• Gut microbiota
• Microglia
• Neurological diseases
• Short-Chain fatty acids

• Humans
• Fatty Acids, Volatile/metabolism
• Gastrointestinal Microbiome/physiology
• Animals
• Microglia/metabolism
• Brain/metabolism
• Brain-Gut Axis/physiology
• Signal Transduction/physiology

• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• tscx202312104 Taishan Industry Leading Talents Project of Shandong province
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• ZR2022LZY021 Natural Science Foundation of Shandong Province (Joint Fundation for Innovation and Development)
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• 2024CXPT074 Key R&D Program of Shandong Province
• Key R&D Program of Shandong Province

• autism spectrum disorder (ASD)
• human gut microbiome
• potential microbial biomarkers
• stiffness network analysis (SNA)

• Humans
• Autism Spectrum Disorder/microbiology
• Gastrointestinal Microbiome/genetics
• Bacteria/classification
• Bacteria/genetics
• Bacteria/isolation & purification
• RNA, Ribosomal, 16S/genetics
• Child
• Feces/microbiology
• Male
• Female
• Biomarkers
• Child, Preschool

• SCFAs
• gut barrier function
• inflammatory bowel disease
• neuroprotection
• probiotics

• animal models
• maternal influence
• maternal microbiome
• metabolites
• microbiome transfer
• neonatal microbiome
• omics
• pregnancy

• autism spectrum disorder
• behavior
• gut microbiota
• obesity
• physical activity

• Adolescent
• Case-Control Studies
• Child
• Gastrointestinal Microbiome/genetics
• Humans
• Meals
• Mental Health
• Observational Studies as Topic
• RNA, Ribosomal, 16S/genetics

• European Union’s Horizon 2020
• University of Iceland Research Fund
• Landspitali University Hospital Scientific Fund

• autism spectrum disorder
• dietary fibers
• gut microbiota
• microbial therapeutics
• microbiota–gut–brain axis

• Autism Spectrum Disorder
• Fatty Acids, Volatile
• Gastrointestinal Diseases
• Gastrointestinal Microbiome/physiology
• Humans
• Microbiota

• autism spectrum disorder
• gut microbiota
• gut-brain axis
• microbiota transfer therapy
• prebiotics

• National Natural Science Foundation of China

• ADHD
• Autism spectrum disorder
• Children and adolescents
• Pharmacotherapy

• Adolescent
• Attention Deficit Disorder with Hyperactivity/drug therapy
• Attention Deficit Disorder with Hyperactivity/epidemiology
• Autism Spectrum Disorder/drug therapy
• Autism Spectrum Disorder/epidemiology
• Child
• Comorbidity
• Humans
• Intellectual Disability/epidemiology
• Parents

• Medical University of Vienna

• Bacterial metabolites
• Gut microbiota
• Inflammation, Neurological disorders
• SCFAs

• Animals
• Fatty Acids, Volatile/metabolism
• Gastrointestinal Microbiome/physiology
• Humans
• Microbiota/physiology
• Nervous System Diseases/metabolism
• Nervous System Diseases/microbiology

• risk factors
• experimental models of disease

• ADHD
• Adhesion molecules
• Autism
• Inflammation
• Stimulants

• Gut
• Mental health
• Microbes

Worldwide, up to 20% of children and adolescents experience mental disorders, which are the leading cause of disability in young people. Research shows that serum zonulin levels are associated with increased intestinal permeability (IP), affecting neural, hormonal, and immunological pathways. This systematic review and meta-analysis aimed to summarize evidence from observational studies on IP in children diagnosed with mental disorders. The review follows the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A systematic search of the Cochrane Library, PsycINFO, PubMed, and the Web of Science identified 833 records. Only non-intervention (i.e., observational) studies in children (<18 years) diagnosed with mental disorders, including a relevant marker of intestinal permeability, were included. Five studies were selected, with the risk of bias assessed according to the Newcastle–Ottawa scale (NOS). Four articles were identified as strong and one as moderate, representing altogether 402 participants providing evidence on IP in children diagnosed with attention deficit and hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and obsessive–compulsive disorder (OCD). In ADHD, elevated serum zonulin levels were associated with impaired social functioning compared to controls. Children with ASD may be predisposed to impair intestinal barrier function, which may contribute to their symptoms and clinical outcome compared to controls. Children with ASD, who experience gastro-intestinal (GI) symptoms, seem to have an imbalance in their immune response. However, in children with OCD, serum zonulin levels were not significantly different compared to controls, but serum claudin-5, a transmembrane tight-junction protein, was significantly higher. A meta-analysis of mean zonulin plasma levels of patients and control groups revealed a significant difference between groups (p = 0.001), including the four studies evaluating the full spectrum of the zonulin peptide family. Therefore, further studies are required to better understand the complex role of barrier function, i.e., intestinal and blood–brain barrier, and of inflammation, to the pathophysiology in mental and neurodevelopmental disorders. This review was PROSPERO preregistered, (162208).

• adolescents
• attention deficit and hyperactivity disorder (ADHD)
• autism spectrum disorder (ASD)
• children
• haptoglobin
• intestinal permeability
• mental disorders
• meta-analysis
• obsessive–compulsive disorder (OCD)
• systematic review
• zonulin

• autism spectrum disorder
• behavior
• fatty acid
• gastrointestinal
• microbiota
• valproate acid

Autism spectrum disorder (ASD) is a serious neurodevelopmental disorder characterized by the impairment of the cognitive function of a child. Studies suggested that the intestinal microbiota has a critical role in the function and regulation of the central nervous system, neuroimmune system and neuroendocrine system. Any adverse changes in the gut–brain axis may cause serious disease. Food preferences and dietary patterns are considered as key in influencing the factors of ASD development. Several recent reviews narrated the importance of dietary composition on controlling or reducing the ASD symptoms. It has been known that the consumption of probiotics confers several health benefits by positive amendment of gut microbiota. The influence of probiotic intervention in children with ASD has also been reported and it has been considered as an alternative and complementary therapeutic supplement for ASD. The present manuscript discusses the role of microbiota and diet in the development of ASD. It also summarizes the recent updates on the influence of dietary supplements and the beneficial effect of probiotics on ASD symptoms. An in-depth literature survey suggested that the maternal diet and lifestyle are greatly associated with the development of ASD and other neurodevelopmental disorders. Mounting evidences have confirmed the alteration in the gut microbial composition in children suffering from ASD. However, the unique profile of microbiome has not yet been fully characterized due to the heterogeneity of patients. The supplementation of probiotics amended the symptoms associated with ASD but the results are inconclusive. The current study recommends further detailed research considering the role of microbiome, diet and probiotics in the development and control of ASD.

• autism spectrum disorder
• cognition
• diet
• microbiome
• probiotics

• ADHD
• Aggression
• Borderline personality disorder
• Compulsivity
• Impulsivity
• Microbiome
• Nutrition
• Probiotics
• Synbiotics

• brain-gut
• microbiome
• neurogastroenterology
• second brain
• stress

• Amygdala’s structure/ultrastructure
• Anxiety-like behavior
• Propionic acid
• Rat
• Social behavior

• Brain development
• Diet
• Early life
• Gut-brain axis
• Microbiota
• Neuropsychiatry
• Nutrition
• Stress

• 16S rRNA
• Chinese children
• autism spectrum disorder
• case control
• gut microbiota

• Autism Spectrum Disorder
• gut-brain axis
• immune system
• physiological mechanisms

• Autism Spectrum Disorder/complications
• Autism Spectrum Disorder/psychology
• Bumetanide/therapeutic use
• Disease Progression
• Fecal Microbiota Transplantation/methods
• Humans
• Social Behavior Disorders/etiology
• Social Behavior Disorders/therapy
• Social Skills
• Sodium Potassium Chloride Symporter Inhibitors/therapeutic use
• Vasopressins/metabolism

• ASD
• Autism
• Cytokines
• Gastrointestinal
• Immune
• Microbiota
• Mucosal Immunity
• Zonulin

• Autism Spectrum Disorder/immunology
• Autism Spectrum Disorder/metabolism
• Autism Spectrum Disorder/microbiology
• Child
• Child Development
• Child, Preschool
• Comorbidity
• Cytokines/metabolism
• Female
• Gastrointestinal Diseases
• Gastrointestinal Microbiome/physiology
• Humans
• Leukocytes, Mononuclear/metabolism
• Male
• Microbiota
• Monocytes/metabolism

• P01 ES011269 NIEHS NIH HHS
• R01 DK048373 NIDDK NIH HHS
• R01 ES015359 NIEHS NIH HHS
• U54 HD079125 NICHD NIH HHS
• R21 HD086669 NICHD NIH HHS
• R21 MH116383 NIMH NIH HHS
• AS7567 Autism Speaks
• UL1 RR024146 NCRR NIH HHS
• ASCN5014 Autism Speaks
• UL1 TR001860 NCATS NIH HHS
• R21 ES025560 NIEHS NIH HHS
• P30 ES023513 NIEHS NIH HHS

• Bacterial metabolites
• Colonic microbiota
• L-proline
• Pregnant Huanjiang mini-pigs

• Autism Spectrum Disorder/complications
• Autism Spectrum Disorder/diagnosis
• Bacteria/classification
• Bacteria/genetics
• Bacteria/isolation & purification
• Child
• Computational Biology
• Dental Plaque/microbiology
• Dysbiosis
• High-Throughput Nucleotide Sequencing
• Humans
• Microbiota
• Mouth/microbiology
• Saliva/microbiology
• Sequence Analysis, DNA

The gut microbiome consists of over 10³–10⁴ microorganism inhabitants that together possess 150 times more genes that the human genome and thus should be considered an “organ” in of itself. Such communities of bacteria are in dynamic flux and susceptible to changes in host environment and body condition. In turn, gut microbiome disturbances can affect health status of the host. Gut dysbiosis might result in obesity, diabetes, gastrointestinal, immunological, and neurobehavioral disorders. Such host diseases can originate due to shifts in microbiota favoring more pathogenic species that produce various virulence factors, such as lipopolysaccharide. Bacterial virulence factors and metabolites may be transmitted to distal target sites, including the brain. Other potential mechanisms by which gut dysbiosis can affect the host include bacterial-produced metabolites, production of hormones and factors that mimic those produced by the host, and epimutations. All animals, including humans, are exposed daily to various environmental chemicals that can influence the gut microbiome. Exposure to such chemicals might lead to downstream systemic effects that occur secondary to gut microbiome disturbances. Increasing reports have shown that environmental chemical exposures can target both host and the resident gut microbiome. In this review, we will first consider the current knowledge of how endocrine disrupting chemicals (EDCs), heavy metals, air pollution, and nanoparticles can influence the gut microbiome. The second part of the review will consider how potential environmental chemical-induced gut microbiome changes might subsequently induce pathophysiological responses in the host, although definitive evidence for such effects is still lacking. By understanding how these chemicals result in gut dysbiosis, it may open up new remediation strategies in animals, including humans, exposed to such chemicals.

• air pollution
• arsenic
• endocrine disrupting chemicals
• gastrointestinal system
• gut-microbiome-brain axis
• heavy metals
• lead
• nanoparticles

• Autism
• Functional bowel disease
• Gastrointestinal
• Inflammation
• Microbiome
• Probiotics

• Abdominal Pain/drug therapy
• Abdominal Pain/immunology
• Abdominal Pain/microbiology
• Autism Spectrum Disorder/immunology
• Autism Spectrum Disorder/microbiology
• Child
• Constipation/drug therapy
• Constipation/immunology
• Constipation/microbiology
• Diarrhea/drug therapy
• Diarrhea/immunology
• Diarrhea/microbiology
• Gastrointestinal Diseases/drug therapy
• Gastrointestinal Diseases/immunology
• Gastrointestinal Diseases/microbiology
• Gastrointestinal Microbiome/immunology
• Humans
• Inflammation
• Probiotics/therapeutic use

• Animals
• Brain/microbiology
• Brain/physiology
• Gastrointestinal Microbiome/physiology
• Gastrointestinal Tract/microbiology
• Humans
• Mental Disorders/microbiology
• Mental Disorders/psychology
• Microbiota/physiology
• Neuropsychiatry/methods

• Science Foundation Ireland (IE)
• Irish Health Research council
• Enterprise Ireland (IE)
• Department of Agriculture, Food and the Marine

• allergies
• antibiotic-associated diarrhea
• asthma
• autism spectrum disorders
• colic
• diabetes
• eczema
• fecal transplantation
• fetal microbiome
• irritable bowel syndrome
• microbiome
• necrotizing enterocolitis
• prematurity
• probiotics
• short-chain fatty acids

Gastrointestinal dysfunction and gut microbial composition disturbances have been widely reported in autism spectrum disorder (ASD). This study examines whether gut microbiome disturbances are present in the BTBR^T + tf/j (BTBR) mouse model of ASD and if the ketogenic diet, a diet previously shown to elicit therapeutic benefit in this mouse model, is capable of altering the profile.

Juvenile male C57BL/6 (B6) and BTBR mice were fed a standard chow (CH, 13 % kcal fat) or ketogenic diet (KD, 75 % kcal fat) for 10–14 days. Following diets, fecal and cecal samples were collected for analysis. Main findings are as follows: (1) gut microbiota compositions of cecal and fecal samples were altered in BTBR compared to control mice, indicating that this model may be of utility in understanding gut-brain interactions in ASD; (2) KD consumption caused an anti-microbial-like effect by significantly decreasing total host bacterial abundance in cecal and fecal matter; (3) specific to BTBR animals, the KD counteracted the common ASD phenotype of a low Firmicutes to Bacteroidetes ratio in both sample types; and (4) the KD reversed elevated Akkermansia muciniphila content in the cecal and fecal matter of BTBR animals.

Results indicate that consumption of a KD likely triggers reductions in total gut microbial counts and compositional remodeling in the BTBR mouse. These findings may explain, in part, the ability of a KD to mitigate some of the neurological symptoms associated with ASD in an animal model.

The online version of this article (doi:10.1186/s13229-016-0099-3) contains supplementary material, which is available to authorized users.

• Autism spectrum disorder
• BTBR mouse
• Gut microbiome
• Ketogenic diet

• Autism
• Bacterial translocation
• Diabetes type 2
• Immune inflammation
• Leaky gut
• Oxidative stress

Despite the fact that the prevalence of autism spectrum disorder (ASD) continues to rise, no effective medical treatments have become standard of care. In this paper we review some of the pathophysiological abnormalities associated with ASD and their potential associated treatments. Overall, there is evidence for some children with ASD being affected by seizure and epilepsy, neurotransmitter dysfunction, sleep disorders, metabolic abnormalities, including abnormalities in folate, cobalamin, tetrahydrobiopterin, carnitine, redox and mitochondrial metabolism, and immune and gastrointestinal disorders. Although evidence for an association between these pathophysiological abnormalities and ASD exists, the exact relationship to the etiology of ASD and its associated symptoms remains to be further defined in many cases. Despite these limitations, treatments targeting some of these pathophysiological abnormalities have been studied in some cases with high-quality studies, whereas treatments for other pathophysiological abnormalities have not been well studied in many cases. There are some areas of more promising treatments specific for ASD including neurotransmitter abnormalities, particularly imbalances in glutamate and acetylcholine, sleep onset disorder (with behavioral therapy and melatonin), and metabolic abnormalities in folate, cobalamin, tetrahydrobiopterin, carnitine, and redox pathways. There is some evidence for treatments of epilepsy and seizures, mitochondrial and immune disorders, and gastrointestinal abnormalities, particularly imbalances in the enteric microbiome, but further clinical studies are needed in these areas to better define treatments specific to children with ASD. Clearly, there are some promising areas of ASD research that could lead to novel treatments that could become standard of care in the future, but more research is needed to better define subgroups of children with ASD who are affected by specific pathophysiological abnormalities and the optimal treatments for these abnormalities.

• autism spectrum disorders
• carnitine
• cobalamin
• epilepsy
• folate
• genetic disorders
• mitochondrial dysfunction
• review

Autism spectrum disorders (ASDs) are a group of mental illnesses highly correlated with gut microbiota. Recent studies have shown that some abnormal aromatic metabolites in autism patients are presumably derived from overgrown Clostridium species in gut, which may be used for diagnostic purposes. In this paper, a GC/MS based metabolomic approach was utilized to seek similar biomarkers by analyzing the urinary information in 62 ASDs patients compared with 62 non-ASDs controls in China, aged 1.5–7. Three compounds identified as 3-(3-hydroxyphenyl)-3-hydroxypropionic acid (HPHPA), 3-hydroxyphenylacetic acid (3HPA), and 3-hydroxyhippuric acid (3HHA) were found in higher concentrations in autistic children than in the controls (p < 0.001). After oral vancomycin treatment, urinary excretion of HPHPA (p < 0.001), 3HPA (p < 0.005), and 3HHA (p < 0.001) decreased markedly, which indicated that these compounds may also be from gut Clostridium species. The sensitivity and specificity of HPHPA, 3HPA, and 3HHA were evaluated by receiver-operating characteristic (ROC) analysis. The specificity of each compound for ASDs was very high (>96%). After two-regression analysis, the optimal area under the curve (AUC, 0.962), sensitivity (90.3%), and specificity (98.4%) were obtained by ROC curve of Prediction probability based on the three metabolites. These findings demonstrate that the measurements of the three compounds are strong predictors of ASDs and support the potential clinical utility for identifying a subgroup of ASDs subjects.

Precision medicine is an active component of medical practice today, but aspirations are to both broaden its reach to a greater diversity of individuals and improve its “precision” by enhancing the ability to define even more disease states in combination with associated treatments. Given complexity of human phenotypes, much work is required. In this review, we deconstruct this challenge at a high level to define what is needed to move closer toward these aspirations. In the context of the variables that influence the diverse array of phenotypes across human health and disease – genetics, epigenetics, environmental influences, and the microbiome – we detail the factors behind why an individual's biochemical (metabolite) composition is increasingly regarded as a key element to precisely defining phenotypes. Although an individual's biochemical (metabolite) composition is generally regarded, and frequently shown, to be a surrogate to the phenotypic state, we review how metabolites (and therefore an individual's metabolic profile) are also functionally related to the myriad of phenotypic influencers like genetics and the microbiota. We describe how using the technology to comprehensively measure an individual's biochemical profile – metabolomics – is integrative to defining individual phenotypes and how it is currently being deployed in efforts to continue to elaborate on human health and disease in large population studies. Finally, we summarize instances where metabolomics is being used to assess individual health in instances where signatures (i.e. biomarkers) have been defined.

•

Untargeted biochemical profiling has the potential to phenotype individuals where genetic associations do not seem to show penetrance

• Diagnostics
• Genome Wide Association Study
• Inborn Errors of Metabolism
• Mass Spectrometry
• Metabolomics
• Precision Medicine
• Untargeted Analysis

• ASD
• LC−HRMS
• NMR
• autism spectrum disorder
• data fusion
• metabolomics

• Animals
• Autism Spectrum Disorder/diet therapy
• Autism Spectrum Disorder/immunology
• Autism Spectrum Disorder/microbiology
• Dysbiosis/diet therapy
• Dysbiosis/immunology
• Dysbiosis/microbiology
• Gastrointestinal Microbiome/physiology
• Gastrointestinal Tract/immunology
• Gastrointestinal Tract/microbiology
• Humans
• Microbiota/physiology
• Prebiotics/administration & dosage
• Probiotics/administration & dosage

The probiotic medicinal yeast Saccharomyces cerevisiae HANSEN CBS 5926 (Saccharomyces boulardii CNCM I-745) is used for the prevention and treatment of diarrhea. Its action is based on multiple mechanisms, including immunological effects, pathogen-binding and antitoxinic effects, as well as effects on digestive enzymes. Correlated with these effects, but also due to its inherent properties, S. boulardii is able to create a favorable growth environment for the beneficial intestinal microbiota, while constituting extra protection to the host mucus layer and mucosa. This review focuses on the positive influence of S. boulardii on the composition of the intestinal microbiota. In a dysbiosis, as during diarrhea, the main microbial population (especially Lachnospiraceae, Ruminococcaceae, Bacteroidaceae, and Prevotellaceae) is known to collapse by at least one order of magnitude. This gap generally leads to transient increases in pioneer-type bacteria (Enterobacteriaceae, Bifidobacteriaceae, and Clostridiaceae). Several human studies as well as animal models demonstrate that treatment with S. boulardii in dysbiosis leads to the faster reestablishment of a healthy microbiome. The most relevant effects of S. boulardii on the fecal composition include an increase of short chain fatty acid-producing bacteria (along with a rise in short chain fatty acids), especially of Lachnospiraceae and Ruminococcaceae, as well as an increase in Bacteroidaceae and Prevotellaceae. At the same time, there is a suppression of pioneer bacteria. The previously observed preventive action of S. boulardii, eg, during antibiotic therapy or regarding traveler’s diarrhea, can be explained by several mechanisms, including a stabilizing effect on the healthy microbiota as well as possibly on the mucus layer. Several different dysbiotic situations could profit from the effects of S. boulardii CNCM I-745. Its additional potential lies in a general stabilization of the gut flora for at-risk populations. More studies are needed to explore the full potential of this versatile probiotic yeast.

• SCFA
• Saccharomyces boulardii CNCM I-745
• colonic bioreactor
• diarrhea
• dysbiosis
• intestinal mucus layer
• microbiota
• mucosa
• probiotic

There is a growing body of scientific evidence that the health of the microbiome (the trillions of microbes that inhabit the human host) plays an important role in maintaining the health of the host and that disruptions in the microbiome may play a role in certain disease processes. An increasing number of research studies have provided evidence that the composition of the gut (enteric) microbiome (GM) in at least a subset of individuals with autism spectrum disorder (ASD) deviates from what is usually observed in typically developing individuals. There are several lines of research that suggest that specific changes in the GM could be causative or highly associated with driving core and associated ASD symptoms, pathology, and comorbidities which include gastrointestinal symptoms, although it is also a possibility that these changes, in whole or in part, could be a consequence of underlying pathophysiological features associated with ASD. However, if the GM truly plays a causative role in ASD, then the manipulation of the GM could potentially be leveraged as a therapeutic approach to improve ASD symptoms and/or comorbidities, including gastrointestinal symptoms. One approach to investigating this possibility in greater detail includes a highly controlled clinical trial in which the GM is systematically manipulated to determine its significance in individuals with ASD. To outline the important issues that would be required to design such a study, a group of clinicians, research scientists, and parents of children with ASD participated in an interdisciplinary daylong workshop as an extension of the 1st International Symposium on the Microbiome in Health and Disease with a Special Focus on Autism (www.microbiome-autism.com). The group considered several aspects of designing clinical studies, including clinical trial design, treatments that could potentially be used in a clinical trial, appropriate ASD participants for the clinical trial, behavioral and cognitive assessments, important biomarkers, safety concerns, and ethical considerations. Overall, the group not only felt that this was a promising area of research for the ASD population and a promising avenue for potential treatment but also felt that further basic and translational research was needed to clarify the clinical utility of such treatments and to elucidate possible mechanisms responsible for a clinical response, so that new treatments and approaches may be discovered and/or fostered in the future.

• Clostridia
• autism spectrum disorder
• clinical trials
• fecal microbiota transplantation (FMT)
• gastrointestinal
• microbiome
• mitochondria
• probiotic
• short chain fatty acids
• vancomycin

Increasing prevalences, morbidity, premature mortality and medical needs associated with non-communicable diseases and conditions (NCDs) have reached epidemic proportions and placed a major drain on healthcare systems and global economies. Added to this are the challenges presented by overuse of antibiotics and increased antibiotic resistance. Solutions are needed that can address the challenges of NCDs and increasing antibiotic resistance, maximize preventative measures, and balance healthcare needs with available services and economic realities. Microbiome management including microbiota seeding, feeding, and rebiosis appears likely to be a core component of a path toward sustainable healthcare. Recent findings indicate that: (1) humans are mostly microbial (in terms of numbers of cells and genes); (2) immune dysfunction and misregulated inflammation are pivotal in the majority of NCDs; (3) microbiome status affects early immune education and risk of NCDs, and (4) microbiome status affects the risk of certain infections. Management of the microbiome to reduce later-life health risk and/or to treat emerging NCDs, to spare antibiotic use and to reduce the risk of recurrent infections may provide a more effective healthcare strategy across the life course particularly when a personalized medicine approach is considered. This review will examine the potential for microbiome management to contribute to sustainable healthcare.