I will send a summary of the results separately. Use the link posted to complete the methods as the data from this paper was used.
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0188785
Investigation of environmental risk factors of co-morbid depression and anxiety disorders. Abstract Introduction Comorbid depression and anxiety disorders are commonly prevalent disorders worldwide, both individually & co-existing together. Generalised anxiety disorder (GAD) has a lifetime prevalence of 5.1% or more & according to other estimates, the lifetime prevalence of major depressive disorder (MDD) is 16.2%. Moreover, 62% of people with GAD will also experience an episode of MDD in their lifetime. Bandelow & Michaelis (2015) found that 85% of patients suffering from depression also displayed significant symptoms of anxiety. Likewise, 90% of anxiety patients suffer from depression [2]. The main symptoms associated with these disorders include repeated negative thoughts, a loss of interest in daily activities, feelings of worthlessness, apprehension, a sense of helplessness, confusion, persistent sadness, muscle tension & heart palpitations to name a few [3,4]. Several genetic and environmental risk factors have been highlighted as being associated with co-morbid depression and anxiety such as childhood trauma, poor nutrition, grief, family history and genetics, chronic stress, gender, medications effect, personality traits [5,6,7]. Using a cohort study design, Kwong et al 2019 [8] reported that a major environmental risk factor associated with co-morbid depression and anxiety is linked to childhood trauma or trauma that occurred in young adulthood. Specifically, they found that late childhood trauma and young adulthood trauma are most often correlated with sexual encounters from a young age, polygenic risk scores, maternal postnatal depression, partner cruelty to a child’s mother or a child being bullied. Additionally, Cerda et al., (2010) [9] reported that the most prevalent psychiatric comorbidities (general anxiety disorder, depression, abuse & conduct disorder) can be linked to both genetic and environmental determinants. They mention that the alteration in potential genes; 5HTTLPR, MAOA, and DRD1-DRD4 of the central nervous system may be responsible for the onset of these psychiatric disorders & their ability to display comorbidly. Additionally, they found the most prevalent environmental risk factor linked to these disorders to be pivotal social factors like childhood adversity, adverse life events, family issues, socioeconomic status and academic difficulties. Similarly, Mondragon et al in 2022 [10] used a network analysis study to analyse the influence of polygenic factors and environmental risk factors on depression and psychotic disorders. They found that these disorders when they show up comorbidly can have overlapping genetic and environmental risk factors such as; area-level exposures, deprivation, air pollution, trauma and greenspace. Sugimoto et al. (2015) [11] reviewed the genetic basis of anxiety disorders & report that it often runs in families which came from evidence based on twin studies. They relay that the major source of this familial risk is mainly genetic in origin through a process called global DNA methylation with the heritability of the disease at present being approximately 30–50%. Hetterna et al. (2005) [12] analysed how stressful life events and genetic factors can be responsible for co-morbid depression and anxiety. Using genetic linkage, they found a significant link to chromosome 9q31 in the development of anxiety factors. Interestingly though, Seok (2020) found that general feelings of anxiety are more likely to be caused by environmental than genetic factors. What’s more, they found that combined, the effects of early childhood trauma along with experiencing recent stressors were stronger than their individual effects. That is, the predisposition toward emotional disturbance caused by childhood trauma can be mitigated if stress is not present for an individual at a given time. Similarly, Lesch et al. (2004) [12] reported that depression and many other brain disorders of varied origins have a very complex genetic basis and ambiguous neurobiology. Therefore, as highlighted above, it is clear to see that depression and anxiety disorders are more often than not comorbid in nature and have complex, overlapping and linked genetic and environmental risk factors or predispositions. However, at present, research is still quite novel in discovering the differing effects of the environmental factors and their linked correlation on these disorders. One reason for this is because when depression and anxiety present together, they are frequently more difficult to treat. This is due to the fact that when anxiety and depression are "functioning" together, their symptoms are often more enduring and severe. As a result, folks who experience both depression and anxiety will require more specific treatments. Therefore, the aim of the present study is to assess whether certain environmental risk factors pose a greater risk of comorbid anxiety & depression & how a predisposition towards the disorders may present itself depending on the environment with which one finds themselves in. 2. Methods 2.1 Design Data from The Ulster University Student Wellbeing study (UUSWS) (NAME, 2015) was he UUSWS survey is being carried out as component of the WHO Earth Mental Health International College Learner Plan (WMH-ICS).An observational, longitidunal cohort survey construct is utilized for all studies. Prospective studies, as an example this, could be extremely benefical in that retract reissues are minimised, sequences or patterns of events might be set up and causal relationships may be inferred. Ethical approval was obtained for the Northern Ireland survey from the Ulster University Research Ethics Board (REC/15/0004). 2.2 Sample Using data from the UUSWS, 4,365 first-year undergraduate students studying at Ulster University in 2015-2016 were recruited; 739 of which completed the survey in full & were thus considered for analysis. 462 of these participants were female, 274 male & 3 identified as other (1 transgender male to female, 1 transgender female to male and 1 non-binary). The age range of participants ranged from 18-49, with an average age of 21(M = 20.69, SD = 5.313). International students were excluded from the study. To registered at Ulster University in the year 2015–2016. A week prior to registration an email was circulated to all new first year undergraduate students due to register at the university, with a detailed participant information sheet attached outlining the aims of the study and methodology to be employed. Students were asked to consider participating in the study. Trained researchers recruited students on the various campuses following registration. A total of 1,646 participants provided informed written consent to take part in the study. Saliva/DNA samples (4ml) were collected from each participant using the Oragene-500 (DNA Genotek) self-collection kits according to the manufacturer’s instructions and stored for genetic analysis. Each student was provided with a card containing their unique ID number and a link to the survey. The survey instrument was administered on-line using Qualtrics software. The link to the survey was also emailed to each participant. The survey was fully completed by 739 of the participants. The completed response rate was 16.95% in relation to the total number of first year students registered. While other students partially completed the survey only those who responded to all questions are included in the analyses for the current study (N = 739), of which 462 were female, 274 were male, and three students identified as other (1 transgender male to female, 1 transgender female to male and 1 non-binary). The average age of participants was 21(M = 20.69, SD = 5.313), with an age range of 18 to 49. All participants were residents of the United Kingdom (UK) or the Republic of Ireland (ROI). International students, those repeating first year and students under the age of 18 were excluded from the study. 2.3 Diagnostic Assessments 2.4 Data Analysis Logistic regression analyses were ran to explore the relationship between anxiety, depression & co-morbid anxiety/depression on age, gender, sexuality & place raised. The origial ‘Plos One’ (SOURCE) had weights generated during output to ensure the results were generalisable to the entire student population (Figure 1). These weights were created using gender & age characteristics. 3. Results Descriptive statistics were calculated for gender, age, & presented in Table 1. Table 2 highlights the odds ratio of age, gender, sexuality & level of childhood trauma on anxiety disorder; calculated using Logistic Regression. Similarly, table 3 Lastly, table 4 highlights the odds ratio of the above variables on co-morbid anxiety & depression. Statistical significance was accepted where P < 0.05. 3.1 latent profile analysis (lpa) of adverse childhood trauma 4. discussion references 0.05.="" 3.1="" latent="" profile="" analysis="" (lpa)="" of="" adverse="" childhood="" trauma="" 4.="" discussion="">