The novel coronavirus disease (COVID-19) pandemic has brought a great deal of pressure for medical students, who typically show elevated anxiety rates. Our aim is to investigate the prevalence of anxiety in medical students during this pandemic. This systematic review and mini meta-analysis has been conducted following the PRISMA guidelines. Two researchers independently searched PubMed on 26 August 2020 for cross-sectional studies on medical students during the COVID-19 outbreak, with no language restrictions applied. We then performed a manual search to detect other potentially eligible investigations. To the 1361 records retrieved in the initial search, 4 more were added by manual search on medRxiv. Finally, eight studies were finally included for qualitative and quantitative analysis, which yielded an estimated prevalence of anxiety of 28% (95% CI: 22–34%), with significant heterogeneity between studies. The prevalence of anxiety in medical students is similar to that prior to the pandemic but correlates with several specific COVID-related stressors. While some preventive and risk factors have been previously identified in a non-pandemic context, knowledge and cognitions on COVID-19 transmission, treatment, prognosis and prevention negatively correlate with anxiety, emerging as a key preventive factor that may provide a rationale for why the levels of anxiety have remained stable in medical students during the pandemic while increasing in their non-medical peers and the general population. Other reasons for the invariability of anxiety rates in this population are discussed. A major limitation of our review is that Chinese students comprised 89% the total sample, which could compromise the external validity of our work

Respiratory rate and heart rate variability (HRV) are studied as stress markers in a database of young healthy volunteers subjected to acute emotional stress, induced by a modification of the Trier Social Stress Test. First, instantaneous frequency domain HRV parameters are computed using time-frequency analysis in the classical bands. Then, the respiratory rate is estimated and this information is included in HRV analysis in two ways: 1) redefining the high-frequency (HF) band to be centered at respiratory frequency; 2) excluding from the analysis those instants where respiratory frequency falls within the low-frequency (LF) band. Classical frequency domain HRV indices scarcely show statistical differences during stress. However, when including respiratory frequency information in HRV analysis, the normalized LF power as well as the LF/HF ratio significantly increase during stress (p-value <; 0.05 according to the Wilcoxon test), revealing higher sympathetic dominance. The LF power increases during stress, only being significantly different in a stress anticipation stage, while the HF power decreases during stress, only being significantly different during the stress task demanding attention. Our results support that joint analysis of respiration and HRV obtains a more reliable characterization of autonomic nervous response to stress. In addition, the respiratory rate is observed to be higher and less stable during stress than during relax (p-value <; 0.05 according to the Wilcoxon test) being the most discriminative index for stress stratification (AUC = 88.2%).

Social and medical problems associated with stress are increasing globally and seriously affect mental health and well-being. However, an effective stress-level monitoring method is still not available. This paper presents a quantitative method for monitoring acute stress levels in healthy young people using biomarkers from physiological signals that can be unobtrusively monitored. Two states were induced to 40 volunteers, a basal state generated with a relaxation task and an acute stress state generated by applying a standard stress test that includes five different tasks. Standard psychological questionnaires and biochemical markers were utilized as ground truth of stress levels. A multivariable approach to comprehensively measure the physiological stress response is proposed using stress biomarkers derived from skin temperature, heart rate, and pulse wave signals. Acute physiological stress levels (total-range 0–100 au) were continuously estimated every 1 min showing medians of 29.06 au in the relaxation tasks, while rising from 34.58 to 47.55 au in the stress tasks. Moreover, using the proposed method, five statistically different stress levels induced by the performed tasks were also measured. Results obtained show that, in these experimental conditions, stress can be monitored from unobtrusive biomarkers. Thus, a more general stress monitoring method could be derived based on this approach.

With no effective treatments for cognitive decline or dementia, improving the evidence base for modifiable risk factors is a research priority. This study investigated associations between risk factors and late-life cognitive decline on a global scale, including comparisons between ethno-regional groups. We harmonized longitudinal data from 20 population-based cohorts from 15 countries over 5 continents, including 48,522 individuals (58.4% women) aged 54–105 (mean = 72.7) years and without dementia at baseline. Studies had 2–15 years of follow-up. The risk factors investigated were age, sex, education, alcohol consumption, anxiety, apolipoprotein E ε4 allele (APOE*4) status, atrial fibrillation, blood pressure and pulse pressure, body mass index, cardiovascular disease, depression, diabetes, self-rated health, high cholesterol, hypertension, peripheral vascular disease, physical activity, smoking, and history of stroke. Associations with risk factors were determined for a global cognitive composite outcome (memory, language, processing speed, and executive functioning tests) and Mini-Mental State Examination score. Individual participant data meta-analyses of multivariable linear mixed model results pooled across cohorts revealed that for at least 1 cognitive outcome, age (B = −0.1, SE = 0.01), APOE*4 carriage (B = −0.31, SE = 0.11), depression (B = −0.11, SE = 0.06), diabetes (B = −0.23, SE = 0.10), current smoking (B = −0.20, SE = 0.08), and history of stroke (B = −0.22, SE = 0.09) were independently associated with poorer cognitive performance (p < 0.05 for all), and higher levels of education (B = 0.12, SE = 0.02) and vigorous physical activity (B = 0.17, SE = 0.06) were associated with better performance (p < 0.01 for both). Age (B = −0.07, SE = 0.01), APOE*4 carriage (B = −0.41, SE = 0.18), and diabetes (B = −0.18, SE = 0.10) were independently associated with faster cognitive decline (p < 0.05 for all). Different effects between Asian people and white people included stronger associations for Asian people between ever smoking and poorer cognition (group by risk factor interaction: B = −0.24, SE = 0.12), and between diabetes and cognitive decline (B = −0.66, SE = 0.27; p < 0.05 for both). Limitations of our study include a loss or distortion of risk factor data with harmonization, and not investigating factors at midlife. These results suggest that education, smoking, physical activity, diabetes, and stroke are all modifiable factors associated with cognitive decline. If these factors are determined to be causal, controlling them could minimize worldwide levels of cognitive decline. However, any global prevention strategy may need to consider ethno-regional differences.