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Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
Rasa, S, Nora-Krukle, Z, Henning, N, Eliassen, E, Shikova, E, Harrer, T, Scheibenbogen, C, Murovska, M, Prusty, BK
Journal of translational medicine. 2018;16(1):268
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The causes of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are currently unknown, however viruses have been implicated. The absence of well-designed studies has hindered the understanding of this disease and the aim of this review was to discuss the literature regarding viruses and ME/CFS. Several viruses were discussed including the herpes virus, which is responsible for illnesses such as chicken pox and cold sores. This virus has not always been associated with the onset of ME/CFS, however it may be in certain individuals. The enteroviruses, which are responsible for illnesses such as hand, foot and mouth and polio, were also reviewed and it was concluded that it is unlikely that these have a role in ME/CFS. Several other viruses were also discussed. The authors then went on to describe how these viruses can affect human cells, potentially causing ME/CFS. It was concluded that the data available is controversial and only certain individuals may be affected, better studies are required. This study could be used by healthcare professionals to identify individuals at risk of ME/CFS following viral infection and understanding how ME/CFS may develop.
Abstract
BACKGROUND AND MAIN TEXT Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex and controversial clinical condition without having established causative factors. Increasing numbers of cases during past decade have created awareness among patients as well as healthcare professionals. Chronic viral infection as a cause of ME/CFS has long been debated. However, lack of large studies involving well-designed patient groups and validated experimental set ups have hindered our knowledge about this disease. Moreover, recent developments regarding molecular mechanism of pathogenesis of various infectious agents cast doubts over validity of several of the past studies. CONCLUSIONS This review aims to compile all the studies done so far to investigate various viral agents that could be associated with ME/CFS. Furthermore, we suggest strategies to better design future studies on the role of viral infections in ME/CFS.
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Does the microbiome and virome contribute to myalgic encephalomyelitis/chronic fatigue syndrome?
Newberry, F, Hsieh, SY, Wileman, T, Carding, SR
Clinical science (London, England : 1979). 2018;132(5):523-542
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Myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) (ME/CFS) is a disabling and debilitating disease. Several studies have shown alterations in the gut microbiome (dysbiosis) in patients with ME/CFS. However, in focusing on the bacterial components of the microbiome, the viral component of the microbiome (known as the virome) has been neglected. Viruses can change the microbiome which can influence the health. This area is therefore important for research into ME/CFS. This article provides a comprehensive review of the current evidence supporting microbiome alterations in ME/CFS patients. Additionally, the challenges associated with microbiome studies are discussed. A literature search was done and 11 papers were found that had examined the microbiome ME/CFS patients, dating from 1998 to 2017. It was not possible to compare the studies statistically but from looking at each one individually there is sufficient evidence to support the claim of an altered intestinal microbiome in ME/CFS patients. ME/CFS is multifactorial and potential dysbiosis should be considered to be only part of the picture. Future studies are needed to adopt standardized techniques and analyses. As research increases, it is becoming clear that the virome can directly and indirectly affect host health, and may play a role in the pathogenesis of ME/CFS.
Abstract
Myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) (ME/CFS) is a disabling and debilitating disease of unknown aetiology. It is a heterogeneous disease characterized by various inflammatory, immune, viral, neurological and endocrine symptoms. Several microbiome studies have described alterations in the bacterial component of the microbiome (dysbiosis) consistent with a possible role in disease development. However, in focusing on the bacterial components of the microbiome, these studies have neglected the viral constituent known as the virome. Viruses, particularly those infecting bacteria (bacteriophages), have the potential to alter the function and structure of the microbiome via gene transfer and host lysis. Viral-induced microbiome changes can directly and indirectly influence host health and disease. The contribution of viruses towards disease pathogenesis is therefore an important area for research in ME/CFS. Recent advancements in sequencing technology and bioinformatics now allow more comprehensive and inclusive investigations of human microbiomes. However, as the number of microbiome studies increases, the need for greater consistency in study design and analysis also increases. Comparisons between different ME/CFS microbiome studies are difficult because of differences in patient selection and diagnosis criteria, sample processing, genome sequencing and downstream bioinformatics analysis. It is therefore important that microbiome studies adopt robust, reproducible and consistent study design to enable more reliable and valid comparisons and conclusions to be made between studies. This article provides a comprehensive review of the current evidence supporting microbiome alterations in ME/CFS patients. Additionally, the pitfalls and challenges associated with microbiome studies are discussed.
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Food for Mood: Relevance of Nutritional Omega-3 Fatty Acids for Depression and Anxiety.
Larrieu, T, Layé, S
Frontiers in physiology. 2018;9:1047
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The human brain contains high levels of polyunsaturated fatty acids (PUFAs). Of these PUFAs, omega-3s have been widely studied in relation to many brain diseases, including anxiety and depression. This review focuses on the clinical and experimental data linking dietary intake of omega-3s with depression or anxiety. People diagnosed with anxiety and depressive disorders have lower omega-3s and a higher ratio of omega-6s to omega-3s in their blood and brains compared to healthy subjects. Experiments on omega-3 supplementation for depression and post-traumatic stress have had promising results. Numerous mechanisms have been proposed for the effects of omega-3s. These include direct effects on specific receptors in the brain, regulation of the endocannabinoid system, effects on the hypothalamic-pituitary-adrenal (HPA) axis, and reduction of inflammation in the brain. The authors conclude that more research is needed into the potential of omega-3s as treatment for mood-related diseases.
Abstract
The central nervous system (CNS) has the highest concentration of lipids in the organism after adipose tissue. Among these lipids, the brain is particularly enriched with polyunsaturated fatty acids (PUFAs) represented by the omega-6 (ω6) and omega-3 (ω3) series. These PUFAs include arachidonic acid (AA) and docosahexaenoic acid (DHA), respectively. PUFAs have received substantial attention as being relevant to many brain diseases, including anxiety and depression. This review addresses an important question in the area of nutritional neuroscience regarding the importance of ω3 PUFAs in the prevention and/or treatment of neuropsychiatric diseases, mainly depression and anxiety. In particular, it focuses on clinical and experimental data linking dietary intake of ω3 PUFAs and depression or anxiety. In particular, we will discuss recent experimental data highlighting how ω3 PUFAs can modulate neurobiological processes involved in the pathophysiology of anxiety and depression. Potential mechanisms involved in the neuroprotective and corrective activity of ω3 PUFAs in the brain are discussed, in particular the sensing activity of free fatty acid receptors and the activity of the PUFAs-derived endocannabinoid system and the hypothalamic-pituitary-adrenal axis.
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Impact of vegan diets on gut microbiota: An update on the clinical implications.
Wong, MW, Yi, CH, Liu, TT, Lei, WY, Hung, JS, Lin, CL, Lin, SZ, Chen, CL
Ci ji yi xue za zhi = Tzu-chi medical journal. 2018;30(4):200-203
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Gut microbiota is defined as microbes that collectively inhabit the gut ecosystem. Several factors, including diet, age, birth mode, breast-feeding or formula-feeding, geography, exercise, alcohol consumption, and exposure to antibiotics may influence gut microbiota. Previous conventional culturing together with recent culture-independent molecular studies show that vegan diets appear to affect gut microbiota. Furthermore, recent literature also indicates that vegan diets may have various health benefits, including amelioration of metabolic syndrome, cardiovascular disease and rheumatoid arthritis. Authors conclude that these findings have their limitations. Thus, further research may help to clarify the complex mechanisms and interrelationships between vegan diets and gut microbiota.
Abstract
Numerous studies indicate that microbiota plays an important role in human health. Diet is a factor related to microbiota which also influences human health. The relationships between diet, microbiota, and human health are complex. This review focuses on the current literature on vegan diets and their unique impact on gut microbiota. We also report on the health benefits of a vegan diet for metabolic syndrome, cardiovascular disease, and rheumatoid arthritis concerning relevant impacts from gut microbiota. Despite evidence supporting the clinical relevance of vegan gut microbiota to human health, the whole mechanism awaits further investigation.
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Cardiometabolic risk factors in vegans; A meta-analysis of observational studies.
Benatar, JR, Stewart, RAH
PloS one. 2018;13(12):e0209086
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Healthy, balanced, plant-based diets have been associated with better health outcomes, however the role of dairy and meat products on heart disease and death due to heart disease is not fully understood. Vegan diets are strictly plant-based and could provide an opportunity to investigate the effect of eliminating animal products on heart disease risk. This meta-analysis of 40 observational studies aimed to evaluate the effect of a vegan diet on heart disease risk factors. The results showed that vegans in most countries had improved heart disease risk factors such as a small waist circumference, lower body mass index (BMI) and balanced blood sugars compared to omnivores, however studies from Taiwan failed to show this trend. It was concluded that a vegan diet in most countries is associated with better health outcomes compared to an omnivorous diet. This study could be use by healthcare practitioners to recommend a vegan diet to those at a higher risk of heart disease.
Abstract
BACKGROUND There is increasing evidence that plant based diets are associated with lower cardiovascular risk. OBJECTIVE To evaluate effects of a vegan compared to an omnivorous diet on cardio-metabolic risk factors. METHODS Meta-analysis of observational studies published between 1960 and June 2018 that reported one or more cardio-metabolic risk factors in vegans and controls eating an omnivorous diet were undertaken. Macro-nutrient intake and cardio-metabolic risk factors were compared by dietary pattern. The Newcastle Ottawa Scale (NOS) was used to assess the quality of each study. The inverse-variance method was used to pool mean differences. Statistical analyses were performed using RevMan software version 5•2 (The Nordic Cochrane Centre, The Cochrane Collaboration, Copenhagen. RESULTS 40 studies with 12 619 vegans and 179 630 omnivores were included. From food frequency questionnaires in 28 studies, vegans compared to omnivores consumed less energy (-11%, 95% confidence interval -14 to -8) and less saturated fat (- 51%, CI -57 to -45). Compared to controls vegans had a lower body mass index (-1.72 kg/m2, CI -2.30 to -1.16), waist circumference (-2.35 cm, CI -3.93 to -0.76), low density lipoprotein cholesterol (-0.49 mmol/L CI -0.62 to -0.36), triglycerides (-0.14 mmol/L, CI -0.24 to -0.05), fasting blood glucose (-0.23 mmol/, CI -0.35 to -0.10), and systolic (-2.56 mmHg, CI -4.66 to -0.45) and diastolic blood pressure (-1.33 mmHg, CI -2.67 to -0.02), p<0.0001 for all. Results were consistent for studies with < and ≥ 50 vegans, and published before and after 2010. However in several large studies from Taiwan a vegan diet was not associated with favourable cardio-metabolic risk factors compared to the control diets. CONCLUSION In most countries a vegan diet is associated with a more favourable cardio- metabolic profile compared to an omnivorous diet.
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The Western Diet-Microbiome-Host Interaction and Its Role in Metabolic Disease.
Zinöcker, MK, Lindseth, IA
Nutrients. 2018;10(3)
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The Western diet is characteristically high in ultra-processed foods, which may change the gut microbiome. As the gut microbiome is unique, any alterations may be associated with disease. This review study aimed to highlight how ultra-processing can affect the gut microbiome and its impact on the development of disease to better inform dietary guidelines. Associations between poor health outcomes and ultra-processed foods have been shown with processed meats, refined grains, and processed fish. Traditionally research has focussed on added salt, sugar and fat, however processed foods may contain or be processed in a way that promotes disease. Gut microbial changes can be driven by diet, which could be detrimental, permanent, and inheritable. Food processing such as heat treatment, and additives such as sweeteners and emulsifiers can all alter the gut microbiota, however these do not need to undergo microbiome testing before being approved for consumption. Effects of ultra-processed foods on the gut microbiome need to be extensively investigated in terms of health outcomes to better inform dietary guidelines. This study could be used by healthcare professionals to better understand how ultra-processed foods play a part in diseases beyond that of added salt, fat and sugar and that the microbiome has a pivotal role.
Abstract
The dietary pattern that characterizes the Western diet is strongly associated with obesity and related metabolic diseases, but biological mechanisms supporting these associations remain largely unknown. We argue that the Western diet promotes inflammation that arises from both structural and behavioral changes in the resident microbiome. The environment created in the gut by ultra-processed foods, a hallmark of the Western diet, is an evolutionarily unique selection ground for microbes that can promote diverse forms of inflammatory disease. Recognizing the importance of the microbiome in the development of diet-related disease has implications for future research, public dietary advice as well as food production practices. Research into food patterns suggests that whole foods are a common denominator of diets associated with a low level of diet-related disease. Hence, by studying how ultra-processing changes the properties of whole foods and how these foods affect the gut microbiome, more useful dietary guidelines can be made. Innovations in food production should be focusing on enabling health in the super-organism of man and microbe, and stronger regulation of potentially hazardous components of food products is warranted.
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Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty.
Ferrucci, L, Fabbri, E
Nature reviews. Cardiology. 2018;15(9):505-522
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Inflammageing is a term used to describe elevated blood inflammatory markers that leads to frailty and increases an individual’s risk for heart disease, kidney disease and other physical and mental illnesses. Whether inflammageing is causal in heart disease is still uncertain. This large review of 310 papers aimed to understand the causes and role of inflammageing in heart disease and other illnesses associated with ageing. Causes of inflammageing were discussed and mechanisms are not fully understood. Genetic susceptibility, obesity, gut microbiota, gut permeability, when cells can no longer divide, and chronic infections were all implicated. The role of inflammageing in heart disease was a focus and the authors deduced that it was likely to be both causal and a result of heart disease. However, the administration of anti-inflammatories in heart disease has not always proved a successful treatment. Possible causes of inflammageing are likely to be linked and cumulative and although inflammation may cause age related diseases, its role in protecting the body means that its benefits outweigh its consequences. It was concluded that controlling inflammageing may prevent heart disease and other diseases associated with ageing. This study could be used by healthcare professionals to help understand what inflammageing is and its role in age related diseases.
Abstract
Most older individuals develop inflammageing, a condition characterized by elevated levels of blood inflammatory markers that carries high susceptibility to chronic morbidity, disability, frailty, and premature death. Potential mechanisms of inflammageing include genetic susceptibility, central obesity, increased gut permeability, changes to microbiota composition, cellular senescence, NLRP3 inflammasome activation, oxidative stress caused by dysfunctional mitochondria, immune cell dysregulation, and chronic infections. Inflammageing is a risk factor for cardiovascular diseases (CVDs), and clinical trials suggest that this association is causal. Inflammageing is also a risk factor for chronic kidney disease, diabetes mellitus, cancer, depression, dementia, and sarcopenia, but whether modulating inflammation beneficially affects the clinical course of non-CVD health problems is controversial. This uncertainty is an important issue to address because older patients with CVD are often affected by multimorbidity and frailty - which affect clinical manifestations, prognosis, and response to treatment - and are associated with inflammation by mechanisms similar to those in CVD. The hypothesis that inflammation affects CVD, multimorbidity, and frailty by inhibiting growth factors, increasing catabolism, and interfering with homeostatic signalling is supported by mechanistic studies but requires confirmation in humans. Whether early modulation of inflammageing prevents or delays the onset of cardiovascular frailty should be tested in clinical trials.
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Psoriasis and Microbiota: A Systematic Review.
Benhadou, F, Mintoff, D, Schnebert, B, Thio, HB
Diseases (Basel, Switzerland). 2018;6(2)
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Psoriasis is an autoimmune inflammatory skin disease that causes red, itchy, flaky and scaly skin. Skin integrity and function are critically dependent on the microbial population on it. Based on this systematic review, the immune system's interaction with microbes on the skin was examined and its relationship to psoriasis. T-cell mediated inflammation is characteristic of psoriasis where interaction between type IV collagen and α1β1 integrin, a collagen receptor, occurs. In psoriatic skin lesions, Firmicutes were predominant, while Actinobacteria were less prevalent. Psoriasis exacerbations are also associated with an exacerbated number of fungi, Malassezia species, in skin lesions. As therapeutic strategies for psoriasis, this systematic review suggests adhering to a gluten-free diet and incorporating prebiotics and probiotics such as Lactobacillus. However, further research is needed to develop specific therapeutic and skin modulation strategies. Health care professionals can benefit from this systematic review by understanding the pathophysiology behind psoriasis and possible therapeutic strategies to consider.
Abstract
BACKGROUND Recent advances have highlighted the crucial role of microbiota in the pathophysiology of chronic inflammatory diseases as well as its impact on the efficacy of therapeutic agents. Psoriasis is a chronic, multifactorial inflammatory skin disorder, which has a microbiota distinct from healthy, unaffected skin. AIM: Through an extensive review of the literature, we aim to discuss the skin and gut microbiota and redefine their role in the pathogenesis of psoriasis. CONCLUSIONS Unfortunately, the direct link between the skin microbiota and the pathogenesis of psoriasis remains to be clearly established. Apart from improving the course of psoriasis, selective modulation of the microbiota may increase the efficacy of medical treatments as well as attenuate their side effects.
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Dietary Considerations in Autism Spectrum Disorders: The Potential Role of Protein Digestion and Microbial Putrefaction in the Gut-Brain Axis.
Sanctuary, MR, Kain, JN, Angkustsiri, K, German, JB
Frontiers in nutrition. 2018;5:40
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Children with autism spectrum disorder (ASD) display high incidence of gastrointestinal (GI) co-morbidities. Growing evidence now shows an association between diet and ASD, demonstrating that impaired gut function may worsen both GI and behavioural symptoms associated with ASD. The aim of this review was to examine the existing literature to further understand the connection between gut structure and function and ASD. This review found children with ASD and gut co-morbidities exhibit poor protein digestion, impaired gut-barrier integrity and a compromised gut microbiome. A potential mechanistic explanation is that the elevated level of undigested proteins is negatively affecting the integrity of the gut. Based on these findings, the authors conclude it is urgent to perform more experimental and clinical research on the “fragile gut” in children with ASD in order to move towards advancements in individualised clinical practice.
Abstract
Children with autism spectrum disorders (ASD), characterized by a range of behavioral abnormalities and social deficits, display high incidence of gastrointestinal (GI) co-morbidities including chronic constipation and diarrhea. Research is now increasingly able to characterize the "fragile gut" in these children and understand the role that impairment of specific GI functions plays in the GI symptoms associated with ASD. This mechanistic understanding is extending to the interactions between diet and ASD, including food structure and protein digestive capacity in exacerbating autistic symptoms. Children with ASD and gut co-morbidities exhibit low digestive enzyme activity, impaired gut barrier integrity and the presence of antibodies specific for dietary proteins in the peripheral circulation. These findings support the hypothesis that entry of dietary peptides from the gut lumen into the vasculature are associated with an aberrant immune response. Furthermore, a subset of children with ASD exhibit high concentrations of metabolites originating from microbial activity on proteinaceous substrates. Taken together, the combination of specific protein intakes poor digestion, gut barrier integrity, microbiota composition and function all on a background of ASD represents a phenotypic pattern. A potential consequence of this pattern of conditions is that the fragile gut of some children with ASD is at risk for GI symptoms that may be amenable to improvement with specific dietary changes. There is growing evidence that shows an association between gut dysfunction and dysbiosis and ASD symptoms. It is therefore urgent to perform more experimental and clinical research on the "fragile gut" in children with ASD in order to move toward advancements in clinical practice. Identifying those factors that are of clinical value will provide an evidence-based path to individual management and targeted solutions; from real time sensing to the design of diets with personalized protein source/processing, all to improve GI function in children with ASD.
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Physical activity, diet and other behavioural interventions for improving cognition and school achievement in children and adolescents with obesity or overweight.
Martin, A, Booth, JN, Laird, Y, Sproule, J, Reilly, JJ, Saunders, DH
The Cochrane database of systematic reviews. 2018;3:CD009728
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Obesity in children and teenagers is markedly high worldwide and this has been linked to poor performance in school. While physical activity and diet are known to impact cognitive function, studies have not considered to what extent healthy lifestyle interventions can improve school performance in this cohort. The aim of this systematic review was to explore whether these interventions can improve school performance in children and teenagers with obesity. Based on the current literature, increased nutrition education and improved food offered within schools can lead to moderate improvements in school achievement when compared with standard school practice in children with obesity. The authors conclude that more high quality, school subject-specific research is needed to shed light on the extent of these benefits.
Abstract
BACKGROUND The global prevalence of childhood and adolescent obesity is high. Lifestyle changes towards a healthy diet, increased physical activity and reduced sedentary activities are recommended to prevent and treat obesity. Evidence suggests that changing these health behaviours can benefit cognitive function and school achievement in children and adolescents in general. There are various theoretical mechanisms that suggest that children and adolescents with excessive body fat may benefit particularly from these interventions. OBJECTIVES To assess whether lifestyle interventions (in the areas of diet, physical activity, sedentary behaviour and behavioural therapy) improve school achievement, cognitive function (e.g. executive functions) and/or future success in children and adolescents with obesity or overweight, compared with standard care, waiting-list control, no treatment, or an attention placebo control group. SEARCH METHODS In February 2017, we searched CENTRAL, MEDLINE and 15 other databases. We also searched two trials registries, reference lists, and handsearched one journal from inception. We also contacted researchers in the field to obtain unpublished data. SELECTION CRITERIA We included randomised and quasi-randomised controlled trials (RCTs) of behavioural interventions for weight management in children and adolescents with obesity or overweight. We excluded studies in children and adolescents with medical conditions known to affect weight status, school achievement and cognitive function. We also excluded self- and parent-reported outcomes. DATA COLLECTION AND ANALYSIS Four review authors independently selected studies for inclusion. Two review authors extracted data, assessed quality and risks of bias, and evaluated the quality of the evidence using the GRADE approach. We contacted study authors to obtain additional information. We used standard methodological procedures expected by Cochrane. Where the same outcome was assessed across different intervention types, we reported standardised effect sizes for findings from single-study and multiple-study analyses to allow comparison of intervention effects across intervention types. To ease interpretation of the effect size, we also reported the mean difference of effect sizes for single-study outcomes. MAIN RESULTS We included 18 studies (59 records) of 2384 children and adolescents with obesity or overweight. Eight studies delivered physical activity interventions, seven studies combined physical activity programmes with healthy lifestyle education, and three studies delivered dietary interventions. We included five RCTs and 13 cluster-RCTs. The studies took place in 10 different countries. Two were carried out in children attending preschool, 11 were conducted in primary/elementary school-aged children, four studies were aimed at adolescents attending secondary/high school and one study included primary/elementary and secondary/high school-aged children. The number of studies included for each outcome was low, with up to only three studies per outcome. The quality of evidence ranged from high to very low and 17 studies had a high risk of bias for at least one item. None of the studies reported data on additional educational support needs and adverse events.Compared to standard practice, analyses of physical activity-only interventions suggested high-quality evidence for improved mean cognitive executive function scores. The mean difference (MD) was 5.00 scale points higher in an after-school exercise group compared to standard practice (95% confidence interval (CI) 0.68 to 9.32; scale mean 100, standard deviation 15; 116 children, 1 study). There was no statistically significant beneficial effect in favour of the intervention for mathematics, reading, or inhibition control. The standardised mean difference (SMD) for mathematics was 0.49 (95% CI -0.04 to 1.01; 2 studies, 255 children, moderate-quality evidence) and for reading was 0.10 (95% CI -0.30 to 0.49; 2 studies, 308 children, moderate-quality evidence). The MD for inhibition control was -1.55 scale points (95% CI -5.85 to 2.75; scale range 0 to 100; SMD -0.15, 95% CI -0.58 to 0.28; 1 study, 84 children, very low-quality evidence). No data were available for average achievement across subjects taught at school.There was no evidence of a beneficial effect of physical activity interventions combined with healthy lifestyle education on average achievement across subjects taught at school, mathematics achievement, reading achievement or inhibition control. The MD for average achievement across subjects taught at school was 6.37 points lower in the intervention group compared to standard practice (95% CI -36.83 to 24.09; scale mean 500, scale SD 70; SMD -0.18, 95% CI -0.93 to 0.58; 1 study, 31 children, low-quality evidence). The effect estimate for mathematics achievement was SMD 0.02 (95% CI -0.19 to 0.22; 3 studies, 384 children, very low-quality evidence), for reading achievement SMD 0.00 (95% CI -0.24 to 0.24; 2 studies, 284 children, low-quality evidence), and for inhibition control SMD -0.67 (95% CI -1.50 to 0.16; 2 studies, 110 children, very low-quality evidence). No data were available for the effect of combined physical activity and healthy lifestyle education on cognitive executive functions.There was a moderate difference in the average achievement across subjects taught at school favouring interventions targeting the improvement of the school food environment compared to standard practice in adolescents with obesity (SMD 0.46, 95% CI 0.25 to 0.66; 2 studies, 382 adolescents, low-quality evidence), but not with overweight. Replacing packed school lunch with a nutrient-rich diet in addition to nutrition education did not improve mathematics (MD -2.18, 95% CI -5.83 to 1.47; scale range 0 to 69; SMD -0.26, 95% CI -0.72 to 0.20; 1 study, 76 children, low-quality evidence) and reading achievement (MD 1.17, 95% CI -4.40 to 6.73; scale range 0 to 108; SMD 0.13, 95% CI -0.35 to 0.61; 1 study, 67 children, low-quality evidence). AUTHORS' CONCLUSIONS Despite the large number of childhood and adolescent obesity treatment trials, we were only able to partially assess the impact of obesity treatment interventions on school achievement and cognitive abilities. School and community-based physical activity interventions as part of an obesity prevention or treatment programme can benefit executive functions of children with obesity or overweight specifically. Similarly, school-based dietary interventions may benefit general school achievement in children with obesity. These findings might assist health and education practitioners to make decisions related to promoting physical activity and healthy eating in schools. Future obesity treatment and prevention studies in clinical, school and community settings should consider assessing academic and cognitive as well as physical outcomes.