Background and aim: The novel coronavirus disease 2019 (COVID-19) not only threatens physical health but also psychological well-being. As a result of the pandemic, increased mental health burdens have been recorded in young adults around the world. We sought to understand the association of stressors related to the COVID-19 pandemic with symptoms of psychological and emotional distress in young Canadian adults. Method: Questionnaire respondents were asked about the extent to which they were personally impacted by COVID-19, and symptoms related to depression, anxiety, post-traumatic disorder, and emotional distress. Results: Of 84 respondents, most identified as female (74%; 62/84). Overall, 61% (51/84) reported experiencing symptoms of psychological distress related to depression, anxiety, or post-traumatic stress disorder (PTSD); specifically, 43% (36/84) reported anxiety-related symptoms, 33% (28/84) reported depression-related symptoms, and 6% (5/84) reported PTSD-related symptoms. Individuals with family in settings high risk for COVID-19 infection and individuals who received government aid with a reduction in income were 4.30-fold and 2.80-fold more likely, respectively, to experience symptoms of psychological distress (95% CI 1.31–14.14; p = .013 and 95% CI 1.08–7.25; p = .038, respectively). Visits to social media daily to hourly for COVID-19 related news resulted in a 3.24-fold increase in the likelihood of experiencing depression-related symptoms (95% CI 1.26–8.35; p = .020). Conclusion: We demonstrate a necessity to focus on alleviating the mental health burdens and contributing stressors within young Canadian adults. Though the mental health burdens are currently exacerbated by the effects of the COVID-19 pandemic, they may persist after the pandemic ends if left unaddressed.

Author contributions: P.K.G. worked on the experimental design, genomic analyses, prepared figures, and was responsible for preparation of the manuscript and all edits. J.S.D. compiled the patient database, assisted in the experimental design of the study and manuscript preparation and edits. A. J. B. compiled the patient database and assisted in manuscript edits. A.D.M. isolated DNA samples for all patients. H.C. prepared all of the samples for sequencing. J. W. identified copy-number variants in the patient samples. R.A.H. acquired DNA samples for study and assisted in manuscript preparation and edits. All authors have approved the final article. Data availability statement: To maintain patient privacy, we cannot provide individual-level genetic data. Instead, we provide cohort-level genetic data, which includes annotations of each variant identified in the study cohorts (Supplementary Table 2). We have also included the Fredrickson classification system, as well as SNPs and weights used to calculate each polygenic score (Supplementary Tables 1, 3, and 4).

Purpose of reviewThe relationship between elevated triglyceride levels (i.e. hypertriglyceridemia) and risk of atherosclerotic cardiovascular disease (ASCVD) has been investigated for decades. Recent genetic studies have sought to resolve the decades-old question of a causal relationship. Recent findingsGenetic studies seem to demonstrate associations between elevated triglyceride levels and ASCVD risk. Mendelian randomization studies suggest this association may be causal. However, simultaneous pleiotropic effects of metabolically linked lipid variables -such as non-HDL cholesterol, apolipoprotein B and HDL cholesterol -often go unaccounted for in these studies. Complex underlying pleiotropic interactions of triglycerides with these lipid fractions together with unmeasured intercalated nonlipid-related mechanisms, such as inflammation and coagulation, impair the ability of genetic studies to implicate a direct role for triglycerides on ASCVD risk. One potential mechanism seems largely driven by the cholesterol carried within triglyceride-rich lipoproteins and their remnants, rather than their triglyceride content.

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Purpose of review: Familial combined hyperlipidemia (FCH), defined by concurrently elevated plasma triglyceride (TG) and low-density lipoprotein (LDL) cholesterol, has long been investigated to characterize its genetic basis. Despite almost half a century of searching, a single gene cause for the phenotype has not yet been identified.Recent findings: Recent studies using next-generation genetic analytic methods confirm that FCH has a polygenic basis, with a clear large contribution from the accumulation of small-to-moderate effect common single nucleotide polymorphisms (SNPs) throughout the genome that is associated with raising TG, and probably also those raising LDL cholesterol. On the other hand, rare monogenic variants, such as those causing familial hypercholesterolemia, play a negligible role, if any. Genetic profiling suggests that patients with FCH and hypertriglyceridemia share a strong polygenic basis and show a similar profile of multiple TG-raising common SNPs.Summary: Recent progress in genomics has shown that most if not all of the genetic susceptibility to FCH is polygenic in nature. Future research should include larger cohort studies, with wider ancestral diversity, ancestry-specific polygenic scores, and investigation of epigenetic and lifestyle factors to help further elucidate the causative agents at play in cases where the genetic etiology remains to be defined.