Data-driven collaborative QUality improvement in Cardiac Rehabilitation (QUICR) to increase program completion: protocol for a cluster randomized controlled trial.

BACKGROUND: Coronary heart disease (CHD) is the leading cause of deaths and disability worldwide. Cardiac rehabilitation (CR) effectively reduces the risk of future cardiac events and is strongly recommended in international clinical guidelines. However, CR program quality is highly variable with divergent data systems, which, when combined, potentially contribute to persistently low completion rates. The QUality Improvement in Cardiac Rehabilitation (QUICR) trial aims to determine whether a data-driven collaborative quality improvement intervention delivered at the program level over 12 months: (1) increases CR program completion in eligible patients with CHD (primary outcome), (2) reduces hospital admissions, emergency department presentations and deaths, and costs, (3) improves the proportion of patients receiving guideline-indicated CR according to national and international benchmarks, and (4) is feasible and sustainable for CR staff to implement routinely. METHODS: QUICR is a multi-centre, type-2, hybrid effectiveness-implementation cluster-randomized controlled trial (cRCT) with 12-month follow-up. Eligible CR programs (n = 40) and the individual patient data within them (n ~ 2,000) recruited from two Australian states (New South Wales and Victoria) are randomized 1:1 to the intervention (collaborative quality improvement intervention that uses data to identify and manage gaps in care) or control (usual care with data collection only). This sample size is required to achieve 80% power to detect a difference in completion rate of 22%. Outcomes will be assessed using intention-to-treat principles. Mixed-effects linear and logistic regression models accounting for clusters within allocated groupings will be applied to analyse primary and secondary outcomes. DISCUSSION: Addressing poor participation in CR by patients with CHD has been a longstanding challenge that needs innovative strategies to change the status-quo. This trial will harness the collaborative power of CR programs working simultaneously on common problem areas and using local data to drive performance. The use of data linkage for collection of outcomes offers an efficient way to evaluate this intervention and support the improvement of health service delivery. ETHICS: Primary ethical approval was obtained from the Northern Sydney Local Health District Human Research Ethics Committee (2023/ETH01093), along with site-specific governance approvals. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry (ANZCTR) ACTRN12623001239651 (30/11/2023) ( https://anzctr.org.au/Trial/Registration/TrialReview.aspx?id=386540&isReview=true ).

Depressive symptoms and cognitive decline in older adults.

OBJECTIVES: Few studies have examined the impact of late-life depression trajectories on specific domains of cognitive function. This study aims to delineate how different depressive symptom trajectories specifically affect cognitive function in older adults. DESIGN: Prospective longitudinal cohort study. SETTING: Australia and the United States of America. PARTICIPANTS: In total, 11,035 community-dwelling older adults with a mean age of 75 years. MEASUREMENTS: Depressive trajectories were modelled from depressive symptoms according to annual Centre for Epidemiological Studies Depression Scale 10 (CES-D-10) surveys. Four trajectories of depressive symptoms were identified: low ("nondepressed"), consistently mild ("subthreshold depression"), consistently moderate ("persistent depression"), and initially low but increasing ("emerging depression"). Global cognition (Modified Mini-Mental State Examination [3MS]), verbal fluency (Controlled Oral Word Association Test [COWAT]), processing speed (Symbol Digit Modalities Test [SDMT]), episodic memory (Hopkins Verbal Learning Test - Revised [HVLT-R]), and a composite z-score were assessed over a subsequent median 2 years. RESULTS: Subthreshold depression predicted impaired performance on the SDMT (Cohen's d -0.04) and composite score (-0.03); emerging depression predicted impaired performance on the SDMT (-0.13), HVLT-R (-0.09), 3 MS (-0.08) and composite score (-0.09); and persistent depression predicted impaired performance on the SDMT (-0.08), 3 MS (-0.11), and composite score (-0.09). CONCLUSIONS: Depressive symptoms are associated with later impaired processing speed. These effects are small. Diverse depression trajectories have different impacts on cognitive function.

Time use, time pressure and sleep: is gender an effect modifier?

BACKGROUND: The gendered division of labour contributes to differences in the way time is spent and experienced by women and men. Time spent in paid and unpaid labour is associated with sleep outcomes, therefore, we examined (i) the relationships between time use and time pressure, and sleep, and (ii) whether these relationships were modified by gender. METHODS: Adults from the Household Income and Labour Dynamics in Australia survey were included in the analysis (N = 7611). Two measures of time use (total time commitments, ≥50% of time spent in paid work) were calculated based on estimates of time spent in different activities. One measure of time pressure was also included. Three sleep outcomes (quality, duration and difficulties) were examined. Logistic regression and effect measure modification analyses were employed. RESULTS: Total time commitments were associated with sleep duration, whereby more hours of total time commitments were associated with an increase in the odds of reporting <7 h sleep. Gender was an effect modifier of the association between ≥50% of time spent in paid work and (i) sleep duration on the multiplicative scale, and (ii) sleep difficulties on the multiplicative and additive scales. Men who spent <50% of time in paid work reported more sleep difficulties than men who spent ≥50% of time spent in paid work. Feeling time pressured was associated with poor sleep quality, short sleep duration and sleep difficulties. CONCLUSIONS: Time use and time pressure were associated with sleep, with some effects experienced differently for men and women.

A National Survey of Patient Data Capture, Management, Reporting Practice in Australian Cardiac Rehabilitation Programs.

BACKGROUND: Lack of service data for cardiac rehabilitation limits understanding of program delivery, benchmarking and quality improvement. This study aimed to describe current practices, management, utilisation and engagement with quality indicators in Australian programs. METHOD: Cardiac rehabilitation programs (n=396) were identified from national directories and networks. Program coordinators were surveyed on service data capture, management systems and adoption of published national quality indicators. Text responses were coded and classified. Logistic regression determined independent associates of the use of data for quality improvement. RESULTS: A total of 319 (81%) coordinators completed the survey. Annual patient enrolments/programs were >200 (31.0%), 51-200 (46%) and ≤50 (23%). Most (79%) programs used an electronic system, alongside paper (63%) and/or another electronic system (19%), with 21% completely paper. While 84% knew of the national quality indicators, only 52% used them. Supplementary to patient care, data were used for reports to managers (57%) and funders (41%), to improve quality (56%), support funding (43%) and research (31%). Using data for quality improvement was more likely when enrolments where >200 (Odds ratio [OR] 3.83, 95% Confidence Interval [CI] 1.76-8.34) and less likely in Victoria (OR 0.24 95%, CI 0.08-0.77), New South Wales (OR 0.25 95%, CI 0.08-0.76) and Western Australia (OR 0.16 95%, CI 0.05-0.57). CONCLUSIONS: The collection of service data for cardiac rehabilitation patient data and its justification is diverse, limiting our capacity to benchmark and drive clinical practice. The findings strengthen the case for a national low-burden approach to data capture for quality care.

Brain derived neurotrophic factor in perioperative neurocognitive disorders: Current evidence and future directions.

An increase in the age of surgical patients as well as the volume of surgeries is associated with a rise in perioperative neurocognitive disorders. These disorders encompass acute delirium and longer-term cognitive dysfunctions. Brain derived neurotrophic factor (BDNF) is a neurotrophin that plays a dynamic role in a series of neurological functions including neuroplasticity, neurogenesis and synaptic regulation. Given the possible alterations to brain physiology in response to surgery, this review aims to explore the relationship between changes in central and peripheral BDNF concentrations and perioperative neurocognitive disorders. Higher levels of Brain tissue and blood BDNF have been associated with better cognitive function; however, the nature of the association between BDNF and delirium is uncertain. Preclinical models point to a significant depletion in BDNF expression and signalling within the brain post-operatively, while preliminary human studies demonstrate depletions in serum BDNF concentration after surgery. These findings suggest that the reduced BDNF concentrations may be associated with post-operative cognitive dysfunction. Thus, understanding the BDNF expression/signalling pathways may present a promising avenue for managing perioperative neurocognitive disorders symptoms. Nonetheless, given that results were primarily derived from preclinical models, it is critical for these findings to be validated in humans to confirm the relevance of this promising target.

Biology, Bias, or Both? The Contribution of Sex and Gender to the Disparity in Cardiovascular Outcomes Between Women and Men.

PURPOSE OF REVIEW: Cardiovascular disease (CVD) is the leading cause of mortality and morbidity worldwide for both men and women. However, CVD is understudied, underdiagnosed, and undertreated in women. This bias has resulted in women being disproportionately affected by CVD when compared to men. The aim of this narrative review is to explore the contribution of sex and gender on CVD outcomes in men and women and offer recommendations for researchers and clinicians. RECENT FINDINGS: Evidence demonstrates that there are sex differences (e.g., menopause and pregnancy complications) and gender differences (e.g., socialization of gender) that contribute to the inequality in risk, presentation, and treatment of CVD in women. To start addressing the CVD issues that disproportionately impact women, it is essential that these sex and gender differences are addressed through educating health care professionals on gender bias; offering patient-centered care and programs tailored to women's needs; and conducting inclusive health research.

The kynurenine pathway in major depressive disorder, bipolar disorder, and schizophrenia: a meta-analysis of 101 studies.

The importance of tryptophan as a precursor for neuroactive compounds has long been acknowledged. The metabolism of tryptophan along the kynurenine pathway and its involvement in mental disorders is an emerging area in psychiatry. We performed a meta-analysis to examine the differences in kynurenine metabolites in major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SZ). Electronic databases were searched for studies that assessed metabolites involved in the kynurenine pathway (tryptophan, kynurenine, kynurenic acid, quinolinic acid, 3-hydroxykynurenine, and their associate ratios) in people with MDD, SZ, or BD, compared to controls. We computed the difference in metabolite concentrations between people with MDD, BD, or SZ, and controls, presented as Hedges' g with 95% confidence intervals. A total of 101 studies with 10,912 participants were included. Tryptophan and kynurenine are decreased across MDD, BD, and SZ; kynurenic acid and the kynurenic acid to quinolinic acid ratio are decreased in mood disorders (i.e., MDD and BD), whereas kynurenic acid is not altered in SZ; kynurenic acid to 3-hydroxykynurenine ratio is decreased in MDD but not SZ. Kynurenic acid to kynurenine ratio is decreased in MDD and SZ, and the kynurenine to tryptophan ratio is increased in MDD and SZ. Our results suggest that there is a shift in the tryptophan metabolism from serotonin to the kynurenine pathway, across these psychiatric disorders. In addition, a differential pattern exists between mood disorders and SZ, with a preferential metabolism of kynurenine to the potentially neurotoxic quinolinic acid instead of the neuroprotective kynurenic acid in mood disorders but not in SZ.

Diet and depression: exploring the biological mechanisms of action.

The field of nutritional psychiatry has generated observational and efficacy data supporting a role for healthy dietary patterns in depression onset and symptom management. To guide future clinical trials and targeted dietary therapies, this review provides an overview of what is currently known regarding underlying mechanisms of action by which diet may influence mental and brain health. The mechanisms of action associating diet with health outcomes are complex, multifaceted, interacting, and not restricted to any one biological pathway. Numerous pathways were identified through which diet could plausibly affect mental health. These include modulation of pathways involved in inflammation, oxidative stress, epigenetics, mitochondrial dysfunction, the gut microbiota, tryptophan-kynurenine metabolism, the HPA axis, neurogenesis and BDNF, epigenetics, and obesity. However, the nascent nature of the nutritional psychiatry field to date means that the existing literature identified in this review is largely comprised of preclinical animal studies. To fully identify and elucidate complex mechanisms of action, intervention studies that assess markers related to these pathways within clinically diagnosed human populations are needed.

The effect of vitamin D supplementation on depressive symptoms in adults: A systematic review and meta-analysis of randomized controlled trials.

Neurosteroid and immunological actions of vitamin D may regulate depression-linked physiology. Meta-analyses investigating the effect of vitamin D on depression have been inconsistent. This meta-analysis investigated the efficacy of vitamin D in reducing depressive symptoms among adults in randomized placebo-controlled trials (RCT). General and clinical populations, and studies of ill individuals with systemic diseases were included. Light therapy, co-supplementation (except calcium) and bipolar disorder were exclusionary. Databases Medline, PsycINFO, CINAHL and The Cochrane Library were searched to identify relevant articles in English published before April 2022. Cochrane risk-of-bias tool (RoB 2) and GRADE were used to appraise studies. Forty-one RCTs (n = 53,235) were included. Analyses based on random-effects models were performed with the Comprehensive Meta-analysis Software. Results for main outcome (n = 53,235) revealed a positive effect of vitamin D on depressive symptoms (Hedges' g = -0.317, 95% CI [-0.405, -0.230], p < 0.001, I2 = 88.16%; GRADE: very low certainty). RoB assessment was concerning in most studies. Notwithstanding high heterogeneity, vitamin D supplementation ≥ 2,000 IU/day appears to reduce depressive symptoms. Future research should investigate possible benefits of augmenting standard treatments with vitamin D in clinical depression. PROSPERO registration number: CRD42020149760. Funding: Finnish Medical Foundation, grant 4120 and Juho Vainio Foundation, grant 202100353.

Effectiveness of nutrition and dietary interventions for people with serious mental illness: systematic review and meta-analysis.

OBJECTIVE: To review recent published trials of nutrition and dietary interventions for people with serious mental illness; to assess their effectiveness in improving metabolic syndrome risk factors. STUDY DESIGN: Systematic review and meta-analysis of randomised and non-randomised controlled trials of interventions with a nutrition/diet-related component delivered to people with serious mental illness, published 1 January 2010 - 6 September 2021. Primary outcomes were weight, body mass index (BMI), and waist circumference. Secondary outcomes were total serum cholesterol, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, triglyceride, and blood glucose levels. DATA SOURCES: MEDLINE, EMBASE, PsycINFO, CINAHL, and CENTRAL databases. In addition, reference lists of relevant publications were examined for further additional studies. DATA SYNTHESIS: Twenty-five studies encompassing 26 intervention arms were included in our analysis. Eight studies were at low or some risk of bias, seventeen were deemed to be at high risk. Eight of seventeen intervention arms found statistically significant intervention effects on weight, ten of 24 on BMI, and seven of seventeen on waist circumference. The pooled effects of nutrition interventions on metabolic syndrome risk factors were statistically non-significant. However, we identified small size effects on weight for interventions delivered by dietitians (five studies; 262 intervention, 258 control participants; standardised mean difference [SMD], -0.28; 95% CI, -0.51 to -0.04) and interventions consisting of individual sessions only (three studies; 141 intervention, 134 control participants; SMD, -0.30; 95% CI, -0.54 to -0.06). CONCLUSIONS: We found only limited evidence for nutrition interventions improving metabolic syndrome risk factors in people with serious mental illness. However, they may be more effective when delivered on an individual basis or by dietitians. PROSPERO REGISTRATION: CRD42021235979 (prospective).

Urinary sodium concentration predicts time to major adverse coronary events and all-cause mortality in men with heart failure over a 28-33-year period: a prospective cohort study.

BACKGROUND: Lower urinary sodium concentrations (UNa) may be a biomarker for poor prognosis in chronic heart failure (HF). However, no data exist to determine its prognostic association over the long-term. We investigated whether UNa predicted major adverse coronary events (MACE) and all-cause mortality over 28-33 years. METHODS: One hundred and eighty men with chronic HF from the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD) were included. Baseline data was collected between 1984 and 1989. MACE and all-cause outcomes were obtained using hospital linkage data (1984-2017) with a follow-up of 28-33 years. Cox proportional hazards models were generated using 24-h UNa tertiles at baseline (1 ≤ 173 mmol/day; 2 = 173-229 mmol/day; 3 = 230-491 mmol/day) as a predictor of time-to-MACE outcomes, adjusted for relevant covariates. RESULTS: Overall, 63% and 83% of participants (n = 114 and n = 150) had a MACE event (median 10 years) and all-cause mortality event (median 19 years), respectively. On multivariable Cox Model, relative to the lowest UNa tertile, no significant difference was noted in MACE outcome for individuals in tertiles 2 and 3 with events rates of 28% (HR:0.72; 95% CI: 0.46-1.12) and 21% (HR 0.79; 95% CI: 0.5-1.25) respectively.. Relative to the lowest UNa tertile, those in tertile 2 and 3 were 39% (HR: 0.61; 95% CIs: 0.41, 0.91) and 10% (HR: 0.90; 95% CIs: 0.62, 1.33) less likely to experience to experience all-cause mortality. The multivariable Cox model had acceptable prediction precision (Harrell's C concordance measure 0.72). CONCLUSION: UNa was a significant predictor of all-cause mortality but not MACE outcomes over 28-33 years with 173-229 mmol/day appearing to be the optimal level. UNa may represent an emerging long-term prognostic biomarker that warrants further investigation.

Evaluating telehealth lifestyle therapy versus telehealth psychotherapy for reducing depression in adults with COVID-19 related distress: the curbing anxiety and depression using lifestyle medicine (CALM) randomised non-inferiority trial protocol.

BACKGROUND: There is increasing recognition of the substantial burden of mental health disorders at an individual and population level, including consequent demand on mental health services. Lifestyle-based mental healthcare offers an additional approach to existing services with potential to help alleviate system burden. Despite the latest Royal Australian New Zealand College of Psychiatrists guidelines recommending that lifestyle is a 'first-line', 'non-negotiable' treatment for mood disorders, few such programs exist within clinical practice. Additionally, there are limited data to determine whether lifestyle approaches are equivalent to established treatments. Using an individually randomised group treatment design, we aim to address this gap by evaluating an integrated lifestyle program (CALM) compared to an established therapy (psychotherapy), both delivered via telehealth. It is hypothesised that the CALM program will not be inferior to psychotherapy with respect to depressive symptoms at 8 weeks. METHODS: The study is being conducted in partnership with Barwon Health's Mental Health, Drugs & Alcohol Service (Geelong, Victoria), from which 184 participants from its service and surrounding regions are being recruited. Eligible participants with elevated psychological distress are being randomised to CALM or psychotherapy. Each takes a trans-diagnostic approach, and comprises four weekly (weeks 1-4) and two fortnightly (weeks 6 and 8) 90-min, group-based sessions delivered via Zoom (digital video conferencing platform). CALM focuses on enhancing knowledge, behavioural skills and support for improving dietary and physical activity behaviours, delivered by an Accredited Exercise Physiologist and Accredited Practising Dietitian. Psychotherapy uses cognitive behavioural therapy (CBT) delivered by a Psychologist or Clinical Psychologist, and Provisional Psychologist. Data collection occurs at baseline and 8 weeks. The primary outcome is depressive symptoms (assessed via the Patient Health Questionnaire-9) at 8 weeks. Societal and healthcare costs will be estimated to determine the cost-effectiveness of the CALM program. A process evaluation will determine its reach, adoption, implementation and maintenance. DISCUSSION: If the CALM program is non-inferior to psychotherapy, this study will provide the first evidence to support lifestyle-based mental healthcare as an additional care model to support individuals experiencing psychological distress. TRIAL REGISTRATION: Australia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12621000387820 , Registered 8 April 2021.

Psychological distress as a risk factor for all-cause, chronic disease- and suicide-specific mortality: a prospective analysis using data from the National Health Interview Survey.

PURPOSE: The risk psychological distress (PD) confers on mortality due to specific chronic diseases compared to suicide is unclear. Using the National Health Interview Survey (NHIS), we investigated the association between PD levels and risk of all-cause and chronic disease-specific mortality and compared the contribution of chronic disease-related mortality to that of suicide. METHODS: Data from 195, 531 adults, who participated in the NHIS between 1997 and 2004, were linked to the National Death Index records through to 2006. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and their 95% confidence intervals (CIs) across four levels of PD, measured using the Kessler-6 scale. Outcomes included all-cause mortality, and mortality due to all CVDs and subtypes, all cancers and subtypes, diabetes mellitus, alcoholic liver disease and suicide. RESULTS: During a mean follow-up time of 5.9 years, 7665 deaths occurred. We found a dose-response association between levels of PD and all-cause mortality, with the adjusted HRs (95% CI) elevated for all levels of PD, when compared to asymptomatic levels: subclinical 1.10 (1.03-1.16), symptomatic 1.36 (1.26-1.46) and highly symptomatic 1.57 (1.37-1.81). A similar association was found for all CVDs and certain CVD subtypes, but not for cancers, cerebrovascular diseases diabetes mellitus. Excess mortality attributable to suicide and alcoholic liver disease was evident among those with levels of PD only. CONCLUSION: PD symptoms, of all levels, were associated with an increased risk of all-cause and CVD-specific mortality while higher PD only was associated with suicide. These findings emphasise the need for lifestyle interventions targeted towards improving physical health disparities among those with PD.

Trends and Predictors of Cardiac Rehabilitation Referral Following Percutaneous Coronary Intervention: A Prospective, Multi-Site Study of 41,739 Patients From the Victorian Cardiac Outcomes Registry (2017-2020).

BACKGROUND: Following percutaneous coronary intervention (PCI), outpatient cardiac rehabilitation (CR) is essential for secondary prevention. However uptake of CR is suboptimal, despite strong evidence demonstrating benefits. The aim of this study was to identify contemporary trends and predictors of CR referral of PCI patients in Victoria. METHODS: A prospective, observational study using data extracted from the Victorian Cardiac Outcomes Registry was undertaken. A total of 41,739 patients were discharged following PCI over the study period (2017-2020) and included for analysis. RESULTS: Cardiac rehabilitation referral was 85%, with an increasing trend over time (p<0.001). Multivariable modelling identifying the independent predictors of CR referral included hospitals with high volumes of ST-elevation myocardial infarction patients (STEMI) (OR 4.89, 95% CI 4.41-5.20), STEMI diagnosis (OR 1.90, 95% CI 1.69-2.14), or treatment in a private hospital (OR 1.45, 95% CI 1.33-1.57). Predictors of non-referral included cardiogenic shock (OR 0.54, 95% CI 0.41-0.71), aged over 75 years (OR 0.62, 95% CI 0.57-0.68) and previous PCI (OR 0.66, 95% CI 0.62-0.70). Percutaneous coronary intervention patients with an acute coronary syndrome who were referred to CR were also more likely to be prescribed four or more major preventive pharmacotherapies, compared to those who were not referred (90% vs 82.1%, p<0.001). CONCLUSION: Our contemporary multicentre analysis showed generally high CR referral rates which have increased over time. However, more effort is needed to target patients treated in the public sector, low volume STEMI hospitals or with short lengths of stay.

The cytokine storms of COVID-19, H1N1 influenza, CRS and MAS compared. Can one sized treatment fit all?

An analysis of published data appertaining to the cytokine storms of COVID-19, H1N1 influenza, cytokine release syndrome (CRS), and macrophage activation syndrome (MAS) reveals many common immunological and biochemical abnormalities. These include evidence of a hyperactive coagulation system with elevated D-dimer and ferritin levels, disseminated intravascular coagulopathy (DIC) and microthrombi coupled with an activated and highly permeable vascular endothelium. Common immune abnormalities include progressive hypercytokinemia with elevated levels of TNF-α, interleukin (IL)-6, and IL-1ß, proinflammatory chemokines, activated macrophages and increased levels of nuclear factor kappa beta (NFκB). Inflammasome activation and release of damage associated molecular patterns (DAMPs) is common to COVID-19, H1N1, and MAS but does not appear to be a feature of CRS. Elevated levels of IL-18 are detected in patients with COVID-19 and MAS but have not been reported in patients with H1N1 influenza and CRS. Elevated interferon-γ is common to H1N1, MAS, and CRS but levels of this molecule appear to be depressed in patients with COVID-19. CD4+ T, CD8+ and NK lymphocytes are involved in the pathophysiology of CRS, MAS, and possibly H1N1 but are reduced in number and dysfunctional in COVID-19. Additional elements underpinning the pathophysiology of cytokine storms include Inflammasome activity and DAMPs. Treatment with anakinra may theoretically offer an avenue to positively manipulate the range of biochemical and immune abnormalities reported in COVID-19 and thought to underpin the pathophysiology of cytokine storms beyond those manipulated via the use of, canakinumab, Jak inhibitors or tocilizumab. Thus, despite the relative success of tocilizumab in reducing mortality in COVID-19 patients already on dexamethasone and promising results with Baricitinib, the combination of anakinra in combination with dexamethasone offers the theoretical prospect of further improvements in patient survival. However, there is currently an absence of trial of evidence in favour or contravening this proposition. Accordingly, a large well powered blinded prospective randomised controlled trial (RCT) to test this hypothesis is recommended.

Assessing the feasibility of an m-Health intervention for changing diet quality and mood in individuals with depression: the My Food & Mood program.

Recent randomized controlled trials have shown that improving diet quality reduces symptoms in those with depression. The provision of digital health interventions that can support dietary change in those with depression has important benefits with respect to reach, accessibility convenience and cost. The My Food & Mood study used single arm cohort design to test the feasibility of such an intervention. Participants with current depressive symptoms were recruited and enrolled online to use the My Food & Mood m-Health (smartphone delivered) program for 8 weeks. Participants completed depression (PHQ-8) and dietary questionnaires (MEDAS) at baseline, week 4 and week 8. Metrics of use and intensity of use engagement measures were calculated from system logs and data entries. There was a significant change in both MEDAS score (t = 8.147, df = 44, p < 0.001) and PHQ-8 score (t = -7.199, df = 44, p < 0.001) throughout the study. There was a moderate positive association between change in MEDAS score and activities completed, goals and weeks engaged, and a strong inverse association between change in MEDAS score and change in PHQ-8 score. An m-Health program targeting dietary intervention in those with depression was feasible. Dietary change was associated with higher engagement and reduced depressive symptoms.

How Does Mental Health Impact Women's Heart Health?

From adolescence until old age, women are more vulnerable to common mental disorders (CMDs; depression and anxiety) than men at all stages of the life course. By middle age, women who have clinical depression are at twice the risk of having an incident cardiovascular disease (CVD) than those without. This has important implications for the way we prevent, identify and treat both CMDs and coronary heart disease in women. In this paper, we discuss the various genetic, biological, ethnic/racial, and psychological pathways by which women's vulnerability to CMDs elevate their CVD risk and recovery from a cardiac event. We review the evidence from trials that have, to date, failed to show that treating depression can reduce or delay the onset or recurrence of CVD events, especially for female patients. We discuss the value of lifestyle-based therapies for treating depression, to which women may be more responsive, and finish by discussing how population-based approaches including risk factor assessment could be tailored to consider these factors.

Resting Heart Rate and Heart Rate Variability in the Year Following Acute Coronary Syndrome: How Do Women Fare?

BACKGROUND: Women experience poorer health outcomes following acute coronary syndrome (ACS). Heart rate (HR) and heart rate variability (HRV) have emerged as sensitive and cost-effective markers of autonomic function and prognostic risk factors of poor cardiac outcomes. The aim of the current study was to investigate whether sex-specific differences existed across HR and five parameters of HRV, at 1 and 12 months following ACS diagnosis. METHODS: Between January 2013 and June 2014, a sample of 416 ACS patients was enrolled in the Anxiety Depression & Heart Rate Variability in cardiac patients: Evaluating the impact of Negative emotions on functioning after Twenty four months (ADVENT) longitudinal cohort study. At 1 and 12 months following discharge, patient HR and HRV (root mean square of successive differences [RMSDD], standard deviation of RR intervals [SDRR], high frequency power [HF], low frequency power [LF], very low frequency power [VLF]) was measured via three-lead electrocardiogram. RESULTS: At 1 month post-ACS, sex was a significant predictor of HR and VLF power in fully- adjusted models. At 12 months post-ACS, sex was a predictor of HR, SDRR and VLF power in fully-adjusted models. CONCLUSION: Sex-specific differences in resting HR and HRV were observed in the year following ACS, whereby women had higher HR and lower HRV, suggestive of poorer autonomic function. Further large-scale cohort studies examining autonomic function as a driver of sex-specific outcomes following ACS are required.

Association between sleep duration and mortality risk among adults with type 2 diabetes: a prospective cohort study.

AIMS/HYPOTHESIS: This study aimed to investigate whether the effects of sleep duration interacted with the presence of diabetes. We specifically sought to examine the relationship between sleep duration and all-cause and cause-specific mortality in people with type 2 diabetes across sex, age at diagnosis, duration of diabetes and treatment type. METHODS: The sample consisted of 273,029 adults, including 248,817 without diabetes and 24,212 with type 2 diabetes, who participated in the National Health Interview Survey from 2004 to 2013 and whose data were linked to a mortality database up to 31 December 2015. Sleep duration was measured using self-report, whereby participants were asked 'on average how long do you sleep each day (≤5, 6, 7, 8, 9 or ≥10 h/day)?' The relationship between sleep duration and mortality risk was investigated using Cox proportional hazards regression model, with adjustments for demographics, BMI, lifestyle behaviours and clinical variables. RESULTS: Absolute mortality rate was higher in adults with diabetes and extremes of sleep duration (≤5 h/day, 215.0 per 10,000 person-years; ≥10 h/day, 363.5 per 10,000 person-years). There was a non-significant interaction between sleep duration and the presence of diabetes (p for interaction = 0.08). A J-shaped relationship existed between sleep duration and all-cause mortality risk in people with type 2 diabetes. Compared with the reference group (7 h/day), both shorter and longer sleep durations were associated with increased risk of all-cause mortality (≤5 h/day, HR 1.24 [95% CI 1.09, 1.40]; 6 h/day, HR 1.13 [1.01, 1.28]; 8 h/day, HR 1.17 [1.06, 1.30]; ≥10 h/day, HR 1.83 [1.61, 2.08]). Similar associations were also observed for mortality risk from CVD, cancer, kidney disease, Alzheimer's disease and chronic lower respiratory diseases. Longer sleep duration in those with a younger age at diabetes onset was associated with greater risks of all-cause and CVD mortality. Shorter sleep duration in individuals treated with both insulin and oral glucose-lowering medication was also associated with higher risks of all-cause and CVD mortality. CONCLUSIONS/INTERPRETATION: The associations between sleep duration and mortality risk may be different between diabetic and non-diabetic individuals. In people with type 2 diabetes, sleeping less or more than 7 h/day was associated with increased risk of all-cause and condition-specific mortality. The association was more prominent in those with a younger age at diabetes onset and receiving treatment with both oral glucose-lowering medication and insulin. This population may benefit from targeted sleep-related interventions to reduce the risks of adverse health outcomes. Graphical abstract.

Inequalities and Deteriorations in Cardiovascular Health in Premenopausal US Women, 1990-2016.

Coronary heart disease (CHD) mortality rates in the United States have declined by up to two thirds in recent decades. Closer examination of these trends reveals substantial inequities in the distribution of mortality benefits. It is worrying that the uneven distribution of CHD that exists from lowest to highest social class-the social gradient-has become more pronounced in the United States since 1990 and is most pronounced for women.Here we consider ways in which this trend disproportionately affects premenopausal women aged 35 to 54 years. We apply a social determinants of health framework focusing on intersecting axes of inequalities-notably gender, class, ethnicity, geographical location, access to wealth, and class-among other power relations to which young and middle-aged women are especially vulnerable, and we argue that increasing inequalities may be driving these unprecedented deteriorations. We conclude by discussing interventions and policies to target and alleviate inequality axes that have potential to promote greater equity in the distribution of CHD mortality and morbidity gains.The application of this framework in the context of women's cardiovascular health can help shed light regarding why we are seeing persistently poorer outcomes for premenopausal US women.