Proefschrift Universiteit Maastricht. / Met lit. opg. - Met samenvatting in het Nederlands.

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The authors of this study is Matilda Svensson and Jonna Svensson, currently studying at Linnaeus University in Växjö. The name of the study is “When unemployment kills”. The aim of this study is to analyze Swedish counties and their suicide rates in relation to unemployment rates, depression and  usage of antidepressant medication. The theoretical datum is based in Durkheim's perspective of suicide as a social phenomenon. The study’s thesis is processed into three framing of questions. Is there a correlation between the occurrence of suicide and unemployment on a regional level, is there a correlation between the occurrence of suicide and depression on a regional level, Is there a correlation between the occurrence of suicide and antidepressant medication on a regional level? The data material is of aggregated secondary form, collected from Swedish databases. We did a descriptive overview of all the data, and then performed correlational analyzing and linear regression in SPSS to analyze the data. Our starting point is that there is a correlation between counties suicide rates and unemployment, depression and antidepressant medication. The descriptive overview indicates that there are regional differences between the counties among all the variables. However, the suicide rates are relatively consistent over time. There are also differences between men and women in terms of suicide ideation, depression and antidepressant medication. It’s possible to assume that women tend to be diagnosed with depression to a higher extent than men, and that men tend to commit suicide to a greater extent than women. However, the result does not indicate any significant correlation between the variables, although some counties did indicate that there was a significant correlation among men’s suicide rates and the independent variables. It's not possible to draw any conclusions based on the study's data material, other than the specific counties which did show a significant result.

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Syftet med föreliggande uppsatsarbete är att beskriva erfarenheter av psykofarmaka och psykoterapi. Studien är kvalitativ till sin karaktär och utgår från intervjuer med fyra psykoterapeuter och en läkare. Uppsatsen tar utgångspunkt i ett fenomenologiskt perspektiv. Intervjuerna har analyserats så förutsättningslöst som möjligt utifrån EPP-metoden. Arbetet har haft sin grund utifrån fem övergripande frågeställningar; Hur uppfattar vi lidandets mening i relation till psykofarmaka? Påverkas en individs möjlighet att känna och tänka om denne regelbundet brukar psykofarmaka? Kan den som lider förvänta sig vägledning i de olika enskilda, respektive kombinationsbehandlingar som finns? Minskar det egna lidandet genom att sätta ord på sin ångest i psykoterapi? Hur resonerar läkemedelsindustrin i frågan kring individens psykiska lidande? Dessa frågeställningar har vilat mot en filosofisk fond som ställer frågan: Är medikaliseringen ett sätt att medicinera mot livet självt, att göra samhällets tillkorta-kommanden till ett individuellt problem? Resultaten presenteras i fem synopsis som visar på att; lidande kan ses som kraft till förändring. Antidepressiva läkemedel har en tendens att döva tankar och känslor. Patientens egen vilja är viktig. Mediciner tenderar att bli till substitut för mötet med människor och att relationen till läkemedelföretagen är problematiskt för behandlare då den också är en vinstmaskin. / The purpose of the study is to describe experiences gained from the use of psychotropic drugs and/or psychotherapy. The study is qualitative in nature and based on interviews with four psychotherapists and physicians. The study takes as its basis a phenomenological perspective. The interviews were analyzed as unprejudiced as possible using the EPP method. The work was based on five overreaching issues; How do we perceive suffering, meaning in relation to psychotropic drugs? Is an individual's ability to feel and think affected by regular use of psychotropic drugs? Can an individual who suffers expect guidance via individual treatment or via available combined treatments? Is an individuals suffering reduced by setting words to the anxiety in psychotherapy? How does the pharmaceutical industry discuss the issue of individual mental suffering? These issues have been tested against a philosophical background that asks the question: Is medicalisation a way of medicating against life itself, a way of making society's shortcomings the individual`s problem? The results are presented in five synopsis which say that suffering can be seen as force for change. Antidepressants have a tendency to numb thoughts and feelings. The patient's own will is important. Medication tends to be a substitute for meeting people and the relationship to pharmaceutical companies problematic for therapists as the industry is also a profit machine.

In der Pathophysiologie der Depression könnte das Zusammenspiel von Immun- und Nervensystem eine zentrale Rolle spielen. In den Krankheitsepisoden zeigen depressive Patienten eine gesteigerte Produktion pro-inflammatorischer Zytokine wie z. B. Interleukin (IL)-1β und dem Tumornekrosefaktor (TNF)-α. Es gibt nur begrenzte Informationen bezüglich der Effekte von Antidepressiva auf Zytokine. Die meisten Studien berichten nur über die Veränderungen einzelner Zytokine und keine hat bis jetzt über Effekte von Antidepressiva auf IL-22 berichtet. Wir haben systematisch die Wirkung von drei Antidepressiva, nämlich Citalopram, Escitalopram und Mirtazapin auf die Sekretion der Zytokine IL-1β, IL-2, IL-4, IL-6, IL-17, IL-22 und TNF-α in einem Vollblutverfahren in-vitro untersucht. Als Immunstimulanzien wurden der gegen humanes CD3 gerichtete monoklonale Antikörper OKT3 und der gegen CD40 gerichtete monoklonale Antikörper 5C3 verwendet. Es zeigte sich, dass es unter Citalopram zu einer erhöhten IL-1β, I-6, IL-22 und TNF-α-Produktion und unter Mirtazapin zu einer erhöhten Produktion von IL-1β, IL-22 und TNF-α gegenüber der Kontrollbedingung, in der keine Antidepressiva zugesetzt wurden, kam. Unter Escitalopram kam es zu einer gegenüber der Kontrollbedingung verringerten IL-17-Produktion. Der Einfluss der Antidepressiva auf IL-2 und IL-4 war für alle drei Psychopharmaka nicht signifikant. Verglichen mit Escitalopram führte Citalopram zu höheren IL-1β-, IL-6-, IL-17- und IL-22-Konzentrationen und Mirtazapin führte zu einer höheren IL-1β-, IL-17-, IL-22- und TNF-α-Produktion. Möglicherweise besteht ein Bezug zwischen dem Profil der Zytokinproduktion eines Antidepressivums und seinen therapeutischen Effekten, Nebenwirkungen und seinem Rückfallrisiko. Zur Überprüfung dieser Hypothese sind jedoch in-vivo Studien notwendig. / The interplay between immune and nervous systems plays a pivotal role in the pathophysiology of depression. In depressive episodes, patients show increased production of pro-inflammatory cytokines such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α. There is limited information on the effect of antidepressant drugs on cytokines, most studies report on a limited sample of cytokines and none have reported effects on IL-22. We systematically investigated the effect of three antidepressant drugs, citalopram, escitalopram and mirtazapine, on secretion of cytokines IL-1β, IL-2, IL-4, IL-6, IL-17, IL-22 and TNF-α in a whole blood assay in vitro, using murine anti-human CD3 monoclonal antibody OKT3, and 5C3 monoclonal antibody against CD40, to stimulate T and B cells respectively.Citalopram increased production of IL-1β, IL-6, TNF-α and IL-22. Mirtazapine increased IL-1β, TNF-α and IL-22. Escitalopram decreased IL-17 levels. The influence of antidepressants on IL-2 and IL-4 levels was not significant for all three drugs. Compared to escitalopram, citalopram led to higher levels of IL-1β, IL-6, IL-17 and IL-22; and mirtazapine to higher levels of IL-1β, IL-17, IL-22 and TNF-α. Mirtazapine and citalopram increased IL-22 production. The differing profile of cytokine production may relate to differences in therapeutic effects, risk of relapse and side effects.

Diss. (sammanfattning) Linköping : Univ., 2003. / Härtill 4 uppsatser.

ithium is an important psychopharmacologi- cal agent for the treatment of unipolar as well as bipolar affective disorders. Lithium has a number of side effects such as hypothyroidism and aggravation of psoriasis. On the other hand, lithium has pro-inflammatory effects, which appear beneficial in some disorders associated with immunological deficits, such as human immunodeficiency virus (HIV) infection and systemic lupus erythematosus (SLE). Therefore, immunological characteristics of lithium may be an important consideration in individualized ther- apeutic decisions. We measured the levels of the cytokines interleukin (IL)-1ß, IL-2, IL-4, IL-6, IL-22, IL-17 and tumour necrosis factor (TNF)-a in the stimulated blood of thirty healthy subjects supplemented with lithium alone, the antidepressants citalopram, escitalopram or mirtazapine alone, the combination of each antidepressant with lithium, and a no drug control. These drugs were tested under three blood stimulant conditions: murine anti-human CD3 monoclonal antibody OKT3 and the 5C3 monoclonal antibody (OKT3/5C3), phytohemagglutinin (PHA), and unstimulated blood. Lithium, alone and in combination with any of the tested antidepressants, led to a consistent increase of IL-1ß, IL-6 and TNF-a levels in the unstimulated as well as the stimulated blood. In the OKT3/ 5C3- and PHA-stimulated blood, IL-17 production was significantly enhanced by lithium. Lithium additionally increased IL-2 concentrations significantly in PHA-stimu- lated blood. The data support the view that lithium has pro- inflammatory properties. These immunological character- istics may contribute to side effects of lithium, but may also explain its beneficial effects in patients suffering from HIV infection or SLE.

Depression is a very common public disease that can lead to social and economic burdens in the society and has been shown to increase in recent decades. The symptoms that define depression are melancholic mood, loss of interest in previously enjoyable activities, loss of joy and loss of energy (greater fatigue than usual). More serious symptoms are thoughts of death and eventually even suicide. The pathophysiology is complicated and not yet fully understood. One of the hypotheses is the monoamine hypothesis, which states that the concentrations of serotonin, dopamine and norepinephrine are depleted in depressed patients and that this is the reason why antidepressant drugs work to many people. Another hypothesis states the role of neuroplasticity (e.g., neurogenesis) in depression. Neuroplasticity can be stimulated by various neurotrophins (e.g., BDNF, Brain derived neurotrophic factor) which in turn have been shown to be stimulated by physical activity. The stimulation of neuroplasticity in some regions in the brain (e.g., hippocampus) leads to antidepressant effects.  The purpose of the work was to, based on literature studies, investigate whether mild to moderate depression can be treated with physical activity as alternative treatment instead of antidepressant drugs. This literature study is based on articles from the databases PubMed.  A total of four studies have been reviewed and were Randomized controlled trial (RCT)- studies comparing physical activity with antidepressant drugs. All studies showed a clear reduction in depressive symptoms in participants who exercised. Exercise has been shown to have similar effects as drug use. The advantages of exercise compared to drug use include fewer side effects, no drug-drug interactions and additional health benefits. The disadvantage is poorer compliance and added costs of group training or help from professional staff.  The conclusion that is drawn is that exercise could very well be offered as an alternative to treatment and has promising conditions. However, additional larger studies with more statistically significant results examining the difference between physical activity and antidepressant drugs should be done as well as studies that provide a better understanding of the pathophysiology which in turn could lead to better treating options. / Depression är en mycket vanlig folksjukdom som kan leda till både social och ekonomisk börda i samhället och har visats öka de senaste decennierna. Symtomen som definierar depression är sänkt grundstämning med onormal nedstämdhet, intresseförlust, glädjeförlust och energiförlust (större uttröttbarhet än vanligt). Mer allvarliga symtom är tankar på död och självmord. Patofysiologin är komplicerad och ännu inte helt klarlagd. En av hypotesen är monoaminohypotesen, och går ut på att koncentrationerna av serotonin, dopamin och noradrenalin är uttömda hos deprimerade patienter samt att det är orsaken till att antidepressiva läkemedel fungerar hos många. En annan hypotes är neuroplasticitetens (bl.a. neurogenes) roll i depressionen. Neuroplasticiteten kan stimuleras av olika neurotrofiner (BDNF) som i sin tur har visats stimuleras av fysisk aktivitet. Denna stimulering ger upphov till antidepressiva effekter. Syftet med arbetet var att, baserat på litteraturstudier, undersöka om mild till måttlig depression kan behandlas med fysisk aktivitet som alternativbehandling istället för antidepressiva läkemedel. Denna litteraturstudie var baserad på artiklar från databaserna PubMed. Fyra studier hade sammanlagt granskats, där dessa var RCT-studier som jämförde fysisk aktivitet med antidepressiva läkemedel. Samtliga studier visade en tydlig minskning av depressiva symtom hos deltagare som tränat. Träning har även visats ge liknande effekter som läkemedelsanvändning. Fördelarna med träning jämfört med läkemedelsanvändning är bl.a. färre biverkningar, inga läkemedel-läkemedel interaktioner samt fler hälsofördelar. Nackdelen är sämre följsamhet och eventuella kostnader vid gruppträning eller hjälp från professionell personal. Slutsatsen som dras är att träning mycket väl skulle kunna erbjudas som en alternativbehandling då det har visats ge likvärdiga effekter som antidepressiva läkemedel. Fler större studier med fler statistiskt signifikanta resultat som undersöker skillnaden mellan fysisk aktivitet och antidepressiva läkemedel bör dock göras, samt studier som ger bättre förståelse för patofysiologin.