Browsing by Subject "Depression"

Depressive disorders and especially Major Depressive Disorder (MDD) have recently raised a lot of concerns. According to Bains & Abdijadid, (2022), in 2030 MDD will be the most common concern in terms of mental well-being and Kessler & Bromet (2013) pointed out that MDD “has one of the highest lifetime prevalence among psychiatric disorders”, and for this reason MDD results in a significant burden from an individual and societal perspective (Lépine & Briley, 2011). Anhedonia which is a core symptom of MDD (Gorwood 2008, Liang et al. 2022) can be defined as the “inability to enjoy experiences or activities that normally would be pleasurable” (APA Dictionary of Psychology, n.d.-c). Its effects on cognitive processes such as reward responsiveness has been the interest of various studies. Pizzagalli et al. (2008) demonstrated in their study that individuals suffering from MDD and experiencing anhedonic symptoms have a blunted reward responsiveness compared to some healthy subjects. This master thesis aimed to replicate Pizzagalli et al. (2008) study to reinvestigate anhedonia´s impact on reward responsiveness as well as anxiety´s role since individuals suffering from MDD also face anxiety or anxiety disorder (Xin et al. 2015).Two groups were formed, a clinical group (N=29) based on the DSM-IV criteria and a control group (N=20), and both groups were given the Face Game or the Probabilistic Reward Task (Pizzagalli et al. 2008) to measure reward responsiveness. Reward responsiveness was computed as “response bias” and the perceived difficulty of the task as “discriminability”. The results showed no significant difference in response bias scores between the depressed and healthy participants, and no significant correlations were found between depression scores, anhedonia scores, anxiety scores, and response bias scores. An effect of the experimental task’s blocks on response bias and discriminability scores was found, but no interaction effect (group * block) was found for the response bias and discriminability scores. Thus, we cannot argue in favor of the results obtained by Pizzagalli et al, (2008) that individuals suffering from MDD and especially experiencing anhedonic symptoms are more likely to have a blunted reward sensitivity compared to some healthy subjects. The statistically non-significant results were attributed to the small sample size, the complexity of the task and its design. Therefore, further investigations should focus on getting larger clinical and control groups and they also should redefine some aspects of the experimental task to make it more sensitive to any changes to reward responsiveness among individuals suffering from MDD and experiencing anhedonic symptoms.

Aims: Adolescent sleep is impacted by numerous biological, psychosocial and contextual factors. The sheer number of new elements capable of affecting adolescent sleep has grown steadily, most notably the amount of electronic devices available. In this adolescent-based sample, we first seek to characterize, and secondly investigate the relationship between gaming, and adolescent sleep, depression and anxiety. Methods. Total of 1374 respondents, aged from 15 to 17 years of age, provided sufficient data in SleepHelsinki! Helsinki university research project. The associations between study parameters were analyzed using correlational comparisons and canonical correlations. Gender differences were also evaluated. The relationships between gaming, sleep, depression and anxiety were further studied using mediation model. Results and Conclusions. In our study the adolescents sleep duration averaged 7:10 hours (SD 1:07) which is well under the recommended amount 8-9 hours of sleep per night. Severe restriction of less than 6 hours of sleep existed in 17.3% of respondents. Negative associations between sleep duration and sleep quality were established on depression, anxiety, chronotype, gaming and alcohol consumption. Positive connections were found between good self-control and sleep hygiene. Girls fared systematically worse than their male counterparts: significantly having more severe sleep restrictions, longer sleep onset latency, worse sleep hygiene and sleep quality. The gaming addiction score was found to mediate the effect of both depression and anxiety on total sleep time. The hours of gaming also mediated the effect of anxiety, but not depression. This study confirms many findings indicating both risk factors and protective factors regarding adolescent sleep. The gaming is established as an integral component when examining adolescent sleep – it should be studied in unison with particularly anxiety and depression symptoms.

Objective. Depression is associated with increased risk of chronic disease, which may be at least partly due to poor health behaviors. Growing body of evidence has associated depression with unhealthy diet. However, the association of depression with diet quality in the long run is not well known. Furthermore, it is unclear if dietary interventions could mitigate the harmful association of depression with diet. This study examined the association of depression with diet both cross-sectionally and longitudinally in a population-based prospective cohort. The effectiveness of an early-onset dietary intervention in modifying these associations was investigated. Methods. The sample (n = 457) was from The Special Turku Coronary Risk Factor Intervention Project (STRIP). The intervention group (n = 209) had undergone a dietary intervention lasting from age of 7 months until age of 20 years. Depression was measured at age 20 using Beck Depression Inventory II (BDI-II). Diet quality was assessed at ages 20 and 26 using a diet score calculated based on food diaries. Missing values were replaced using multiple imputation by chained equations. Linear regression analyses were used to analyze the association of depression at age 20 with diet at ages 20 and 26, as well as the modifying effect of intervention group on these associations. Results. No cross-sectional association was found for depression and diet at age 20. Depression at age 20 was longitudinally associated with worse diet quality at age 26. The associations did not differ between intervention and control groups at either of the time points. Conclusions. Contrary to previous research, this study did not find cross-sectional association for depression with diet. However, this study offers novel information on longitudinal associations, suggesting that depression may have effects on diet quality that can manifest after several years. Dietary intervention was not found effective in modifying these associations. Since long-term effects on diet may be an important factor explaining the association of depression with chronic diseases, ways to mitigate the adverse consequences of depression for diet should be explored further.

Current treatments for major depressive disorder have notable limitations including the delay achieving the therapeutic effect. Ketamine has been shown to alleviate the symptoms of depression rapidly and promising findings have also been found when using nitrous oxide. However, the mechanisms behind rapid antidepressant effect are not fully discovered. It seems that rapid-acting treatments alter brain energy metabolism, enhance synaptic plasticity, and repair neuronal dysfunction connected to depression. Particularly, the activation of brain derived neurotrophic factor (BDNF) mediated tropomyosin receptor kinase B (TrkB) signaling has been connected to rapid antidepressant effect. Fasting is also known to induce BDNF production and it is thought to activate BDNF-TrkB signaling. In addition, both of these treatments alter the brain energy metabolism. The objective of this study was to find out how fasting and nitrous oxide alone and in combination affect the rapid antidepressant effect and synaptic plasticity related BDNF-TrkB signaling in mice. Another aim of the research was to determine whether the body temperature changes after these treatments as a marker of metabolic rate. The analyzed brain samples of the mice were collected 15 minutes after cessation of nitrous oxide administration. As a result, it was found that the fasting protocol used in this study did not activate the studied BDNF-TrkB signaling. However, after nitrous oxide administration, the studied signaling and markers related to synaptic plasticity were partly activated. The results from the combination of nitrous oxide and fasting were similar compared to nitrous oxide administration only. It is therefore conceivable, that the effects were caused exclusively by nitrous oxide. Furthermore, a fascinating finding related to energy metabolism was that nitrous oxide reduced the body temperature of the mice significantly 15 minutes after cessation of the gas administration. Overall, these results are promising and consistent with previous research indicating that nitrous oxide administration could be related to induced synaptic plasticity and therefore have antidepressant associated effects. Nitrous oxide could be used to understand the mechanisms behind rapid antidepressant effect and it could be a potential option to treat depression in the future. Based on these results, it seems that energy metabolism could be related to rapid antidepressant effect. It also supports the observations that all different rapid-acting treatments alter the brain energy metabolism.

Masennus on yleinen sairaus väestötasolla ja kansantaloudellisesti hyvin merkittävä, sillä masennus on merkittävä syy työkyvyttömyyseläkkeelle siirtymiseen. Unettomuus on yleinen oire masennuksen yhteydessä, mutta sen on havaittu olevan myös itsenäinen riskitekijä masennuksen puhkeamiselle. Unettomuus ei myöskään ole pelkkä oire, vaan usein itsenäinen liitännäissairaus masennuksen rinnalla. Masennuksen ja unettomuuden välillä on havaittu useita yhteisiä tekijöitä, vaikka nämä kaksi sairautta yhdistävää tarkkaa mekanismia ei vielä tiedetä. Tutkielman tarkoituksena on selvittää FinTerveys 2017 -tutkimuksen pohjalta masennuksen ja unettomuuden yleisyyttä suomalaisväestössä sekä selvittää regressiomallilla, assosioituvatko unettomuuteen liittyvät oireet masennukseen ja psyykkiseen oireiluun. Aineistosta havaitaan, että lääkärin toteamaa masennusta on 6,5 prosentilla ja usein koettua unettomuusoireilua 10 prosentilla. Usein koettu unettomuusoireilu on 5,47-kertaisesti (95 % CI = 4,05–7,40) yleisempää ihmisillä, joilla on lääkärin toteama masennus kuin ihmisillä, joilla masennusta ei ole. Lisäksi havaitaan, että kaikki huonosta unesta kielivät oireet (unettomuus, päiväväsymys, mielipide riittämättömästä unesta ja unilääkkeiden käyttö) näyttäisivät lisäävän riskiä masennukselle ja päiväväsymys assosioituu vahvimmin masennukseen. Tulokset vahvistavat unettomuuden yhteyttä masennukseen ja sen tärkeyttä, että unettomuuden taustalta on hyvä tunnistaa mahdolliset muut sairaudet, ja toisinpäin sitä, että masennuksen yhteydessä olevaa unettomuutta pitää tarkastella omana merkittävänä kokonaisuutenaan.

Masennus on kansanterveydellisesti merkittävä ongelma, sillä suomalaisista n. 5 % sairastuu vuoden aikana. Sairaus vaikuttaa selvästi elämänlaatuun heikentämällä toiminta- ja työkykyä. Erilaisia neuromodulaatiomenetelmiä on käytetty jo pitkään masennuksen hoidossa, erityisesti hoitoresistentissä taudissa. Vanhin niistä on sähköhoito, jota on käytetty jo 1930-luvulta lähtien. Viime aikoina on myös kehitetty uusia, ei-invasiivisia hoitoja. Uusin niistä on tDCS, eli transkraniaalinen tasavirtastimulaatio. Tähän työhön liittyy lyhyt katsaus masennuksesta ja erilaisista neuromodulaatiomenetelmistä. Tämän lisäksi tehtiin HYKS psykiatrian kautta pilottitutkimus tasavirtastimulaatiohoidosta. Tutkimuksen tarkoituksena oli selvittää hoitomenetelmän hyötyä vaikeahoitoisten masennuspotilailla. Potilaita rekrytoitiin HUS alueelta Keravalta ja Järvenpäästä. Yhteensä tutkimukseen osallistui 15 potilasta. Tutkimuksessa annettiin 2 mA tasavirtastimulaatiohoitoa 30 minuutin ajan 5 päivänä viikossa 3 viikon ajan. Tuloksia mitattiin ensijaisesti PHQ9-oirekyselyllä, lisäksi potilaat täyttivät BDI-, Oasis-, Sheehan toimintakykyasteikko-, Core5- ja 15D-kaavakkeet. Kaavakkeita kerättiin potilailta hoidon alussa ja jokaisen hoitoviikon jälkeen. Tutkimuksella ei osoitettu tilastollisesti merkittävää hyötyä tDCS-hoidosta. Potilaiden PHQ9 pisteet vähenivät keskimäärin n. 20 %. Kolme potilasta, eli 20 % osallistuneista, saavuttivat remission, joka määriteltiin 50 % laskuksi PHQ9 pisteissä. Pisteet vähenivät keskiarvoltaan 18,80 (SD ±6,3) pisteestä 15,00 (SD±7,3) pisteeseen. P-arvo oli 0,06. Tutkimuksen tulokset viittaavat aiempiin tutkimuksiin vertaillen heikompaan tehoon, mikä osittain voi selittyä vaikeahoitoisemmalla potilasmateriaalilla ja tutkimuksen pienellä otoksella.

Depression is a common debilitating mental disorder. It is suffered by more than 320 million people globally and can involve symptoms such as loss of appetite and interest, frequent sadness, rumination, inactivity, and possible suicidal ideation. The World Health Organization has described the condition as the leading cause of global disability, a health crisis that causes significant human suffering and financial losses, both of which are avoidable through treatment. However, the causal relations of the condition are ambiguous as many of the symptoms have been found to be predispositions, comorbid, as well as causes of the disorder, which has led to a myriad of competing theories on the causes and treatment of depression. Focusing on the psychological theories of depression, these differences can not only be understood through historical debates, but also as fundamental contemporary questions relating to what mental health is and how an individual possibly evaluates subjective well-being (SWB). These are not definitive concepts, as presented in this paper, but a social psychological perspective can help the reader to create a more nuanced picture that assists in discerning the examined phenomenon. Despite the many uncertainties on what depression is and how best to treat it, the disorder has for the last four decades been most often diagnosed as Major Depressive Disorder and successfully treated through Cognitive Behavioural Therapy (CBT). However, this treatment has recently been gaining criticism for being too costly and unnecessarily complicated, in addition to showing evidence of selection and publication bias. One persuasive alternative to CBT is the cost-effective Behavioural Activation treatment (BA), a method that aims to behaviourally reactivate the patient through goals that are set in a handful of sessions, but as a relatively recent method, more research is needed on, among other things, the goal characteristics. There is potential that reactivating the social life among the depressed presents a more effective goal than other goals defined during treatment. As a functioning social life is emphasised by researchers on mental health and SWB, it could be that breaking the habit of social withdrawal is key for cost-effective depression treatment. The aim of this master’s thesis is therefore to present a wide array of research on mental health and depression, to situate BA to modern understandings of depression, and to argue for the potential in defining social goals in BA. This is investigated through multi-level modelling and linear regression analyses on survey data that was gathered in England from participants who were enrolled in BA as a part of their Low Intensity Cognitive Behavioural Therapy for depression. The results were non-significant, indicating heterogenous data, extraneous variables, and mixed results – factors that are not entirely surprising given the variability relating to the syndrome and utilised methods. These are subsequently summarised in a conducive discussion held at the end of the paper along with a review of limitations and future research.

Current pharmacological treatments for major depressive disorder leave many patients unresponsive to treatment or treatment response is delayed by weeks. More effective treatments with quicker effect onset are therefore needed. Ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonists has demonstrated sustained rapid antidepressant activity after single dose. Precise mechanisms behind this effect are unknown, however some crucial contributors to ketamine-induced behavioural effects in rodents include phosphorylation of Tropomyosin receptor kinase B (TrkB), ribosomal protein s6 kinase (p70s6k), glycogen synthase kinase 3 (GSK3), mitogen activated protein kinases (MAPKs), and activation of α-amino-3-hydroxy-5- methyl-4- isoxazolepropionic acid receptors (AMPAR). Similar TrkB related signaling cascades are also activated with another NMDA receptor antagonist and a putative rapid-acting antidepressant, nitrous oxide (N2O). During acute effects of N2O, cortical excitation increases MAPK phosphorylation and upregulates expression of activity dependent immediate early genes (IEG; c-Fos and Bdnf IV). Phosphorylation of TrkB, GSK3 and p70s6k appearing only after N2O has been eliminated suggest that TrkB signaling is induced as an adaptive response to treatment. The first objective of this study was to corroborate previous results from our group to validate our gas administration set up and protein analysis protocol. To analyze N2O-induced phosphorylation of proteins implicated in ketamine’s behavioral effects in mice, we treated C57BL/6J male mice with either room air (control) or 65% nitrous oxide for 20 minutes. After gas exposure and 15-minute washout period, medial prefrontal cortex samples were dissected to be analyzed with western blotting. In this study nitrous oxide exposure did not induce increased TrkB signaling in nitrous oxide withdrawal. Another aim of this study was to investigate the involvement of AMPARs in inducing cortical excitation with N2O. Pretreatment of AMPAR antagonist (10 mg/kg, NBQX) or saline was given to C57BL/6J male mice 10 minutes prior to 1 hour exposure to 50 % O2 or 50 % N2O, a N2O dose previously shown to induce IEG expression. One hour after gas exposure mice were euthanized and mPFCs were dissected and analyzed with reverse transcriptase quantitative PCR (RT-qPCR). No regulation in IEG expression was induced with nitrous oxide, NBQX pretreatment or combination compared to control. Additional studies factoring in limitations of this study are needed to uncover the involvement of AMPAR in inducing cortical excitation and antidepressant-like behavioral effects of N2O in preclinical models of depression.