<p>Den här uppsatsen analyserar informationssajten om depression Depressionslinjen, som ges ut av läkemedelsföretaget Pfizer. Analysen görs enligt Fairclough (2001a; 2001b; 2002). Analysen visar att läsaren/patienten konstitueras som passiv medan SSRI och läkaren konstitueras som aktiva och handlande. Terapi och andra alternativ till läkemedel nämns, men olika diskursiva grepp används som ger intrycket av att dessa kommer i andra hand. Lågt Serotonin framstår som orsak till depression. Med utgångspunkt från texter av Filip Kotler (1991) visar uppsatsen att Depressionslinjen har åtskilliga inslag av marknadsföring. Tre alternativa sätt att se på depression föreslås: Depression som samhällsproblem, depression som existensiell utmaning och depression som minne. Slutsatsen är att Depressionslinjen har en idologisk roll i och med att sidan för fram en professionell lösning på depression där serotoninet får skulden till problemet.</p>

Den här uppsatsen analyserar informationssajten om depression Depressionslinjen, som ges ut av läkemedelsföretaget Pfizer. Analysen görs enligt Fairclough (2001a; 2001b; 2002). Analysen visar att läsaren/patienten konstitueras som passiv medan SSRI och läkaren konstitueras som aktiva och handlande. Terapi och andra alternativ till läkemedel nämns, men olika diskursiva grepp används som ger intrycket av att dessa kommer i andra hand. Lågt Serotonin framstår som orsak till depression. Med utgångspunkt från texter av Filip Kotler (1991) visar uppsatsen att Depressionslinjen har åtskilliga inslag av marknadsföring. Tre alternativa sätt att se på depression föreslås: Depression som samhällsproblem, depression som existensiell utmaning och depression som minne. Slutsatsen är att Depressionslinjen har en idologisk roll i och med att sidan för fram en professionell lösning på depression där serotoninet får skulden till problemet.

Major depressive disorder (MDD) is a mood disorder majorly responsible for disability and mortality worldwide. With a lifetime prevalence of 15-20%, it is the main cause of functional impairment in Western societies as well as the fourth most debilitating illness in the world. Although the pathophysiology of MDD is not yet fully understood, some evidence that suggest the presence of a neuroanatomical deficiency have given rise to the theory of a specific imbalance in the monoamine neurotransmitters noradrenaline (NA) and/or serotonin (5-HT) levels in the brain. Overall, the various classes of antidepressant agents that have been developed to increase monoamine levels on the basis of this proposal have been successful. However, facts relating to prevalent escalation in the illness and recurring episodes of depression point towards a need to enhance clinical treatment. Most conventional antidepressants such as selective serotonin reuptake inhibitors (SSRI) and selective serotonin and noradrenaline inhibitors (SNRI) pose problems in symptomatic improvement. These include therapeutic lag, safety and tolerability issues, making more than 30% patients with MDD unable to reach adequate relief. In this respect, the action mechanism has moved beyond conventional SSRI and lead to the introduction of vilazodone, a novel antidepressant with an additional 5-HT1A partial agonist profile argued to be of potential benefit for a greater efficacy, faster onset of action and better tolerability. Using secondary data, this project aimed to evaluate the role of vilazodone as a SPARI-drug in the overall clinical treatment of MDD as well as its potential in addressing some of the most common obstacles in antidepressant treatment. Study results proved vilazodone’s efficacy to be superior to placebo. Patients across all studies showed significant improvement in depressive symptoms measured in MADRS and HAMD17. Vilazodone was also shown to be generally safe and tolerable but was not positively distinguished from placebo with regards to adverse effects. An overall, meaningful improvement in depressive symptoms was demonstrated in vilazodone, which reinforces its merit as an important treatment option for patients with MDD.

Major depressive disorder (MDD) is a mood disorder majorly responsible for disability and mortality worldwide. With a lifetime prevalence of 15-20%, it is the main cause of functional impairment in Western societies as well as the fourth most debilitating illness in the world. Although the pathophysiology of MDD is not yet fully understood, some evidence that suggest the presence of a neuroanatomical deficiency have given rise to the theory of a specific imbalance in the monoamine neurotransmitters noradrenaline (NA) and/or serotonin (5-HT) levels in the brain. Overall, the various classes of antidepressant agents that have been developed to increase monoamine levels on the basis of this proposal have been successful. However, facts relating to prevalent escalation in the illness and recurring episodes of depression point towards a need to enhance clinical treatment. Most conventional antidepressants such as selective serotonin reuptake inhibitors (SSRI) and selective serotonin and noradrenaline inhibitors (SNRI) pose problems in symptomatic improvement. These include therapeutic lag, safety and tolerability issues, making more than 30% patients with MDD unable to reach adequate relief. In this respect, the action mechanism has moved beyond conventional SSRI and lead to the introduction of vilazodone, a novel antidepressant with an additional 5-HT1A partial agonist profile argued to be of potential benefit for a greater efficacy, faster onset of action and better tolerability. Using secondary data, this project aimed to evaluate the role of vilazodone as a SPARI-drug in the overall clinical treatment of MDD as well as its potential in addressing some of the most common obstacles in antidepressant treatment. Study results proved vilazodone’s efficacy to be superior to placebo. Patients across all studies showed significant improvement in depressive symptoms measured in MADRS and HAMD17. Vilazodone was also shown to be generally safe and tolerable but was not positively distinguished from placebo with regards to adverse effects. An overall, meaningful improvement in depressive symptoms was demonstrated in vilazodone, which reinforces its merit as an important treatment option for patients with MDD.