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Nutrition and CNS: In Health and Disease

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: closed (4 December 2020) | Viewed by 57892

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Special Issue Editors

Dr. Ruth M. Barrientos

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Guest Editor

Institute for Behavioral Medicine Research and Department of Psychiatry, The Ohio State University, Columbus, Ohio, USA
Interests: Behavioral Neuroscience, Aging, Neuroinflammation, Learning and Memory

Dr. Luba Sominsky

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Guest Editor

School of Health and Biomedical Sciences, RMIT University, Melbourne, Australia
Interests: Neuroendocrinology, Neuroimmunology, Reproductive Physiology

Special Issue Information

Dear Colleagues,

Over the last 100 years, dietary habits and trends in the developed world have shifted to largely favor the consumption of saturated fats and refined sugars. Not surprisingly, these trends have contributed to the obesity epidemic across all segments of society, and this, in turn, has contributed to disease vulnerability and progression. At the same time, other foods have emerged as beneficial powerhouses that help prevent and combat disease, and maintain a healthy homeostasis. There is abundant evidence supporting both angles, thanks in large part to the work coming out of your laboratories. Thus, we are reaching out to you to request that you consider contributing to our Special Issue.

The aim of this Special Issue is to update knowledge on the nutritional contribution to health and disease across the lifespan as it relates specifically to the central nervous system. The scope is broad and includes, but is not limited, to intermittent fasting/caloric restriction; effects of ketogenic, high-fat, high-sugar, and anti-oxidant diets on brain cancer, epilepsy, multiple sclerosis, migraines, spinal cord injury, Alzheimer’s disease, neuroendocrinology, olfaction, stress, addiction, and depression. We welcome different types of manuscript submissions, including original research articles and up-to-date reviews (systematic reviews and meta-analyses).

Dr. Ruth M. Barrientos
Dr. Luba Sominsky
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Diet
Neurological Disease
Disease Progression
Disease Amelioration

Published Papers (9 papers)

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Research

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20 pages, 4614 KiB

Open AccessArticle

Effects of Early-Life Stress, Postnatal Diet Modulation and Long-Term Western-Style Diet on Peripheral and Central Inflammatory Markers

by Silvie R. Ruigrok, Maralinde R. Abbink, Jorine Geertsema, Jesse E. Kuindersma, Nina Stöberl, Eline M. van der Beek, Paul J. Lucassen, Lidewij Schipper and Aniko Korosi

Nutrients 2021, 13(2), 288; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13020288 - 20 Jan 2021

Cited by 11 | Viewed by 3231

Abstract

Early-life stress (ES) exposure increases the risk of developing obesity. Breastfeeding can markedly decrease this risk, and it is thought that the physical properties of the lipid droplets in human milk contribute to this benefit. A concept infant milk formula (IMF) has been developed that mimics these physical properties of human milk (Nuturis^®, N-IMF). Previously, we have shown that N-IMF reduces, while ES increases, western-style diet (WSD)-induced fat accumulation in mice. Peripheral and central inflammation are considered to be important for obesity development. We therefore set out to test the effects of ES, Nuturis^® and WSD on adipose tissue inflammatory gene expression and microglia in the arcuate nucleus of the hypothalamus. ES was induced in mice by limiting the nesting and bedding material from postnatal day (P) 2 to P9. Mice were fed a standard IMF (S-IMF) or N-IMF from P16 to P42, followed by a standard diet (STD) or WSD until P230. ES modulated adipose tissue inflammatory gene expression early in life, while N-IMF had lasting effects into adulthood. Centrally, ES led to a higher microglia density and more amoeboid microglia at P9. In adulthood, WSD increased the number of amoeboid microglia, and while ES exposure increased microglia coverage, Nuturis^® reduced the numbers of amoeboid microglia upon the WSD challenge. These results highlight the impact of the early environment on central and peripheral inflammatory profiles, which may be key in the vulnerability to develop metabolic derangements later in life. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

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19 pages, 2482 KiB

Open AccessArticle

Iron Deficiency Reprograms Phosphorylation Signaling and Reduces O-GlcNAc Pathways in Neuronal Cells

by Luke N. Erber, Ang Luo, Yao Gong, Montana Beeson, Maolin Tu, Phu Tran and Yue Chen

Nutrients 2021, 13(1), 179; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13010179 - 08 Jan 2021

Cited by 9 | Viewed by 3096

Abstract

Micronutrient sensing is critical for cellular growth and differentiation. Deficiencies in essential nutrients such as iron strongly affect neuronal cell development and may lead to defects in neuronal function that cannot be remedied by subsequent iron supplementation. To understand the adaptive intracellular responses to iron deficiency in neuronal cells, we developed and utilized a Stable Isotopic Labeling of Amino acids in Cell culture (SILAC)-based quantitative phosphoproteomics workflow. Our integrated approach was designed to comprehensively elucidate the changes in phosphorylation signaling under both acute and chronic iron-deficient cell models. In addition, we analyzed the differential cellular responses between iron deficiency and hypoxia (oxygen-deprived) in neuronal cells. Our analysis identified nearly 16,000 phosphorylation sites in HT-22 cells, a hippocampal-derived neuronal cell line, more than ten percent of which showed at least

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2-fold changes in response to either hypoxia or acute/chronic iron deficiency. Bioinformatic analysis revealed that iron deficiency altered key metabolic and epigenetic pathways including the phosphorylation of proteins involved in iron sequestration, glutamate metabolism, and histone methylation. In particular, iron deficiency increased glutamine-fructose-6-phosphate transaminase (GFPT1) phosphorylation, which is a key enzyme in the glucosamine biosynthesis pathway and a target of 5′ AMP-activated protein kinase (AMPK), leading to reduced GFPT1 enzymatic activity and consequently lower global O-GlcNAc modification in neuronal cells. Taken together, our analysis of the phosphoproteome dynamics in response to iron and oxygen deprivation demonstrated an adaptive cellular response by mounting post-translational modifications that are critical for intracellular signaling and epigenetic programming in neuronal cells. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

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19 pages, 2609 KiB

Open AccessArticle

High Maternal Omega-3 Supplementation Dysregulates Body Weight and Leptin in Newborn Male and Female Rats: Implications for Hypothalamic Developmental Programming

by Soniya Xavier, Jasmine Gili, Peter McGowan, Simin Younesi, Paul F. A. Wright, David W. Walker, Sarah J. Spencer and Luba Sominsky

Nutrients 2021, 13(1), 89; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13010089 - 30 Dec 2020

Cited by 5 | Viewed by 3164

Abstract

Maternal diet is critical for offspring development and long-term health. Here we investigated the effects of a poor maternal diet pre-conception and during pregnancy on metabolic outcomes and the developing hypothalamus in male and female offspring at birth. We hypothesised that offspring born to dams fed a diet high in fat and sugar (HFSD) peri-pregnancy will have disrupted metabolic outcomes. We also determined if these HFSD-related effects could be reversed by a shift to a healthier diet post-conception, in particular to a diet high in omega-3 polyunsaturated fatty acids (ω3 PUFAs), since ω3 PUFAs are considered essential for normal neurodevelopment. Unexpectedly, our data show that there are minimal negative effects of maternal HFSD on newborn pups. On the other hand, consumption of an ω3-replete diet during pregnancy altered several developmental parameters. As such, pups born to high-ω3-fed dams weighed less for their length, had reduced circulating leptin, and also displayed sex-specific disruption in the expression of hypothalamic neuropeptides. Collectively, our study shows that maternal intake of a diet rich in ω3 PUFAs during pregnancy may be detrimental for some metabolic developmental outcomes in the offspring. These data indicate the importance of a balanced dietary intake in pregnancy and highlight the need for further research into the impact of maternal ω3 intake on offspring development and long-term health. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

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14 pages, 1389 KiB

Open AccessArticle

Diet-Induced Obesity Disrupts Trace Element Homeostasis and Gene Expression in the Olfactory Bulb

by Melissa S. Totten, Derek M. Pierce and Keith M. Erikson

Nutrients 2020, 12(12), 3909; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12123909 - 21 Dec 2020

Cited by 6 | Viewed by 3215

Abstract

The aim of this study was to determine the impact of diet-induced obesity (DIO) on trace element homeostasis and gene expression in the olfactory bulb and to identify potential interaction effects between diet, sex, and strain. Our study is based on evidence that obesity and olfactory bulb impairments are linked to neurodegenerative processes. Briefly, C57BL/6J (B6J) and DBA/2J (D2J) male and female mice were fed either a low-fat diet or a high-fat diet for 16 weeks. Brain tissue was then evaluated for iron, manganese, copper, and zinc concentrations and mRNA gene expression. There was a statistically significant diet-by-sex interaction for iron and a three-way interaction between diet, sex, and strain for zinc in the olfactory bulb. Obese male B6J mice had a striking 75% increase in iron and a 50% increase in manganese compared with the control. There was an increase in zinc due to DIO in B6J males and D2J females, but a decrease in zinc in B6J females and D2J males. Obese male D2J mice had significantly upregulated mRNA gene expression for divalent metal transporter 1, alpha-synuclein, amyloid precursor protein, dopamine receptor D2, and tyrosine hydroxylase. B6J females with DIO had significantly upregulated brain-derived neurotrophic factor expression. Our results demonstrate that DIO has the potential to disrupt trace element homeostasis and mRNA gene expression in the olfactory bulb, with effects that depend on sex and genetics. We found that DIO led to alterations in iron and manganese predominantly in male B6J mice, and gene expression dysregulation mainly in male D2J mice. These results have important implications for health outcomes related to obesity with possible connections to neurodegenerative disease. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

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11 pages, 1639 KiB

Open AccessArticle

Relationship between Dietary Fiber Intake and the Prognosis of Amytrophic Lateral Sclerosis in Korea

by Haelim Yu, Seung Hyun Kim, Min-Young Noh, Sanggon Lee and Yongsoon Park

Nutrients 2020, 12(11), 3420; https://0-doi-org.brum.beds.ac.uk/10.3390/nu12113420 - 07 Nov 2020

Cited by 11 | Viewed by 2929

Abstract

The gut microbiota has been suggested as an important factor in the pathogenic mechanisms of amyotrophic lateral sclerosis (ALS). This study aimed to investigate whether the intake of different kinds of dietary fiber was related to the disease progression rate (∆FS) and survival time. In total, 272 Korean sporadic ALS patients diagnosed according to the revised EI Escorial criteria were recruited starting in March 2011 and were followed until the occurrence of events or the end of September 2020. The events included percutaneous endoscopic gastrostomy, tracheostomy, and death. Dietary fiber intake was calculated based on a 24-h dietary recall and classified according to five major fiber-rich foods: vegetables, fruits, grains, legumes, and nuts/seeds. Among the total participants, the group with ∆FS values lower than the mean ∆FS (0.75) was noted in the highest tertiles of total and vegetable fiber intake. Participants in the highest tertile for vegetable fiber intake showed longer survival in the Kaplan–Meier analysis (p = 0.033). Notably, vegetable fiber intake was negatively correlated with pro-inflammatory cytokine (interleukin (IL)-1β, IL-6, and monocyte chemoattractant protein-1) levels in the cerebrospinal fluid. This study showed that vegetable fiber intake could influence the disease progression rate and survival time. Further clinical trials are needed to confirm whether dietary fiber supplementation improves the prognosis of ALS. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

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Review

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19 pages, 366 KiB

Open AccessReview

The Role of the Gut Microbiome, Immunity, and Neuroinflammation in the Pathophysiology of Eating Disorders

by Michael J. Butler, Alexis A. Perrini and Lisa A. Eckel

Nutrients 2021, 13(2), 500; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13020500 - 03 Feb 2021

Cited by 34 | Viewed by 8038

Abstract

There is a growing recognition that both the gut microbiome and the immune system are involved in a number of psychiatric illnesses, including eating disorders. This should come as no surprise, given the important roles of diet composition, eating patterns, and daily caloric intake in modulating both biological systems. Here, we review the evidence that alterations in the gut microbiome and immune system may serve not only to maintain and exacerbate dysregulated eating behavior, characterized by caloric restriction in anorexia nervosa and binge eating in bulimia nervosa and binge eating disorder, but may also serve as biomarkers of increased risk for developing an eating disorder. We focus on studies examining gut dysbiosis, peripheral inflammation, and neuroinflammation in each of these eating disorders, and explore the available data from preclinical rodent models of anorexia and binge-like eating that may be useful in providing a better understanding of the biological mechanisms underlying eating disorders. Such knowledge is critical to developing novel, highly effective treatments for these often intractable and unremitting eating disorders. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

29 pages, 1037 KiB

Open AccessReview

Associations of Dietary Intake on Biological Markers of Inflammation in Children and Adolescents: A Systematic Review

by Melissa Bujtor, Anne I. Turner, Susan J. Torres, Laura Esteban-Gonzalo, Carmine M. Pariante and Alessandra Borsini

Nutrients 2021, 13(2), 356; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13020356 - 25 Jan 2021

Cited by 46 | Viewed by 8171

Abstract

Background: In children and adolescents, chronic low-grade inflammation has been implicated in the pathogenesis of co- and multi-morbid conditions to mental health disorders. Diet quality is a potential mechanism of action that can exacerbate or ameliorate low-grade inflammation; however, the exact way dietary intake can regulate the immune response in children and adolescents is still to be fully understood. Methods: Studies that measured dietary intake (patterns of diet, indices, food groups, nutrients) and any inflammatory biomarkers in children and adolescents aged 2 to19 years and published until November 2020 were included in this systematic review, and were selected in line with PRISMA guidelines through the following databases: Academic Search Complete, CINAHL, Global Health, Medline COMPLETE and Web of Science–Core Collection. A total of 53 articles were identified. Results: Results show that adequate adherence to healthful dietary patterns such as the Mediterranean diet, or food groups such as vegetables and fruit, or macro/micro nutrients such as fibre or vitamin C and E, are associated with decreased levels of pro-inflammatory biomarkers, mainly c-reactive protein (CRP), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α), whereas adherence to a Western dietary pattern, as well as intake of food groups such as added sugars, macro-nutrients such as saturated fatty acids or ultra-processed foods, is associated with higher levels of the same pro-inflammatory biomarkers. Conclusions: This is the first systematic review examining dietary intake and biological markers of inflammation in both children and adolescents. A good quality diet, high in vegetable and fruit intake, wholegrains, fibre and healthy fats ameliorates low-grade inflammation, and therefore represents a promising therapeutic approach, as well as an important element for disease prevention in both children and adolescents. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

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23 pages, 387 KiB

Open AccessFeature PaperReview

Mechanisms Underlying the Cognitive and Behavioural Effects of Maternal Obesity

by Kyoko Hasebe, Michael D. Kendig and Margaret J. Morris

Nutrients 2021, 13(1), 240; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13010240 - 15 Jan 2021

Cited by 27 | Viewed by 5345

Abstract

The widespread consumption of ‘western’-style diets along with sedentary lifestyles has led to a global epidemic of obesity. Epidemiological, clinical and preclinical evidence suggests that maternal obesity, overnutrition and unhealthy dietary patterns programs have lasting adverse effects on the physical and mental health of offspring. We review currently available preclinical and clinical evidence and summarise possible underlying neurobiological mechanisms by which maternal overnutrition may perturb offspring cognitive function, affective state and psychosocial behaviour, with a focus on (1) neuroinflammation; (2) disrupted neuronal circuities and connectivity; and (3) dysregulated brain hormones. We briefly summarise research implicating the gut microbiota in maternal obesity-induced changes to offspring behaviour. In animal models, maternal obesogenic diet consumption disrupts CNS homeostasis in offspring, which is critical for healthy neurodevelopment, by altering hypothalamic and hippocampal development and recruitment of glial cells, which subsequently dysregulates dopaminergic and serotonergic systems. The adverse effects of maternal obesogenic diets are also conferred through changes to hormones including leptin, insulin and oxytocin which interact with these brain regions and neuronal circuits. Furthermore, accumulating evidence suggests that the gut microbiome may directly and indirectly contribute to these maternal diet effects in both human and animal studies. As the specific pathways shaping abnormal behaviour in offspring in the context of maternal obesogenic diet exposure remain unknown, further investigations are needed to address this knowledge gap. Use of animal models permits investigation of changes in neuroinflammation, neurotransmitter activity and hormones across global brain network and sex differences, which could be directly and indirectly modulated by the gut microbiome. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

16 pages, 1519 KiB

Open AccessReview

Evolution of the Human Diet and Its Impact on Gut Microbiota, Immune Responses, and Brain Health

by Brigitte M. González Olmo, Michael J. Butler and Ruth M. Barrientos

Nutrients 2021, 13(1), 196; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13010196 - 10 Jan 2021

Cited by 55 | Viewed by 19676

Abstract

The relatively rapid shift from consuming preagricultural wild foods for thousands of years, to consuming postindustrial semi-processed and ultra-processed foods endemic of the Western world less than 200 years ago did not allow for evolutionary adaptation of the commensal microbial species that inhabit the human gastrointestinal (GI) tract, and this has significantly impacted gut health. The human gut microbiota, the diverse and dynamic population of microbes, has been demonstrated to have extensive and important interactions with the digestive, immune, and nervous systems. Western diet-induced dysbiosis of the gut microbiota has been shown to negatively impact human digestive physiology, to have pathogenic effects on the immune system, and, in turn, cause exaggerated neuroinflammation. Given the tremendous amount of evidence linking neuroinflammation with neural dysfunction, it is no surprise that the Western diet has been implicated in the development of many diseases and disorders of the brain, including memory impairments, neurodegenerative disorders, and depression. In this review, we discuss each of these concepts to understand how what we eat can lead to cognitive and psychiatric diseases. Full article

(This article belongs to the Special Issue Nutrition and CNS: In Health and Disease)

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