Adjusted odds ratios for PTSD by ethnicity and immigrant status a Canadian-born visible minority vs Canadian-born white. b Immigrant white vs Canadian-born white. c Immigrant visible minority vs Canadian white. Model 1: Demographic, social, and economic characteristics: Immigrant status, sex, age, education, household income. Model 2: Model 1 + Physical Health: Co-morbidities, hypertension, chronic pain. Model 3: Model 2 + Health Behaviours: smoking, binge drinking, physical activity. Model 4: Model 3 + Over-nutrition: Disease risk, percent body fat, waist-to-hip ratio, waist-to-height ratio. Model 5: Model 4 + Poor nutrition: Grip strength, nutrition risk (SCREEN™), skeletal muscle index, T-scores, anemia screen, Model 6: Model 5 + Dietary Intakes: Fiber, pulses/nuts, fat sources, fish sources, omega-3 eggs, fruits and vegetables, pure fruit juice, salty snacks, calcium sources with high vitamin D content, calcium sources with low vitamin D content, pastries, chocolate bars. Model 7: Full Model: All variables in models 1–7

Adjusted odds ratios for PTSD by ethnicity and immigrant status a Canadian-born visible minority vs Canadian-born white. b Immigrant white vs Canadian-born white. c Immigrant visible minority vs Canadian white. Model 1: Demographic, social, and economic characteristics: Immigrant status, sex, age, education, household income. Model 2: Model 1 + Physical Health: Co-morbidities, hypertension, chronic pain. Model 3: Model 2 + Health Behaviours: smoking, binge drinking, physical activity. Model 4: Model 3 + Over-nutrition: Disease risk, percent body fat, waist-to-hip ratio, waist-to-height ratio. Model 5: Model 4 + Poor nutrition: Grip strength, nutrition risk (SCREEN™), skeletal muscle index, T-scores, anemia screen, Model 6: Model 5 + Dietary Intakes: Fiber, pulses/nuts, fat sources, fish sources, omega-3 eggs, fruits and vegetables, pure fruit juice, salty snacks, calcium sources with high vitamin D content, calcium sources with low vitamin D content, pastries, chocolate bars. Model 7: Full Model: All variables in models 1–7

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PurposeThis study aimed to address knowledge gaps about post-traumatic stress disorder (PTSD) in mid-age and older adults, with particular attention to the relationship of PTSD with nutrition and with ethnicity and immigrant status.Methods Binary logistic regression analysis of weighted comprehensive cohort data from the baseline Canadian Longitudi...

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... A low level of education has been reported to predict PTSD in other settings [35], but this finding was not confirmed in the present case. Inversely, being older than 65 had a protective role in the development of a diagnosis of PTSD and its symptoms over time, confirming previous findings on the general pathogenesis of PTSD [36]. Age, however, was not multivariately associated with chronic PTSD. ...
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Background: Coronavirus disease (COVID-19) hospitalization has been related to Post-Traumatic Stress Disorder (PTSD). Available information is limited by insufficient follow-up and lack of longitudinal studies. Baseline factors (e.g., sex; obesity) have been related to PTSD, but post-hospitalization factors have not been studied. Objective: This study aimed to analyse prevalence, baseline, post-discharge factors and possible clinical courses of PTSD after hospitalization for COVID-19. Method: 109 patients (94.7% of the original sample) completed a programme of three follow-up telephone assessments during the year following hospitalization. Data included clinical and sociodemographic factors as well as psychometric tools assessing PTSD, social support, and perception of threat to life (PTL). Mixture model analysis was performed to study the longitudinal course of PTSD symptoms. Chronic (>6 months) PTSD predictors were also analysed. Results: 1-year PTSD period prevalence was 23.9%, peaking at six months; 11% of the patients suffered chronic PTSD. Pre- and post-hospitalization factors influenced the onset and course of PTSD over time. These included working status, PTL, and lack of social support. Interestingly, obesity, pulmonary diseases and family cluster infection seem specifically related to PTSD following COVID-19. Inversely, clinical interventions, older age and male gender were protective. Conclusions: PTSD following COVID-19 hospitalization is common. The analysed demographic, social, clinical, and psychological factors predict PTSD symptomatology over time and can modify odds of a chronic course. Clinicians could better identify cases at risk of a chronic PTSD course. Finally, treatment as usual appeared related to a better outcome and should be proposed to patients with PTSD.
... Specific to PTSD, a longitudinal study of middleaged and older adults revealed that "minority" immigrant Canadians had a higher chance of PTSD compared to nonimmigrant Canadians, while White immigrants had a lower chance of PTSD [88]. It is very likely that this difference in the relationship between PTSD and ethnicity may be moderated by discrimination and racism. ...
... Although the preceding Table 1 Research-to-date summary of mental health outcomes due to racism Asterisk means the symptom was reported higher in women. [86][87][88] • PTSD [66,67,79,[88][89][90] literature gives inferences into the environmental ramifications of racial trauma, the overall amount of supporting literature remains inadequate. ...
... Although the preceding Table 1 Research-to-date summary of mental health outcomes due to racism Asterisk means the symptom was reported higher in women. [86][87][88] • PTSD [66,67,79,[88][89][90] literature gives inferences into the environmental ramifications of racial trauma, the overall amount of supporting literature remains inadequate. ...
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Purpose of Review While research has identified racial trauma in other contexts, it is often overlooked amongst Canadian society. Racial trauma occurs as a result of an event of racism or cumulative events over time whereby an individual experiences stress and consequent mental health sequelae. Given that the BIPOC (Black, Indigenous, and/or Person of Colour) population in Canada is increasing, it is imperative to identify racial discrimination and the subsequent stress and trauma associated with being racialized in Canada, which subjects BIPOC Canadians to various forms of racism, including microaggressions. Recent Findings This paper reviews the published literature on racism and racial discrimination that identifies or infers racial trauma as the source of the mental health implications for various groups (e.g., Indigenous people, Black Canadians, Asian Canadians, immigrants, and refugees). In addition, intersectionality of racialized persons is prominent to their psychological well-being as their psychosocial and socioeconomic position are complex. Therefore, this paper both provides insight into the Canadian experience as a person of colour and signifies the need for further research on racial trauma in a Canadian context. Summary Despite Canada’s emphasis on multiculturalism, racialized individuals are at risk for racial trauma due to prejudice and discrimination. The politicization of multiculturalism has permitted Canada to deny claims of racism, yet the historical basis of established institutions results in irrefutable systemic and systematic barriers for Canadian people of colour.
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Objective Canada exhibits one of highest lifetime prevalence for post-traumatic stress disorder (PTSD), but the etiology of this debilitating mental health condition still remains largely unknown. This study aims to examine the genetics of PTSD in the Canadian Longitudinal Study on Aging (CLSA) to identify potential genetic factors involved in the development of PTSD. Method The CLSA sample was screened for primary (PTSD status) and secondary outcomes (avoidance, detachment, guardedness, and nightmares) based on the Primary Care PTSD Screen Scale (PC-PTSD). After GWAS quality control and whole-genome imputation, single-marker, gene-based, and polygenic risk score (PRS) analyses were performed. Results Based on available genotype and phenotype data, N = 16,535 individuals were selected for the analyses. While genome-wide analyses did not show significant findings for our primary and secondary outcomes, PRS analyses showed variable levels of association between PC-PTSD items with trauma, major depressive disorder, schizophrenia, bipolar disorder, educational attainment, and insomnia (p < 5e-4). Conclusion This is the first GWAS of PTSD status and individual PC-PTSD items in a population sample of older adults from Canada. This study was also able to replicate findings from previous studies. Genetic investigations into individual symptom components of PTSD may help untangle the complex genetic architecture of PTSD.
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Muscle sympathetic nerve activity (MSNA) increases during isometric exercise via increased firing of low-threshold action potentials (AP), recruitment of larger, higher-threshold APs, and synaptic delay modifications. Recent work found that women with post-traumatic stress disorder (PTSD) demonstrate exaggerated early-onset MSNA responses to exercise; however, it is unclear how PTSD affects AP recruitment patterns during fatiguing exercise. We hypothesized that women with PTSD (n = 11, 43 [11] [SD] years) would exhibit exaggerated sympathetic neural recruitment compared to women without PTSD (controls; n = 13, 40 [8] years). MSNA and AP discharge patterns (via microneurography and a continuous wavelet transform) were measured during 1 min of baseline, isometric handgrip exercise (IHG) to fatigue, 2 min of post-exercise circulatory occlusion (PECO), and 3 min of recovery. Women with PTSD were unable to increase AP content per burst compared to controls throughout IHG and PECO (main effect of group: P = 0.026). Furthermore, relative to controls, women with PTSD recruited fewer AP clusters per burst during the first (controls: ∆1.3 [1.2] vs. PTSD: ∆-0.2 [0.8]; P = 0.016) and second minute (controls: ∆1.2 [1.1] vs. PTSD: ∆-0.1 [0.8]; P = 0.022) of PECO, and fewer subpopulations of larger, previously silent axons during the first (controls: ∆5 [4] vs. PTSD: ∆1 [2]; P = 0.020) and second minute (controls: ∆4 [2] vs. PTSD: ∆1 [2]; P = 0.021) of PECO. Conversely, PTSD did not modify the AP cluster size-latency relationship during baseline, the end of IHG, or PECO (all P = 0.658-0.745). Collectively, these data indicate that women with PTSD demonstrate inherent impairments in the fundamental neural coding patterns elicited by the sympathetic nervous system during IHG and exercise pressor reflex activation.
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Background Patients with post-traumatic stress disorder (PTSD) have an increased risk for cardiovascular disease. The underlying mechanisms are unclear but impaired autonomic function may contribute. However, research in this field has shown contradictory results and the causal links between PTSD, autonomic dysfunction, and cardiovascular risk remain unknown. This brief review summarizes the current knowledge on alterations in autonomic function and cardiovascular risk in patients with PTSD. Literature search strategy A PubMed search of the literature was performed using the following keywords: autonomic function, heart rate variability, blood pressure variability, sympathetic activity, baroreflex function, and cardiovascular risk in combination with PTSD. Evidence-based studies conducted between 2000 and 2021 were selected. Results In total 1221 articles were identified and of these, 61 (48 original research papers, 13 review articles) were included in this review. Many, though not all, studies have reported increased activity of the sympathetic nervous system and decreased activity of the parasympathetic nervous system (namely, autonomic imbalance) in PTSD patients. There seems to be enough evidence to suggest impairments in baroreflex function in PTSD, leading to blood pressure dysregulation. It appears that the chronicity of PTSD diagnosis and symptom severity are independent risk factors for cardiovascular disease, which may be linked with impaired autonomic function. Conclusions Increased cardiovascular risk may be associated with autonomic dysfunction in PTSD. Whether autonomic dysfunction can serve as a biomarker for the onset and progression of PTSD remains to be determined. It also needs to determine if autonomic imbalance increases the risk of developing PTSD.