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      Nutrition and behavioral health disorders: depression and anxiety

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          Abstract

          Suboptimal nutrition has been implicated in the underlying pathology of behavioral health disorders and may impede treatment and recovery. Thus, optimizing nutritional status should be a treatment for these disorders and is likely important for prevention. The purpose of this narrative review is to describe the global burden and features of depression and anxiety, and summarize recent evidence regarding the role of diet and nutrition in the prevention and management of depression and anxiety. Current evidence suggests that healthy eating patterns that meet food-based dietary recommendations and nutrient requirements may assist in the prevention and treatment of depression and anxiety. Randomized controlled trials are needed to better understand how diet and nutrition-related biological mechanisms affect behavioral health disorders, to assist with the development of effective evidence-based nutrition interventions, to reduce the impact of these disorders, and promote well-being for affected individuals.

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          Most cited references126

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          Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association

          Circulation, 139(10)
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            Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

            Non-fatal health outcomes from diseases and injuries are a crucial consideration in the promotion and monitoring of individual and population health. The Global Burden of Disease (GBD) studies done in 1990 and 2000 have been the only studies to quantify non-fatal health outcomes across an exhaustive set of disorders at the global and regional level. Neither effort quantified uncertainty in prevalence or years lived with disability (YLDs). Of the 291 diseases and injuries in the GBD cause list, 289 cause disability. For 1160 sequelae of the 289 diseases and injuries, we undertook a systematic analysis of prevalence, incidence, remission, duration, and excess mortality. Sources included published studies, case notification, population-based cancer registries, other disease registries, antenatal clinic serosurveillance, hospital discharge data, ambulatory care data, household surveys, other surveys, and cohort studies. For most sequelae, we used a Bayesian meta-regression method, DisMod-MR, designed to address key limitations in descriptive epidemiological data, including missing data, inconsistency, and large methodological variation between data sources. For some disorders, we used natural history models, geospatial models, back-calculation models (models calculating incidence from population mortality rates and case fatality), or registration completeness models (models adjusting for incomplete registration with health-system access and other covariates). Disability weights for 220 unique health states were used to capture the severity of health loss. YLDs by cause at age, sex, country, and year levels were adjusted for comorbidity with simulation methods. We included uncertainty estimates at all stages of the analysis. Global prevalence for all ages combined in 2010 across the 1160 sequelae ranged from fewer than one case per 1 million people to 350,000 cases per 1 million people. Prevalence and severity of health loss were weakly correlated (correlation coefficient -0·37). In 2010, there were 777 million YLDs from all causes, up from 583 million in 1990. The main contributors to global YLDs were mental and behavioural disorders, musculoskeletal disorders, and diabetes or endocrine diseases. The leading specific causes of YLDs were much the same in 2010 as they were in 1990: low back pain, major depressive disorder, iron-deficiency anaemia, neck pain, chronic obstructive pulmonary disease, anxiety disorders, migraine, diabetes, and falls. Age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010. Regional patterns of the leading causes of YLDs were more similar compared with years of life lost due to premature mortality. Neglected tropical diseases, HIV/AIDS, tuberculosis, malaria, and anaemia were important causes of YLDs in sub-Saharan Africa. Rates of YLDs per 100,000 people have remained largely constant over time but rise steadily with age. Population growth and ageing have increased YLD numbers and crude rates over the past two decades. Prevalences of the most common causes of YLDs, such as mental and behavioural disorders and musculoskeletal disorders, have not decreased. Health systems will need to address the needs of the rising numbers of individuals with a range of disorders that largely cause disability but not mortality. Quantification of the burden of non-fatal health outcomes will be crucial to understand how well health systems are responding to these challenges. Effective and affordable strategies to deal with this rising burden are an urgent priority for health systems in most parts of the world. Bill & Melinda Gates Foundation. Copyright © 2012 Elsevier Ltd. All rights reserved.
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              Distribution of the vitamin D receptor and 1 alpha-hydroxylase in human brain.

              Despite a growing body of evidence that Vitamin D is involved in mammalian brain functioning, there has been a lack of direct evidence about its role in the human brain. This paper reports, for the first time, the distribution of the 1,25-dihydroxyvitamin D3 receptor (VDR), and 1alpha-hydroxylase (1alpha-OHase), the enzyme responsible for the formation of the active vitamin in the human brain. The receptor and the enzyme were found in both neurons and glial cells in a regional and layer-specific pattern. The VDR was restricted to the nucleus whilst 1alpha-OHase was distributed throughout the cytoplasm. The distribution of the VDR in human brain was strikingly similar to that reported in rodents. Many regions contained equivalent amounts of both the VDR and 1alpha-OHase, however the macrocellular cells within the nucleus basalis of Meynert (NBM) and the Purkinje cells in the cerebellum expressed 1alpha-OHase in the absence of VDR. The strongest immunohistochemical staining for both the receptor and enzyme was in the hypothalamus and in the large (presumably dopaminergic) neurons within the substantia nigra. The observed distribution of the VDR is consistent with the proposal that Vitamin D operates in a similar fashion to the known neurosteroids. The widespread distribution of 1alpha-OHase and the VDR suggests that Vitamin D may have autocrine/paracrine properties in the human brain.
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                Author and article information

                Contributors
                (View ORCID Profile)
                Journal
                Nutrition Reviews
                Oxford University Press (OUP)
                0029-6643
                1753-4887
                March 01 2021
                February 11 2021
                May 24 2020
                March 01 2021
                February 11 2021
                May 24 2020
                : 79
                : 3
                : 247-260
                Affiliations
                [1 ]Department of Nutritional Sciences, Pennsylvania State University, University Park, Pennsylvania, USA
                [2 ]National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, Maryland, USA
                [3 ]Mayo Clinic, Rochester, Minnesota, USA
                [4 ]Substance Abuse and Mental Health Services Administration, Rockville, Maryland, USA
                [5 ]Milken Institute School of Public Health, George Washington University, Washington, DC, USA
                [6 ]Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut, USA
                [7 ]Nutrition Policy Institute, University of California, Agriculture and Natural Resources, Berkeley, California, USA
                Article
                10.1093/nutrit/nuaa025
                32447382
                53f5d4c7-ba69-45f4-b14c-256544265ddb
                © 2020

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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