the launch of this recommendations paper, which addresses depression as one of the most important challenges that needs to be addressed in occupational health and safety, if we are to ensure the sustainability of work life in Europe. Alejandro Cercas Member of the European Parliament from Spain for the Group of the Progressive Alliance of Socialists and Democrats As a contributor to the Stephen Hughes Initiative on Depression in the Workplace, I am pleased to see that our work over the past two years is coming together in this highly relevant paper. However this is only the frst step towards tackling depression in the workplace, and much work is still left to be done. Going forward I am particularly keen to work towards seeing these recommendations refected in concrete policy action by the European Parliament. Starting with the forthcoming revision of the Strategy on Health and Safety at work, I am committed to fght this important battle towards the inclusion of depression and psychosocial risks as a priority in all relevant policies, together with my colleagues from the different political groups. Martin Kastler Member of the European Parliament from Germany for the European Peoples Party The signifcance of addressing depression in the workplace is immense, and it is crucial that this is not overlooked when developing future health and safety at work policies. As Rapporteur for the proposal for a decision of the European Parliament and of the Council on the European Year for Active Ageing (2012), I am especially aware of the signifcance of ensuring good mental health and preventing depression, as a prerequisite for keeping individuals active and healthy throughout their working life, which is a necessity to ensure that Europe develops in a sustainable way in the face of an ageing population. This recommendations paper makes an important contribution to addressing the cognitive effects of depression in the workplace that leads to loss of workability, and I am happy to support this important initiative. Introduction We are at a defning moment in the way in which we approach the challenge of depressiona among our working populations across Europe. Depression has a corrosive effect on the individuals ability to function at home, at work, and within everyday social networks. Less well understood are the cognitive symptoms of depression that directly affect an employees ability to function both inside and outside the workplace. Examples of cognitive symptoms of depression are lack of concentration, indecisiveness and forget- fulness. If adequately managed, people with depression can lead productive lives and make valuable contributions to society as a whole: the barriers to societal participation are being progressively weakened by advances in medi- cal management of this frequently disabling disease. The cognitive symptoms of depression can have a large impact in the workplace, and it is important that this is de- fned and better understood. From there we are in a stronger position to develop effective treatment strategies. The peer-reviewed literature makes the case all too often that application of guideline-supported standards of care can help restore the lives and productivity of many. When depression has been diagnosed, multidimensional treatment strategies can reduce cognitive and other symptoms of depression. Such intervention can directly increase atten- dance at work and productivity while at work. Healthcare professionals working in communities and hospitals strive to apply the accepted standards of care to their patients. Moreover, many with depression struggle to make sense of what they are experiencing, and all too often will be unwilling or unable to seek professional help. These obstacles can lead to a downward spiral of performance at work causing fnancial loss to both the employer and the employee, further escalating to become a burden on society at large as worsening illness is left untreated. There are important differences between the employer-employee relationship, and the doctor-patient interaction. While healthcare professionals rely on the individuals to explain the scope of any problems, employers have objec- tive measures of productivity and subjective reports of social function provided by the affected employees and their colleagues. In addition, employers have specifc and well-defned reasons to discuss an employees performance and where necessary to encourage changes in behaviour. This creates an opportunity for policy makers to better support effective interventions by employers. Indeed it is the prerogative of policy makers to support employers in their efforts to reduce the impact of depressi- on on the individual employee, society and ultimately businesses across Europe. Such initiatives will yield benefts that extend beyond the workplace; this is as much about broader health policy as employment policy. Moreover, any changes may also beneft the large numbers of unpaid workers, such as carers and those supporting family businesses, who are often in similar situations and exposed to the same risks as paid workers. As authors of these policy recommendations, it is our objective to improve understanding of depression in the workplace and how specifc facets of this disease can place a devastating burden on businesses in Europe and their competitiveness worldwide.