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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. Supplementary Information The online version contains supplementary material available at 10.1007/s00127-021-02116-7.

Summary A growing body of evidence suggests that diet quality may predict muscle health. This study found that a “Traditional” dietary pattern predicted greater muscle mass, and an anti-inflammatory diet predicted greater muscle mass and better muscle function over 15 years. These findings reinforce the importance of optimising dietary behaviours for healthy ageing. Introduction Research investigating the roles of individual nutrients in muscle health fails to account for the synergistic relationships between foods and nutrients. This study aimed to investigate the predictive value of diet quality and dietary patterns for muscle mass and function in men over a 15-year period. Methods This longitudinal study was conducted in 522 men from the Geelong Osteoporosis Study with complete dietary and muscle mass or muscle function data at both baseline and 15-year follow-up assessments. Dietary exposures were extracted from food frequency questionnaires and included the Australian Recommended Food Score, the Dietary Inflammatory Index (DII®), and three a posteriori dietary patterns: Plant-focused, Western, and Traditional (Anglo-Australian). Outcome variables included dual-energy X-ray absorptiometry–derived skeletal muscle index (SMI) and muscle function measured with the timed up-and-go (TUG) test. Results An anti-inflammatory diet and higher scores on a Traditional dietary pattern both predicted greater SMI ((B: −0.04 (95%CI −0.08, −0.00) kg/m2) and (B: 0.12 (95%CI 0.04, 0.20) kg/m2), respectively), while a pro-inflammatory diet predicted slower TUG (B: 0.11 (95%CI 0.001, 0.21) sec) over the 15-year follow-up period. These associations remained significant following adjustment for confounding variables. There were no associations observed for other dietary exposures. Conclusion A Traditional dietary pattern higher in vegetables, wholegrain cereals, and animal protein was associated with greater skeletal muscle mass, and an anti-inflammatory diet, also rich in vegetables, fruit, and wholegrain cereals, was associated with greater skeletal muscle mass and better muscle function over 15 years. Supplementary Information The online version contains supplementary material available at 10.1007/s00198-021-06012-3.

Background Attention Deficit Hyperactivity Disorder (ADHD) is a prevalent neurodevelopmental disorder. Effective long-term treatment options are limited, which warrants increased focus on potential modifiable risk factors. The aim of this study was to investigate associations between maternal diet quality during pregnancy and child diet quality and child ADHD symptoms and ADHD diagnosis. Methods This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). We assessed maternal diet quality with the Prenatal Diet Quality Index (PDQI) and Ultra-Processed Food Index (UPFI) around mid-gestation, and child diet quality using the Diet Quality Index (CDQI) at 3 years. ADHD symptoms were assessed at child age 8 years using the Parent Rating Scale for Disruptive Behaviour Disorders. ADHD diagnoses were retrieved from the Norwegian Patient Registry. Results In total, 77,768 mother-child pairs were eligible for studying ADHD diagnoses and 37,787 for ADHD symptoms. Means (SD) for the PDQI, UPFI and CDQI were 83.1 (9.3), 31.8 (9.7) and 60.3 (10.6), respectively. Mean (SD) ADHD symptom score was 8.4 (7.1) and ADHD diagnosis prevalence was 2.9% (male to female ratio 2.6:1). For one SD increase in maternal diet index scores, we saw a change in mean (percent) ADHD symptom score of − 0.28 (− 3.3%) (CI: − 0.41, − 0.14 (− 4.8, − 1.6%)) for PDQI scores and 0.25 (+ 3.0%) (CI: 0.13, 0.38 (1.5, 4.5%)) for UPFI scores. A one SD increase in PDQI score was associated with a relative risk of ADHD diagnosis of 0.87 (CI: 0.79, 0.97). We found no reliable associations with either outcomes for the CDQI, and no reliable change in risk of ADHD diagnosis for the UPFI. Conclusions We provide evidence that overall maternal diet quality during pregnancy is associated with a small decrease in ADHD symptom score at 8 years and lower risk for ADHD diagnosis, with more robust findings for the latter outcome. Consumption of ultra-processed foods was only associated with increased ADHD symptom score of similar magnitude as for overall maternal diet quality, and we found no associations between child diet quality and either outcome. No causal inferences should be made based on these results, due to potential unmeasured confounding.

Depression is a disabling, highly prevalent, frequently chronic, and difficult-to-treat disorder with an immense cognitive, social, and economic burden. Given that many of the advances in other non-communicable disorders like cancer have been in prevention rather than treatment, the prevention of depression is currently an unmet public health priority. We sought to provide an overview of the meta-analytic literature through conducting a systematic umbrella review of universally delivered preventive interventions for depression. The search was conducted on March 18, 2021 utilising the following databases (all accessed through EBSCOHost); Allied and Complementary Medicine Database, CINAHL Complete, Global Health, Health Source: Nursing/Academic Edition, MEDLINE Complete and APA PsychArticles. The following search terms related to depression, prevention, and trial study design. Two authors independently screened articles and a third resolved discrepancies. Eligibility criteria sought to identify meta-analyses that investigated the prevention of depression (i.e., reduced incidence) through intervention studies that were universal, in that they were designed to be delivered to entire populations Six meta-analyses on psychological interventions, two school-based meta-analyses, and one eHealth meta-analysis were included in this umbrella review. Findings indicated that all identified studies were of good quality and one was of fair quality. One previous meta-review that examined physical activity to prevent depression was included in results, comprising eight meta-analyses. Preventive interventions have primarily and successfully utilized psychological therapeutic components, delivered at the school, community, and workplace settings. Both school- and eHealth-based interventions hold some utility for depression prevention. There is meta-analytic evidence that physical activity is efficacious for depression prevention. However, universal prevention is inconsistently defined. There is a pressing need for well-designed randomized controlled preventative interventions for depression before recommendations can be universally accepted with convincing level of evidence.

Lifestyle factors including diet, sleep, physical activity, and substance use cessation, are recognised as treatment targets for common mental disorders (CMDs). As the field of lifestyle-based mental health care evolves towards effectiveness trials and real-world translation, it is timely to consider how such innovations can be integrated into clinical practice. This paper discusses the utility and scale-up of lifestyle interventions for CMDs and draws on diabetes prevention literature to identify enablers and barriers to translation efforts. We discuss the extent to which lifestyle interventions aimed at managing CMDs and preventing diabetes share commonalities (program content, theoretical underpinnings, program structures, interventionists, frameworks promoting fidelity, quality, sustainability). Specific considerations when utilising these programs for mental health include personalising content with respect to symptoms and trajectories of depression and anxiety, medication regimen and genetic risk profile. As this field moves from efficacy to effectiveness and implementation, it is important to ensure issues in implementation science, including “voltage drop”, “program drift”, logistics, funding, and resourcing, are in line with evidence-based models that are effective in research settings. Ongoing considerations includes who is best placed to deliver this care and the need for models to support implementation including long-term financing, workforce training, supervision, stakeholder and organisational support.

Highlights: • The Australian Recommended Food Score predicted SMI over 5-years. • A less inflammatory diet and a ‘traditional’ diet predicted SMI over 5-years. • Neither a ‘plant-focused’ nor ‘western’ diet predicted SMI over 5-years., Low muscle mass is associated with reduced independence and increased risk for falls and fractures. Identification of modifiable risk factors for low muscle mass is thus imperative. This study aimed to examine the longitudinal relationship between both diet quality and patterns and lean mass in Australian women. Data from n = 494 participants of the Geelong Osteoporosis Study’s 10- and 15-year women’s follow-ups were used (conducted in 2004–08 and 2011–14, respectively), and participants were aged 21–89 years. Self-reported lifestyle and demographics were collected, and food frequency questionnaire data informed the dietary exposure variables: the Australian Recommended Food Score (ARFS); the Dietary Inflammatory Index (DII); and a posteriori dietary patterns. The outcome, Skeletal Muscle Index (SMI), was calculated from DXA-derived appendicular lean mass (ALM) relative to height (ALM kg/m2). Analyses employed Generalised Estimating Equations. A higher ARFS score positively predicted SMI over 5-years, and adjustments for age and physical activity did not attenuate this relationship (B:0.044, (95%CI 0.004, 0.084) kg/m2). Following adjustment, both an anti-inflammatory diet (B:-0.034, (95%CI −0.070, −0.002) kg/m2) and a ‘traditional’ dietary pattern predicted higher SMI (B:0.081, (95%CI 0.004, 0.158) kg/m2). No other associations were observed. Our study reinforces the importance of diet quality for healthy, aging muscle mass. Furthermore, a less inflammatory diet and a diet comprising a wide variety of plant and animal foods may be conducive to maintenance of muscle mass in women. Further studies investigating diet quality’s impact on various muscle health measures over longer time periods are warranted.

Background Online interventions can be a cost-effective and efficient way to deliver programs to large numbers of people regardless of geographic location. However, attrition in web-based interventions is often an issue. Developing ways to keep participants engaged is important for ensuring validity and limiting potential biases. We developed a web-based dietary intervention as part of The My Food & Mood study which aimed to optimize ways to engage participants with low mood or depressive symptoms to promote dietary behavior change. Different versions of the My Food & Mood program were tested during optimization. Iterations were developed based on user feedback and usage analysis. Objective The purpose of this study was to compare engagement and nonusage attrition across 4 program iterations—which differed by platform format, delivery mode, and activity type—to create an optimized version. Methods Each program version contained modular videos with key activities with respect to implementing behavior change techniques of equivalent levels of required participation and length: version 1.0, desktop program and smartphone app; version 2.1, desktop or smartphone program; version 2.2, desktop program; and version 3.0, smartphone app. Adults with PHQ-8 scores of 5 or greater were recruited online and assigned to 1 of the 4 versions. Participants were asked to use the program for 8 weeks and complete measures at weeks 4 and 8. Engagement data were collected from the web-based platform system logs and customized reports. Cox regression survival analysis examined nonusage attrition and Kruskal-Wallis tests compared engagement across each cohort. Results A total of 614 adults participated. Kruskal-Wallis tests showed significant differences across the 4 cohorts in all engagement measures. The smartphone app (version 3.0) had the greatest engagement as measured by weeks engaged, total usage time, total time key activities, number of active sessions, percentage of activities completed against protocol, goals completed, and percentage of videos watched. Cox regression multivariate survival analysis showed referral from a health practitioner (hazard ratio [HR] 0.344, P=.001) and greater proficiency with computers (HR 0.796, P=.049) reduced the risk of nonusage attrition. Computer confidence was associated with an increased risk of nonusage attrition. Conclusions My Food & Mood version 3.0, a dietary intervention delivered via smartphone app with self-monitoring tools for diet quality and mood monitoring, was the version with greatest engagement in a population with low mood or depression. The iterative design techniques employed and analysis of feedback from participants resulted in a program that achieved lower rates of nonusage attrition and higher rates of intensity of use.

Background: Murine studies demonstrate that maternal prenatal gut microbiota influences brain development and behaviour of offspring. No human study has related maternal gut microbiota to behavioural outcomes during early life. This study aimed to evaluate relationships between the prenatal faecal microbiota, prenatal diet and childhood behaviour. Methods: A sub-cohort of 213 mothers and 215 children were selected from a longitudinal pre-birth cohort. Maternal prenatal exposure measures collected during the third trimester included the faecal microbiota (generated using 16S rRNA amplicon sequencing), and dietary intake. The behavioural outcome used the Childhood Behaviour Checklist at age two. Models were adjusted for prenatal diet, smoking, perceived stress, maternal age and sample batch. Findings: We found evidence that the alpha diversity of the maternal faecal microbiota during the third trimester of pregnancy predicts child internalising behaviour at two years of age (−2·74, (−4·71, −0·78), p = 0·01 (Wald test), R2=0·07). Taxa from butyrate-producing families, Lachnospiraceae and Ruminococcaceae, were more abundant in mothers of children with normative behaviour. A healthy prenatal diet indirectly related to decreased child internalising behaviours via higher alpha diversity of maternal faecal microbiota. Interpretation: These findings support animal studies showing that the composition of maternal prenatal gut microbiota is related to offspring brain development and behaviour. Our findings highlight the need to evaluate potential impacts of the prenatal gut microbiota on early life brain development. Funding: This study was funded by the National Health and Medical Research Council of Australia (1082307, 1147980), Murdoch Children's Research Institute, Barwon Health and Deakin University.

Numerous observational studies have investigated the role of the Dietary Inflammatory Index (DII®) in chronic disease risk. The aims of this umbrella review and integrated meta-analyses were to systematically synthesize the observational evidence reporting on the associations between the DII and health outcomes based on meta-analyses, and to assess the quality and strength of the evidence for each associated outcome. This umbrella review with integrated meta-analyses investigated the association between the DII and a range of health outcomes based on meta-analyses of observational data. A credibility assessment was conducted for each outcome using the following criteria: Statistical heterogeneity, 95% prediction intervals, evidence for small-study effect and/or excess significance bias, as well as effect sizes and P values using calculated random effects meta-analyses. In total, 15 meta-analyses reporting on 38 chronic disease-related outcomes were included, incorporating a total population of 4,360,111 subjects. Outcomes (n = 38) were examined through various study designs including case-control (n = 8), cross-sectional (n = 5), prospective (n = 5), and combination (n = 20) study designs. Adherence to a pro-inflammatory dietary pattern had a significant positive association with 27 (71%) of the included health outcomes (P value < 0.05). Using the credibility assessment, Class I (Convincing) evidence was identified for myocardial infarction only, Class II (Highly suggestive) evidence was identified for increased risk of all-cause mortality, overall risk of incident cancer, and risk of incident site-specific cancers (colorectal, pancreatic, respiratory, and oral cancers) with increasing (more pro-inflammatory) DII score. Most outcomes (n = 31) presented Class III (Suggestive) or lower evidence (Weak or No association). Pro-inflammatory dietary patterns were nominally associated with an increased risk of many chronic disease outcomes. However, the strength of evidence for most outcomes was limited. Further prospective studies are required to improve the precision of the effect size. © 2021 The Author(s). Published by Oxford University Press on behalf of the American Society for Nutrition.

The intestinal microbiome has been identified as a key modifier for a variety of health conditions. Fecal Microbiota Transplantation (FMT) has emerged as a fast, safe, and effective means by which to modify the intestinal microbiome and potentially treat a variety of health conditions. Despite extensive research of FMT for CDI, there is a lack of clarity informed by systematic synthesis of data regarding the safety and efficacy of FMT for other health conditions. This systematic review used PRISMA guidelines and was prospectively registered with PROSPERO (CRD42018104243). In March 2020, a search of MEDLINE, EMBASE, and PsycINFO was conducted. We identified 26 eligible studies. A meta-analysis of FMT for active Ulcerative Colitis (UC) showed that FMT significantly improved rates of clinical remission (OR = 3.634, 95% CI = 1.940 to 6.808, I2 = 0%, p

The association between dairy product consumption and biomarkers of inflammation, adipocytokines, and oxidative stress is poorly studied in children. Therefore, these associations were examined in a representative subsample of 1338 schoolchildren with a mean age of 11.5 (&plusmn, 0.7) years in the Healthy Growth Study. Information on dairy product consumption was collected by dietary recalls. Total dairy consumption was calculated by summing the intake of milk, yogurt, and cheese. Inflammatory markers, i.e., high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and adipocytokines, i.e., leptin, adiponectin, and the antioxidant enzyme glutathione peroxidase (GPx) were analysed. Due to the skewed distribution hs-CRP, IL-6, and leptin were log transformed. Multivariable regression analyses adjusted for age, sex, energy intake, physical activity, parental education, Tanner stage, and fat mass were used to assess the associations between consumption of total dairy, milk, yogurt, cheese, and markers of inflammation, adipocytokines, oxidative stress, and adiponectin&minus, leptin ratio. Our results showed that milk consumption was inversely associated with leptin (&beta, &minus, 0.101, 95% CI: &minus, 0.177, &minus, 0.025, p = 0.009) and positively associated with the adiponectin&minus, leptin ratio (&beta, 0.116, 95% CI: 0.020, 0.211, p = 0.018), while total dairy, cheese, and yogurt consumption were not associated with inflammatory, adipocytokine, or antioxidant markers. Further prospective studies are needed to confirm these results.

© 2020 The Author(s). Published with license by Taylor & Francis Group, LLC. The effects of dairy and dairy-derived products on the human gut microbiota remains understudied. A systematic literature search was conducted using Medline, CINAHL, Embase, Scopus, and PubMed databases with the aim of collating evidence on the intakes of all types of dairy and their effects on the gut microbiota in adults. Risk of bias was assessed using the Cochrane risk-of-bias tool.The search resulted in 6,592 studies, of which eight randomized controlled trials (RCTs) met pre-determined eligibility criteria for inclusion, consisting of a total of 468 participants. Seven studies assessed the effect of type of dairy (milk, yogurt, and kefir) and dairy derivatives (whey and casein) on the gut microbiota, and one study assessed the effect of the quantity of dairy (high dairy vs low dairy). Three studies showed that dairy types consumed (milk, yogurt, and kefir) increased the abundance of beneficial genera Lactobacillus and Bifidobacterium. One study showed that yogurt reduced the abundance of Bacteroides fragilis, a pathogenic strain. Whey and casein isolates and the quantity of dairy consumed did not prompt changes to the gut microbiota composition. All but one study reported no changes to bacterial diversity in response to dairy interventions and one study reported reduction in bacterial diversity in response to milk intake.In conclusion, the results of this review suggest that dairy products such as milk, yogurt, and kefir may modulate the gut microbiota composition in favor to the host. However, the broader health implications of these findings remain unclear and warrant further studies.

Blueberries are rich in polyphenols that may be beneficial to cognitive performance and mood. The aim of this systematic review was to evaluate randomized controlled trials investigating the effects of blueberries and blueberry products on measures of cognition and mood. In total, eleven articles (that included 12 studies) were identified using freeze-dried blueberries (n=9 studies), whole blueberries (n=2) and blueberry concentrate (n=1). These studies were conducted in children (n=5), young adults (n=1), and older people with either no known cognitive impairment (n=4) or indicated cognitive impairment (n=2). Eight studies reported blueberry consumption or supplementation at various doses and time lengths to improve measures of cognitive performance, particularly short- and long-term memory and spatial memory. For mood, one study reported significant between-group improvements in positive affect from blueberry products, whereas four studies reported no improvement. Low risk of bias were observed across all studies. Based on the current evidence, blueberries may improve some measures of cognitive performance when consumed for up to six months in duration. However, considerable differences in study design, dosages, and anthocyanin content hinder between-study comparison. The use of standardized blueberry interventions, consideration of placebo formulations, and consistently reported cognitive performance tools are recommended in future trials. PROSPERO registration no. CRD42018100888.

There is increasing academic and clinical interest in how "lifestyle factors" traditionally associated with physical health may also relate to mental health and psychological well-being. In response, international and national health bodies are producing guidelines to address health behaviors in the prevention and treatment of mental illness. However, the current evidence for the causal role of lifestyle factors in the onset and prognosis of mental disorders is unclear. We performed a systematic meta-review of the top-tier evidence examining how physical activity, sleep, dietary patterns and tobacco smoking impact on the risk and treatment outcomes across a range of mental disorders. Results from 29 meta-analyses of prospective/cohort studies, 12 Mendelian randomization studies, two meta-reviews, and two meta-analyses of randomized controlled trials were synthesized to generate overviews of the evidence for targeting each of the specific lifestyle factors in the prevention and treatment of depression, anxiety and stress-related disorders, schizophrenia, bipolar disorder, and attention-deficit/hyperactivity disorder. Standout findings include: a) convergent evidence indicating the use of physical activity in primary prevention and clinical treatment across a spectrum of mental disorders; b) emerging evidence implicating tobacco smoking as a causal factor in onset of both common and severe mental illness; c) the need to clearly establish causal relations between dietary patterns and risk of mental illness, and how diet should be best addressed within mental health care; and d) poor sleep as a risk factor for mental illness, although with further research required to understand the complex, bidirectional relations and the benefits of non-pharmacological sleep-focused interventions. The potentially shared neurobiological pathways between multiple lifestyle factors and mental health are discussed, along with directions for future research, and recommendations for the implementation of these findings at public health and clinical service levels. ispartof: WORLD PSYCHIATRY vol:19 issue:3 pages:360-380 ispartof: location:Italy status: published

Background Recently, the efficacy of dietary improvement as a therapeutic intervention for moderate to severe depression was evaluated in a randomised controlled trial. The SMILES trial demonstrated a significant improvement in Montgomery–Åsberg Depression Rating Scale scores favouring the dietary support group compared with a control group over 12 weeks. We used data collected within the trial to evaluate the cost-effectiveness of this novel intervention. Methods In this prospective economic evaluation, sixty-seven adults meeting DSM-IV criteria for a major depressive episode and reporting poor dietary quality were randomised to either seven sessions with a dietitian for dietary support or to an intensity matched social support (befriending) control condition. The primary outcome was Quality Adjusted Life Years (QALYs) as measured by the AQoL-8D, completed at baseline and 12 week follow-up (endpoint) assessment. Costs were evaluated from health sector and societal perspectives. The time required for intervention delivery was costed using hourly wage rates applied to the time in counselling sessions. Food and travel costs were also included in the societal perspective. Data on medications, medical services, workplace absenteeism and presenteesim (paid and unpaid) were collected from study participants using a resource-use questionnaire. Standard Australian unit costs for 2013/2014 were applied. Incremental cost-effectiveness ratios (ICERs) were calculated as the difference in average costs between groups divided by the difference in average QALYs. Confidence intervals were calculated using a non-parametric bootstrap procedure. Results Compared with the social support condition, average total health sector costs were $856 lower (95% CI -1247 to − 160) and average societal costs were $2591 lower (95% CI -3591 to − 198) for those receiving dietary support. These differences were driven by lower costs arising from fewer allied and other health professional visits and lower costs of unpaid productivity. Significant differences in mean QALYs were not found between groups. However, 68 and 69% of bootstrap iterations showed the dietary support intervention was dominant (additional QALYs at less cost) from the health sector and societal perspectives. Conclusions This novel dietary support intervention was found to be likely cost-effective as an adjunctive treatment for depression from both health sector and societal perspectives. Trial registration Australia and New Zealand Clinical Trials Register (ANZCTR): ACTRN12612000251820. Registered on 29 February 2012. Electronic supplementary material The online version of this article (10.1186/s12889-018-5504-8) contains supplementary material, which is available to authorized users.

Supplemental digital content is available in the text., Objective Poor diet can be detrimental to mental health. However, the overall evidence for the effects of dietary interventions on mood and mental well-being has yet to be assessed. We conducted a systematic review and meta-analysis examining effects of dietary interventions on symptoms of depression and anxiety. Methods Major electronic databases were searched through March 2018 for all randomized controlled trials of dietary interventions reporting changes in symptoms of depression and/or anxiety in clinical and nonclinical populations. Random-effects meta-analyses were conducted to determine effect sizes (Hedges' g with 95% confidence intervals [CI]) for dietary interventions compared with control conditions. Potential sources of heterogeneity were explored using subgroups and meta-regression analyses. Results Sixteen eligible randomized controlled trials (published in English) with outcome data for 45,826 participants were included; the majority of which examined samples with nonclinical depression (n = 15 studies). Nonetheless, dietary interventions significantly reduced depressive symptoms (g = 0.275, 95% CI = 0.10 to 0.45, p = .002). Similar effects were observed among high-quality trials (g = 0.321, 95% CI = 0.12 to 0.53, p = .002) and when compared with both inactive (g = 0.308, 95% CI = 0.02 to 0.60, p = .038) and active controls (g = 0.174, 95% CI = 0.01 to 0.34, p = .035). No effect of dietary interventions was observed for anxiety (k = 11, n = 2270, g = 0.100, 95% CI = −0.04 to 0.24, p = .148). Studies with female samples observed significantly greater benefits from dietary interventions, for symptoms of both depression and anxiety. Conclusions Dietary interventions hold promise as a novel intervention for reducing symptoms of depression across the population. Future research is required to determine the specific components of dietary interventions that improve mental health, explore underlying mechanisms, and establish effective schemes for delivering these interventions in clinical and public health settings. Registration PROSPERO Online Protocol: CRD42018091256.

The SMILES trial was the first intervention study to test dietary improvement as a treatment strategy for depression. Molendijk et al. propose that expectation bias and difficulties with blinding might account for the large effect size. While we acknowledge the issue of expectation bias in lifestyle intervention trials and indeed discuss this as a key limitation in our paper, we observed a strong correlation between dietary change and change in depression scores, which we argue is consistent with a causal effect and we believe unlikely to be an artefact of inadequate blinding. Since its publication, our results have been largely replicated and our recent economic evaluation of SMILES suggests that the benefits of our approach extend beyond depression. We argue that the SMILES trial should be considered an important, albeit preliminary, first step in the field of nutritional psychiatry research. Electronic supplementary material The online version of this article (10.1186/s12916-018-1228-y) contains supplementary material, which is available to authorized users.

The link between falls and depression has been researched in the elderly; however, little information is available on this association in younger adults, particularly men. This study sought to investigate the link between major depressive disorder (MDD) and falls in a population-based sample of 952 men (24-97 years). MDD was diagnosed utilizing the Structured Clinical Interview for DSM-IV-TR Research Version, Non-Patient edition, and categorized as 12-month/past/never. Body mass index and gait were measured; falls, smoking status, psychotropic medication use, and alcohol intake were self-reported as part of the Geelong Osteoporosis Study 5-year follow-up assessment. Thirty-four (3.6%) men met criteria for 12-month MDD, and 110 (11.6%) for past MDD. Of the 952 men, 175 (18.4%) reported falling at least once during the past 12 months. Fallers were older (66 [interquartile range: 48-79] vs. 59 [45-72] years, p = .001) and more likely to have uneven gait ( n = 16, 10% vs. n = 31, 4%, p = .003) than nonfallers. Participants with 12-month MDD had more than twice the odds of falling (age-adjusted odds ratio: 2.22, 95% confidence interval [1.03, 4.80]). The odds of falling were not associated with past depression ( p = .4). Further adjustments for psychotropic drug use, gait, body mass index, smoking status, blood pressure, and alcohol did not explain these associations. Given the 2.2-fold greater likelihood of falling associated with depression was not explained by age or psychotropic drug use, further research is warranted.

Background:Bipolar disorder (BD) is a psychiatric disorder with an uncertain aetiology. Recently, special attention has been given to homocysteine (Hcy), as it has been suggested that alterations in 1-carbon metabolism might be implicated in diverse psychiatric disorders. However, there is uncertainty regarding possible alterations in peripheral Hcy levels in BD.Methods:This study comprises a meta-analysis comparing serum and plasma Hcy levels in persons with BD and healthy controls. We conducted a systematic search for all eligible English and non-English peer-reviewed articles.Results:Nine cross-sectional studies were included in the meta-analyses, providing data on 1547 participants. Random-effects meta-analysis showed that serum and plasma levels of Hcy were increased in subjects with BD in either mania or euthymia when compared to healthy controls, with a large effect size in the mania group (g= 0.98, 95% CI: 0.8–1.17,P< 0.001,n= 495) and a small effect in the euthymia group (g= 0.3, 95% CI: 0.11–0.48,P= 0.002,n= 1052).Conclusions:Our meta-analysis provides evidence that Hcy levels are elevated in persons with BD during mania and euthymia. Peripheral Hcy could be considered as a potential biomarker in BD, both of trait (since it is increased in euthymia), and also of state (since its increase is more accentuated in mania). Longitudinal studies are needed to clarify the relationship between bipolar disorder and Hcy, as well as the usefulness of peripheral Hcy as both a trait and state biomarker in BD.

Multiple studies have demonstrated an association between cigarette smoking and increased anxiety symptoms or disorders, with early life exposures potentially predisposing to enhanced anxiety responses in later life. Explanatory models support a potential role for neurotransmitter systems, inflammation, oxidative and nitrosative stress, mitochondrial dysfunction, neurotrophins and neurogenesis, and epigenetic effects, in anxiety pathogenesis. All of these pathways are affected by exposure to cigarette smoke components, including nicotine and free radicals. This review critically examines and summarizes the literature exploring the role of these systems in increased anxiety and how exposure to cigarette smoke may contribute to this pathology at a biological level. Further, this review explores the effects of cigarette smoke on normal neurodevelopment and anxiety control, suggesting how exposure in early life (prenatal, infancy, and adolescence) may predispose to higher anxiety in later life. A large heterogenous literature was reviewed that detailed the association between cigarette smoking and anxiety symptoms and disorders with structural brain changes, inflammation, and cell-mediated immune markers, markers of oxidative and nitrosative stress, mitochondrial function, neurotransmitter systems, neurotrophins and neurogenesis. Some preliminary data were found for potential epigenetic effects. The literature provides some support for a potential interaction between cigarette smoking, anxiety symptoms and disorders, and the above pathways; however, limitations exist particularly in delineating causative effects. The literature also provides insight into potential effects of cigarette smoke, in particular nicotine, on neurodevelopment. The potential treatment implications of these findings are discussed in regards to future therapeutic targets for anxiety. The aforementioned pathways may help mediate increased anxiety seen in people who smoke. Further research into the specific actions of nicotine and other cigarette components on these pathways, and how these pathways interact, may provide insights that lead to new treatment for anxiety and a greater understanding of anxiety pathogenesis.

Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype-the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.

Background Healthy Together Victoria (HTV) - a complex ‘whole of system’ intervention, including an embedded cluster randomized control trial, to reduce chronic disease by addressing risk factors (physical inactivity, poor diet quality, smoking and harmful alcohol use) among children and adults in selected communities in Victoria, Australia (Healthy Together Communities). Objectives To describe the methodology for: 1) assessing changes in the prevalence of measured childhood obesity and associated risks between primary and secondary school students in HTV communities, compared with comparison communities; and 2) assessing community-level system changes that influence childhood obesity in HTC and comparison communities. Methods Twenty-four geographically bounded areas were randomized to either prevention or comparison (2012). A repeat cross-sectional study utilising opt-out consent will collect objectively measured height, weight, waist and self-reported behavioral data among primary [Grade 4 (aged 9-10y) and Grade 6 (aged 11-12y)] and secondary [Grade 8 (aged 13-14y) and Grade 10 (aged 15-16y)] school students (2014 to 2018). Relationships between measured childhood obesity and system causes, as defined in the Foresight obesity systems map, will be assessed using a range of routine and customised data. Conclusion This research methodology describes the beginnings of a state-wide childhood obesity monitoring system that can evolve to regularly inform progress on reducing obesity, and situate these changes in the context of broader community-level system change.

While the underlying pathophysiology of mood disorders (MD) is not fully understood, there is now an extensive body of data showing they are associated with a chronic, low-grade inflammatory response (Berk et al., 2013a). Further support has come from studies of patient groups with immune-related diseases, with which depression is highly comorbid (Dantzer et al., 2008) and studies where infusion of cytokines robustly induces symptoms of depression (DellaGioia and Hannestad, 2010). Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) primarily used in the treatment of hypercholesterolemia and prevention of cardiovascular disease, and aspirin (acetylsalicylic acid), primarily used as an analgesic and/or antiplatelet agent, both have antiinflammatory properties (Dinarello, 2010). Given these agents are now known to reduce the risk of a number of diseases characterized by inflammation and our previous finding of an inverse association with depression in women (Pasco et al., 2010), we aimed to determine whether a similar relationship exists for men. Data were derived from an age-stratified, random population-based sample of men enrolled in the Geelong Osteoporosis Study, a large, ongoing study located in southeastern Australia (Pasco et al., 2012). Further details of the study have been published elsewhere (Pasco et al., 2012). Briefly, between 2001 and 2006, 1540 men (response 67.0%) were recruited from the Australian Commonwealth electoral rolls for the Barwon Statistical Division. Of the 1540 participants, 978 returned for 5-year follow-up assessment between 2006 and 2011 (81.0% response for those alive and contactable). For the current analyses, participants for whom psychiatric data were not available (n=17) were excluded, resulting in a sample of 961 men aged 24 to 98 years. The study was approved by the Barwon Health Human Research Ethics Committee, and written informed consent was obtained from all participants. The Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Non-patient edition was conducted at the Geelong Osteoporosis Study 5-year follow-up and used to assess lifetime history of MD. Self-reported medication use was documented by questionnaires administered at each visit. Participants were asked to bring a list of medications or containers to assist with accurate recording of details. Anthropometry was measured and information on lifestyle factors was obtained via written questionnaire. Socio-economic status was ascertained using Socio-Economic Index For Areas index scores. Two study designs were utilized: a nested case-control and a retrospective cohort study. The former identified ‘cases’ as subjects diagnosed with a MD and ‘controls’ were MD-free (ever). Exposure to statins and/or aspirin was recognized if exposure preceded the first-onset MD episode for cases and the 5-year assessment for controls. Multivariable logistic regression was used to calculate odds ratios (ORs) with 95% CI for de novo MD for those exposed to antiinflammatory agents in comparison with those not exposed. The latter design comprised participants without a history of MD at baseline who were followed from baseline until a first episode of MD or until the end of the 5-year follow-up period. The risk for de novo MD associated with exposure to antiinflammatory agents was examined using multivariable Cox proportional hazards regression models. Covariates including age, weight, height, alcohol, smoking, physical activity, socio-economic status, and use of antidepressants, sex hormones, nonsteroidal antiinflammatory drugs, other hyperlipidaemia agents, and other anticoagulants were tested as confounders or effect modifiers in each multivariable model. Among 961 men, 165 were diagnosed with a MD (cases) and 796 had no history of MD (controls). Twenty-three cases were excluded due to participants having an episode of MD prior to exposure to either statins or aspirin, and one control was excluded because of an unknown medication status. Thus, 142 cases and 795 controls were considered. Participant characteristics are shown in Table 1. At the time of interview, 182 men (19.4%) were exposed to statins; 50 (27.5%) used Simvastatin, 87 (47.8%) used Atorvastatin, 28 (15.4%) used Pravastatin, and 17 (9.3%) used Rosuvastatin. Median duration of use was 6.3 (IQR 2.4–10.2) years. Exposure to statins was documented for 4 of 142 (2.8%) cases and 178 of 795 (22.4%) controls (P

Background Atheoretical large-scale data mining techniques using machine learning algorithms have promise in the analysis of large epidemiological datasets. This study illustrates the use of a hybrid methodology for variable selection that took account of missing data and complex survey design to identify key biomarkers associated with depression from a large epidemiological study. Methods The study used a three-step methodology amalgamating multiple imputation, a machine learning boosted regression algorithm and logistic regression, to identify key biomarkers associated with depression in the National Health and Nutrition Examination Study (2009–2010). Depression was measured using the Patient Health Questionnaire-9 and 67 biomarkers were analysed. Covariates in this study included gender, age, race, smoking, food security, Poverty Income Ratio, Body Mass Index, physical activity, alcohol use, medical conditions and medications. The final imputed weighted multiple logistic regression model included possible confounders and moderators. Results After the creation of 20 imputation data sets from multiple chained regression sequences, machine learning boosted regression initially identified 21 biomarkers associated with depression. Using traditional logistic regression methods, including controlling for possible confounders and moderators, a final set of three biomarkers were selected. The final three biomarkers from the novel hybrid variable selection methodology were red cell distribution width (OR 1.15; 95% CI 1.01, 1.30), serum glucose (OR 1.01; 95% CI 1.00, 1.01) and total bilirubin (OR 0.12; 95% CI 0.05, 0.28). Significant interactions were found between total bilirubin with Mexican American/Hispanic group (p = 0.016), and current smokers (p

OBJECTIVE: To examine the relationship between diet quality and depressive symptomology amongst a community-based sample of Fijian adolescents. METHODS: Participants included 7,237 adolescents (52.6% girls; mean age 15.6 years) at baseline (2005) and 2,948 (56% girls; mean age 17.4 years) at follow-up (2007/2008), from the Pacific Obesity Prevention in Communities Project. Intervention schools (n = 7) were selected from Nasinu, near Suva on the main Fijian island Viti Levu, and comparison schools (n = 11) were chosen from towns on the opposite, west side of the island. A dietary questionnaire was used to measure diet quality. Factor analysis clustered dietary variables into two unique and independent factors, referred to as healthy diet quality and unhealthy diet quality. Depressive symptomology was assessed via the emotional subscale of the Paediatric Quality of Life Inventory. Both measures were self-reported and self-administered. Multiple linear regression was used to test cross-sectional associations (at baseline and follow-up) between diet quality and depressive symptomology. Variables controlled for included gender, age, ethnicity, study condition, BMI-z scores, and physical activity. FINDINGS: Strong, positive dose-response associations between healthy diet and high emotional scores (lower depressive symptomology) were found in cross-sectional analyses at baseline and follow-up, among boys and girls. No association was found between emotional health and unhealthy diet. CONCLUSIONS: This study suggests that cross-sectional relationships exist between a high quality diet during adolescence and less depressive symptoms, however more evidence is required to determine if these two variables are linked causally. Trial population health strategies that use dietary interventions as a mechanism for mental health promotion provide an opportunity to further test these associations. If this is indeed a true relationship, these forms of interventions have the potential to be inexpensive and have substantial reach, especially in Low and Middle Income Countries. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry ACTRN12608000345381.

Background The possible therapeutic impact of dietary changes on existing mental illness is largely unknown. Using a randomised controlled trial design, we aimed to investigate the efficacy of a dietary improvement program for the treatment of major depressive episodes. Methods ‘SMILES’ was a 12-week, parallel-group, single blind, randomised controlled trial of an adjunctive dietary intervention in the treatment of moderate to severe depression. The intervention consisted of seven individual nutritional consulting sessions delivered by a clinical dietician. The control condition comprised a social support protocol to the same visit schedule and length. Depression symptomatology was the primary endpoint, assessed using the Montgomery–Åsberg Depression Rating Scale (MADRS) at 12 weeks. Secondary outcomes included remission and change of symptoms, mood and anxiety. Analyses utilised a likelihood-based mixed-effects model repeated measures (MMRM) approach. The robustness of estimates was investigated through sensitivity analyses. Results We assessed 166 individuals for eligibility, of whom 67 were enrolled (diet intervention, n = 33; control, n = 34). Of these, 55 were utilising some form of therapy: 21 were using psychotherapy and pharmacotherapy combined; 9 were using exclusively psychotherapy; and 25 were using only pharmacotherapy. There were 31 in the diet support group and 25 in the social support control group who had complete data at 12 weeks. The dietary support group demonstrated significantly greater improvement between baseline and 12 weeks on the MADRS than the social support control group, t(60.7) = 4.38, p

Background Recent meta-analyses confirm a relationship between diet quality and both depression and cognitive health in adults. While the biological pathways that underpin these relationships are likely multitudinous, extensive evidence from animal studies points to the involvement of the hippocampus. The aim of this study was to examine the association between dietary patterns and hippocampal volume in humans, and to assess whether diet was associated with differential rates of hippocampal atrophy over time. Methods Data were drawn from the Personality and Total Health Through Life Study and focused on a subsample of the cohort (n = 255) who were aged 60–64 years at baseline in 2001, completed a food frequency questionnaire, and underwent two magnetic resonance imaging scans approximately 4 years apart. Longitudinal generalized estimating equation linear regression models were used to assess the association between dietary factors and left and right hippocampal volumes over time. Results Every one standard deviation increase in healthy “prudent” dietary pattern was associated with a 45.7 mm3 (standard error 22.9 mm3) larger left hippocampal volume, while higher consumption of an unhealthy “Western” dietary pattern was (independently) associated with a 52.6 mm3 (SE 26.6 mm3) smaller left hippocampal volume. These relationships were independent of covariates including age, gender, education, labour-force status, depressive symptoms and medication, physical activity, smoking, hypertension and diabetes. While hippocampal volume declined over time, there was no evidence that dietary patterns influenced this decline. No relationships were observed between dietary patterns and right hippocampal volume. Conclusions Lower intakes of nutrient-dense foods and higher intakes of unhealthy foods are each independently associated with smaller left hippocampal volume. To our knowledge, this is the first human study to demonstrate associations between diet and hippocampal volume concordant with data previously observed in animal models.

International audience; Psychiatry is at an important juncture, with the current pharmacologically focused model having achieved modest benefits in addressing the burden of poor mental health worldwide. Although the determinants of mental health are complex, the emerging and compelling evidence for nutrition as a crucial factor in the high prevalence and incidence of mental disorders suggests that diet is as important to psychiatry as it is to cardiology, endocrinology, and gastroenterology. Evidence is steadily growing for the relation between dietary quality (and potential nutritional deficiencies) and mental health, and for the select use of nutrient-based supplements to address deficiencies, or as monotherapies or augmentation therapies. We present a viewpoint from an international collaboration of academics (members of the International Society for Nutritional Psychiatry Research), in which we provide a context and overview of the current evidence in this emerging field of research, and discuss the future direction. We advocate recognition of diet and nutrition as central determinants of both physical and mental health.

Background Historically, the focus of Non Communicable Disease (NCD) prevention and control has been cardiovascular disease (CVD), type 2 diabetes mellitus (T2DM), cancer and chronic respiratory diseases. Collectively, these account for more deaths than any other NCDs. Despite recent calls to include the common mental disorders (CMDs) of depression and anxiety under the NCD umbrella, prevention and control of these CMDs remain largely separate and independent. Discussion In order to address this gap, we apply a framework recently proposed by the Centers for Disease Control with three overarching objectives: (1) to obtain better scientific information through surveillance, epidemiology, and prevention research; (2) to disseminate this information to appropriate audiences through communication and education; and (3) to translate this information into action through programs, policies, and systems. We conclude that a shared framework of this type is warranted, but also identify opportunities within each objective to advance this agenda and consider the potential benefits of this approach that may exist beyond the health care system.

Background Maternal smoking during pregnancy (MSDP) is associated with multiple adverse childhood outcomes including externalizing behaviors. However, the association between MSDP and internalizing (anxiety and depressive) behaviors in offspring has received less investigation. We aimed to assess the association between MSDP and childhood internalizing (anxiety and depressive) behaviors in a very large, well-characterized cohort study. Methods We assessed the association between MSDP and internalizing behaviors in offspring utilizing information drawn from 90,040 mother-child pairs enrolled in the Norwegian Mother and Child Cohort Study. Mothers reported smoking information, including status and frequency of smoking, twice during pregnancy. Mothers also reported their child’s internalizing behaviors at 18 months, 36 months, and 5 years. Associations between MSDP and childhood internalizing behaviors, including dose-response and timing of smoking in pregnancy, were assessed at each time point. Results MSDP was associated with increased internalizing behaviors when offspring were aged 18 months (B = 0.11, P 20 cigarettes per day) were associated with higher levels of internalizing behaviors. Maternal smoking during early pregnancy appeared to be the critical period for exposure. Conclusions We found evidence supporting a potential role for MSDP in increasing internalizing (anxiety and depressive) behaviors in offspring. We also found evidence supportive of a possible causal relationship, including dose-dependency and support for a predominant role of early pregnancy exposure. Further investigation utilizing genetically informed designs are warranted to assess this association.

Leptin and ghrelin have been implicated in the pathogenesis of major depression. However, evidence is lacking among apparently healthy people. This study examined the relationship of these appetite hormones to depressive symptoms in a Japanese working population. A cross-sectional study was conducted in 2009 among 497 Japanese employees (287 men and 210 women) aged 20–68 years. Fasting serum leptin and ghrelin levels were measured using a Luminex suspension bead-based multiplexed array. Depressive symptoms were assessed using the Center for Epidemiologic Studies Depression (CES-D) scale. Logistic regression analysis was performed to estimate odds ratio (OR) and 95% confidence interval (CI) for depressive symptoms with adjustment for potential confounders. The prevalence of depressive symptoms (CES-D ≥16) was 26.5% and 33.3% among men and women, respectively. Women in the middle and highest tertiles of leptin levels showed lower odds for depressive symptoms compared with those in the lowest level, although the trend association was not statistically significant (P trend = 0.14). Higher ghrelin levels were associated with increased odds for depressive symptoms in women (P trend = 0.02). The multivariable adjusted OR (95% CI) of having depressive symptoms for the lowest through highest tertiles of ghrelin levels were 1.00 (reference), 1.71 (0.76 - 3.86), and 2.69 (1.16 - 6.28), respectively. Neither leptin nor ghrelin was associated with depressive symptoms in men. Results suggest that lower leptin and higher ghrelin levels may be related to higher prevalence of depressive status among Japanese women.

Introduction Recent research suggests that diet quality influences depression risk; however, a lack of experimental evidence leaves open the possibility that residual confounding explains the observed relationships. The aim of this study was to document the cross-sectional and longitudinal associations between dietary patterns and symptoms of depression and to undertake a detailed examination of potential explanatory factors, particularly socioeconomic circumstances, in the diet-depression relationship. Methods Data were drawn from the Personality and Total Health (PATH) Through Life Study, a longitudinal community study following three age cohorts (20+; 40+; 60+yrs) from south-eastern Australia over three assessment periods (n = 3663). Regression analyses evaluated the cross-sectional and longitudinal relationships between dietary patterns, depressive symptoms, age, detailed measures of socioeconomic circumstances, other health behaviours, and cardiovascular risk factors. Results The lowest tertile of prudent (healthy) dietary pattern and the highest tertile of western (unhealthy) dietary pattern were associated with an increased likelihood of depressive symptoms. However, these contemporaneous associations were explained by adjustment for detailed measures of socioeconomic circumstances and physical activity. In prospective analyses, lower scores on the healthy dietary pattern and higher scores on the unhealthy dietary pattern independently predicted increased depressive symptoms across time, before and after adjustment for potential confounders and baseline depressive symptoms, but only for those in the oldest cohort. Dietary patterns did not explain the relationship between socioeconomic position and depressive symptoms. Conclusion The results of this study confirm that the relationship between habitual dietary intake and depressive symptoms is somewhat explained by socioeconomic circumstances and other health behaviours, but suggest that long term exposure to unhealthy dietary habits independently predisposes to depression over the lifecourse.

There is a need for the development of effective universal preventive approaches to the common mental disorders, depression and anxiety, at a population level. Poor diet, physical inactivity and smoking have long been recognized as key contributors to the high prevalence noncommunicable diseases. However, there are now an increasing number of studies suggesting that the same modifiable lifestyle behaviors are also risk factors for common mental disorders. In this paper we point to the emerging data regarding lifestyle risk factors for common mental disorders, with a particular focus on and critique of the newest evidence regarding diet quality. On the basis of this most recent evidence, we consequently argue for the inclusion of depression and anxiety in the ranks of the high prevalence noncommunicable diseases influenced by habitual lifestyle practices. We believe that it is both feasible and timely to begin to develop effective, sustainable, population-level prevention initiatives for the common mental illnesses that build on the established and developing approaches to the noncommunicable somatic diseases.