Are the gut bacteria telling us to eat or not to eat? reviewing the role of gut microbiota in the etiology, disease progression and treatment of eating disorders

Classified as probably not a substantial claim.

The gut-brain axis is a bi-directional communication system connected via neural, hormonal, and immunological pathways, initially recognized for regulating digestive function and food intake.

“The gut–brain axis, connected via neural, hormonal, and immunological pathways, is a bi-directional communication system that is initially recognized for its role in regulating digestive function and food intake [33,34].”

• cites [33] Murphy, 2006, Gut hormones and the regulation of energy homeostasis, Nature sourceNot checked yet

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• cites [34] Holzer, 2012, Neuropeptide, Y, peptide YY and pancreatic polypeptide in the gut-brain axis, Neuropeptides sourceNot checked yet

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Probably not a substantial claim: may not pass S4 (based). May combine two claims.

Compensatory behaviors such as purging and laxative abuse, and conventional treatment such as nutritional rehabilitation, would be expected to impact the gut microbiota, and this change may feed back to modify disease progress.

“More importantly, compensatory behaviors, e.g., purging and laxative abuse, and conventional treatment (nutritional rehabilitation) would be expected to impact on the gut microbiota and this change may feed back to modify the disease progress further.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Microbiota is considered an integral part of gut-brain communication, with some advocating for microbiota as an independent component of the axis.

“Recent advances in our knowledge of the gut microbiota have shed new light on the interactions between the brain and the gastrointestinal tract, with microbiota now being considered an integral part of the gut–brain communication—some even advocate for microbiota being an independent component of the axis [37,38].”

• cites [37] Cryan, 2012, Mind-altering microorganisms: The impact of the gut microbiota on brain and behaviour, Nat. Rev. Neurosci. sourceNot checked yet

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• cites [38] Raybould, 2010, Gut chemosensing: Interactions between gut endocrine cells and visceral afferents, Auton. Neurosci. sourceNot checked yet

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There is a high prevalence of co-morbidity between psychiatric and gastrointestinal symptoms, with 40-60% of patients with functional gastrointestinal disorders experiencing psychiatric symptoms and up to 50% of psychiatric patients diagnosed with irritable bowel syndrome.

“There is a high prevalence of co-morbidity between psychiatric and gastrointestinal symptoms, e.g., 40–60% of patients with functional gastrointestinal disorders experience psychiatric symptoms [35] and up to 50% of psychiatric patients are diagnosed with irritable bowel syndrome [36], which clearly suggests broader implications of this axis on gastrointestinal and brain functions.”

• cites [35] Levy, 2006, Psychosocial aspects of the functional gastrointestinal disorders, Gastroenterology sourceNot checked yet

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• cites [36] Garakani, 2003, Comorbidity of irritable bowel syndrome in psychiatric patients: A review, Am. J. Ther. sourceNot checked yet

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Altered gut-brain communication is evident in eating disorders, with dysregulated appetite control and a distorted perception of satiety among the key biological drivers of extreme feeding behaviors.

“Altered gut–brain communication is evident in eating disorders with dysregulated appetite control and a distorted perception of satiety among the key biological drivers of extreme feeding behaviors.”

May combine two claims.

Literature on gut microbial profile in eating disorders is scarce, with only a handful of studies measuring gut microbial profile in patients with anorexia nervosa and no data available on other forms of eating disorders.

“Surprisingly though, literature on this area is scarce, with only a handful of studies measuring gut microbial profile in patients with AN [29,30,31,32] and no data are available on other forms of eating disorders.”

• cites [29] Morita, C., Tsuji, H., Hata, T., Gondo, M., Takakura, S., Kawai, K., Yoshihara, K., Ogata, K., Nomoto, K., and Miyazaki, K. (2015). Gut Dysbiosis in Patients with Anorexia Nervosa. PLoS ONE, 10. sourceNot checked yet

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• cites [30] Kleiman, 2015, The Intestinal Microbiota in Acute Anorexia Nervosa and During Renourishment: Relationship to Depression, Anxiety, and Eating Disorder Psychopathology, Psychosom. Med. sourceNot checked yet

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• cites [31] Armougom, F., Henry, M., Vialettes, B., Raccah, D., and Raoult, D. (2009). Monitoring bacterial community of human gut microbiota reveals an increase in Lactobacillus in obese patients and Methanogens in anorexic patients. PLoS ONE, 4. sourceNot checked yet

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• cites [32] Mack, 2016, Weight gain in anorexia nervosa does not ameliorate the faecal microbiota, branched chain fatty acid profiles, and gastrointestinal complaints, Sci. Rep. sourceNot checked yet

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• AssumptionThe authors state this as an assumption: There is at least an associative relationship between eating disorders and an altered gut microbiota.

May combine two claims.

An altered gut microbial profile is likely to play a role in the co-morbidities of eating disorders, with altered immune function, short-chain fatty acid production, and the gut barrier being key mechanistic links.

“Given the established causality between dysbiosis and metabolic diseases, an altered gut microbial profile is likely to play a role in the co-morbidities of eating disorders with altered immune function, short-chain fatty acid production, and the gut barrier being the key mechanistic links.”

May combine two claims.

Different bacteria have distinct nutritional requirements, for example Prevotella thrive on carbohydrate and Bacteroides appear to prefer protein and animal fat.

“From an evolutionary perspective, it is not difficult to envisage a role of gut microbiota in modifying host feeding behavior as different bacteria have distinct nutritional requirements, e.g., Prevotella thrive on carbohydrate and Bacteroides appear to have a preference for protein and animal fat [39].”

• cites [39] Wu, 2011, Linking long-term dietary patterns with gut microbial enterotypes, Science sourceNot checked yet

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Many microorganisms express receptors for eukaryotic hormonal signals that primarily act by regulating gene expression; for example, when exposed to norepinephrine, Campylobacter jejuni exhibits increased growth and virulence-associated properties in vitro.

“Known as inter-kingdom signaling, many microorganisms express receptors for eukaryotic hormonal signals that primarily act by regulating gene expression [63], e.g., when exposed to norepinephrine, Campylobacter jejuni exhibited increased growth and virulence-associated properties in vitro [64].”

• cites [63] Hughes, 2008, Inter-kingdom signalling: Communication between bacteria and their hosts, Nat. Rev. Microbiol. sourceNot checked yet

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• cites [64] Cogan, 2007, Norepinephrine increases the pathogenic potential of Campylobacter jejuni, Gut sourceNot checked yet

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Lipopolysaccharide disrupts the blood-brain barrier by increasing permeability, thereby increasing the impact of circulating cytokines on central appetite regulation.

“LPS disrupts the blood–brain barrier (i.e., increases permeability) [41] to increase the impact of circulating cytokines on central appetite regulation;”

• cites [41] Banks, 2015, Lipopolysaccharide-induced blood-brain barrier disruption: Roles of cyclooxygenase, oxidative stress, neuroinflammation, and elements of the neurovascular unit, J. Neuroinflamm. sourceNot checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing).

Stress-induced dysbiosis, with subsequent impaired intestinal barrier and bacterial translocation, has been proposed as a key molecular mechanism that stimulates innate immune activity and contributes to the association between chronic psychological stressors and systemic inflammation in humans.

“Stress-induced dysbiosis (and the subsequent impaired intestinal barrier and bacterial translocation) has been proposed as a key molecular mechanism that stimulates innate immune activity and contributes to the association between chronic psychological stressors and systemic inflammation in humans [69,70].”

• cites [69] Preacher, 2003, Chronic stress and age-related increases in the proinflammatory cytokine IL-6, Proc. Natl. Acad. Sci. USA sourceNot checked yet

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• cites [70] Gouin, 2012, Chronic stress, daily stressors, and circulating inflammatory markers, Health Psychol. sourceNot checked yet

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Gut microbes exhibit time-specific changes in composition and functions that align with the host circadian clock, with up to 10% of all microbes in humans shown to display diurnal oscillations that contribute to distinct functional entities throughout the day.

“Gut microbes exhibit time-specific changes in composition and functions that align with the host circadian clock, with up to 10% of all microbes in humans shown to display diurnal oscillations that contribute to distinct functional entities throughout the day, e.g., energy metabolism pathways dominate during daytime and the detoxification pathways are most active at night [78].”

• cites [78] Thaiss, 2014, Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis, Cell sourceNot checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Some animal data suggest that lipopolysaccharide directly initiates an anorexic response by activating the Toll-like receptor 4/MyD88 signaling pathway in the central nervous system, although it has also been proven otherwise.

“some animal data suggest that LPS directly initiates an anorexic response (i.e., inflammation-induced anorexia) by activating the Toll-like receptor 4/MyD88 signaling pathway in the central nervous system [42,43], although it has also been proven otherwise [44].”

• cites [42] Wisse, 2007, Evidence that lipopolysaccharide-induced anorexia depends upon central, rather than peripheral, inflammatory signals, Endocrinology sourceNot checked yet

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• cites [43] Hrupka, 2004, Role for CD14, TLR2, and TLR4 in bacterial product-induced anorexia, Am. J. Physiol. Regul. Integr. Comp. Physiol. sourceNot checked yet

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• cites [44] Ruud, 2013, Inflammation- and tumor-induced anorexia and weight loss require MyD88 in hematopoietic/myeloid cells but not in brain endothelial or neural cells, FASEB J. sourceNot checked yet

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There is an early-life window during which gut microbes are required for normal programming of the hypothalamic-pituitary-adrenal axis; neonatal colonization with a pathogen-free microbiome reversed the exaggerated HPA stress response in germ-free mice but was without effect when microbes were introduced later in life.

“There appears to be a window early in life during which gut microbes are required for normal programming of the HPA axis. Colonization with a pathogen-free microbiome at the neonate stage reversed the exaggerated HPA stress response in germ-free mice but was without effect when the microbes were introduced later in life, which would implicate a role of neonatal dysbiosis (or infection) in predis”

• cites [56] Sudo, 2004, Postnatal microbial colonization programs the hypothalamic-pituitary-adrenal system for stress response in mice, J. Physiol. sourceNot checked yet

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The effects of gut bacteria on behavior are primarily mediated by their actions on the hypothalamic-pituitary-adrenal axis, which is fundamental to the etiology and progression of eating disorders.

“The effects of gut bacteria on behavior are primarily mediated by their actions on the hypothalamic–pituitary–adrenal (HPA) axis, a major neuroendocrine system that regulates the response to both psychological and physical stressors and is fundamental to the etiology and progression of eating disorders [55].”

• cites [55] Ravaldi, 2008, Stress, hypothalamic-pituitary-adrenal axis and eating disorders, Neuropsychobiology sourceNot checked yet

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Behavioral traits are transmissible via gut microbes, providing strong evidence for causality between gut microbiota and psychobehavioral characteristics.

“These data suggest that behavioral traits are transmissible via gut microbes, thus providing strong evidence for causality between gut microbiota and psychobehavioral characteristics.”

May combine two claims.

Lipopolysaccharide induces cytokine production, notably interleukin-1, interleukin-6, and tumor necrosis factor-α, from immune cells and triggers immune-endocrine-nervous changes that subsequently activate the hypothalamic-pituitary-adrenal axis.

“By binding to its receptors on macrophages, lymphocytes, and granulocytes, LPS induces cytokine production (notably interleukin-1, interleukin-6 and tumor necrosis factor-α) from immune cells and triggers a series of changes in the immune-endocrine-nervous system that subsequently activates the HPA axis (for details please refer to a comprehensive review by Tilders and colleagues [59]).”

• cites [59] Tilders, 1994, Activation of the hypothalamus-pituitary-adrenal axis by bacterial endotoxins: Routes and intermediate signals, Psychoneuroendocrinology sourceNot checked yet

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Circulating lipopolysaccharide does not pass the blood-brain barrier to impact neurons or glial cells per se, but it modulates blood-brain barrier function by affecting tight junction proteins and brain endothelial cells to regulate immune cell trafficking and cytokine transport.

“Finally, although circulating LPS does not pass the blood–brain barrier to impact on neurons or glial cells per se [59], LPS modulates the blood–brain barrier function by its direct effect on the tight junction proteins and thus barrier permeability, as well as its interactions with the brain endothelial cells to regulate immune cell trafficking and cytokine transport as an indirect way for gut”

• cites [59] Tilders, 1994, Activation of the hypothalamus-pituitary-adrenal axis by bacterial endotoxins: Routes and intermediate signals, Psychoneuroendocrinology sourceNot checked yet

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• cites [61] Banks, 2010, The blood-brain barrier and immune function and dysfunction, Neurobiol. Dis. sourceNot checked yet

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A subgroup of patients with anorexia nervosa and bulimia nervosa had autoantibodies that bind to α-melanocyte-stimulating hormone, and the circulating level of these autoantibodies was correlated with psychological traits of eating disorders.

“Fetissov and colleagues [45,46] revealed that a subgroup of patients with AN and BN had autoantibodies that bind to the α-melanocyte-stimulating hormone (MSH), and the circulating level of these autoantibodies was correlated with the psychological traits of eating disorders.”

• cites [45] Fetissov, 2002, Autoantibodies against alpha -MSH, ACTH, and LHRH in anorexia and bulimia nervosa patients, Proc. Natl. Acad. Sci. USA sourceNot checked yet

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• cites [46] Fetissov, 2005, Autoantibodies against neuropeptides are associated with psychological traits in eating disorders, Proc. Natl. Acad. Sci. USA sourceNot checked yet

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The abundance of the mucin-degrading taxa Verrucomicrobia is significantly increased in anorexia nervosa patients at baseline and returns to levels similar to healthy controls after weight gain.

“Following this notion, the abundance of the mucin-degrading taxa Verrucomicrobia was significantly increased in AN patients at baseline and returned to levels similar to that in healthy controls after weight gain [32].”

• cites [32] Mack, 2016, Weight gain in anorexia nervosa does not ameliorate the faecal microbiota, branched chain fatty acid profiles, and gastrointestinal complaints, Sci. Rep. sourceNot checked yet

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May combine two claims.

Limited food choice is a direct selective pressure on gut microbes because different microbes have preferred substrates; for example, Roseburia and Bacteroides are sensitive to dietary carbohydrate and protein, respectively, and the proportion of Bacteroidetes depends on the type of dietary fiber that reaches the colon.

“Limited food choice is a direct selective pressure as different microbes have their preferred substrates, e.g., Roseburia and Bacteroides are sensitive to dietary carbohydrate and protein, respectively, and the proportion of Bacteroidetes is dependent on the type of dietary fiber that reaches the colon [71,72,73].”

• cites [71] Maukonen, 2015, Human gut microbiota: Does diet matter?, Proc. Nutr. Soc. sourceNot checked yet

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• cites [72] Chung, W.S., Walker, A.W., Louis, P., Parkhill, J., Vermeiren, J., Bosscher, D., Duncan, S.H., and Flint, H.J. (2016). Modulation of the human gut microbiota by dietary fibres occurs at the species level. BMC Biol., 14. sourceNot checked yet

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• cites [73] Dominianni, C., Sinha, R., Goedert, J.J., Pei, Z., Yang, L., Hayes, R.B., and Ahn, J. (2015). Sex, body mass index, and dietary fiber intake influence the human gut microbiome. PLoS ONE, 10. sourceNot checked yet

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Germ-free mice receiving cecal content transplant express behavioral phenotypes that mimic the donors, and mice receiving fecal transplant from patients with major depressive disorder display more depression-like behaviors than those colonized with microbiota from healthy controls.

“Further, germ-free mice receiving cecal content transplant expressed behavioral phenotypes that mimicked the donors [54], and those that had fecal transplant from patients with major depressive disorder also displayed more depression-like behaviors, as compared to those colonized with microbiota from healthy controls [50].”

• cites [54] Bercik, 2011, The intestinal microbiota affect central levels of brain-derived neurotropic factor and behavior in mice, Gastroenterology sourceNot checked yet

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• cites [50] Zheng, 2016, Gut microbiome remodeling induces depressive-like behaviors through a pathway mediated by the host’s metabolism, Mol. Psychiatry sourceNot checked yet

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May combine two claims.

Food restriction in patients with eating disorders changes energy substrate availability for gut microbes and leads to distinct microbial profiles.

“Food restriction in patients with eating disorders changes energy substrate availability (type, amount, and duration) for the gut microbes and leads to distinct microbial profiles.”

May combine two claims.

Bacteria produce neurotransmitters and neuromodulators, such as γ-amino butyric acid from Bifidobacterium spp. that controls anxiety and serotonin from Enterococcus spp. that modulates mood, which act directly on afferent axons or interact with intestinal epithelial cells and the enteric nervous system to modify neural signaling to the central nervous system.

“Bacteria produce many neurotransmitters and neuromodulators, e.g., γ-amino butyric acid (GABA) from Bifidobacterium spp. controls anxiety and serotonin from Enterococcus spp. modulates mood regulation, that either act directly on afferent axons or interact with the intestinal epithelial cells and thus the enteric nervous system to modify neural signaling to the central nervous system [37].”

• cites [37] Cryan, 2012, Mind-altering microorganisms: The impact of the gut microbiota on brain and behaviour, Nat. Rev. Neurosci. sourceNot checked yet

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May combine two claims.

Cycling of microbial abundance aligns with the feeding schedule that overrides the effect of the host circadian rhythm, implicating a role of irregular feeding patterns in contributing to dysbiosis in eating disorders.

“Cycling of microbial abundance appears to align with the feeding schedule that overrides the effect of the host circadian rhythm, which would implicate a role of irregular feeding patterns in contributing to dysbiosis in eating disorders.”

May combine two claims.

Experimentally-induced anorexia nervosa increased barrier permeability and reduced tight junction protein expression in the mouse colon, but was without effect in the jejunum.

“Experimentally-induced AN increased barrier permeability and reduced tight junction protein expression in the mouse colon, but was without effect in the jejunum [102].”

• cites [102] Jesus, 2014, Alteration of intestinal barrier function during activity-based anorexia in mice, Clin. Nutr. sourceNot checked yet

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Microbiome-targeted interventions could potentially supplement existing treatments and increase treatment efficacy in eating disorders.

“Achieving and maintaining a healthy gut microbiome, therefore, could potentially be a gut-specific approach to increase treatment efficacy in eating disorders.”

• Also stated in: § 4. Therapeutic Potential of Microbiome-Based Treatments for Eating Disorders · hedged

  “we can already see the possibility of using microbiome-targeted interventions to supplement what is already available for the patients.”

• AssumptionRests on an assumption: Compliance to nutritional rehabilitation in eating disorders is often hindered by gastrointestinal symptoms associated with the illness.

May combine two claims.

Gut microbes do not directly disrupt the gut barrier; rather, they alter butyrate availability for colonocytes that change colonic mucosal functions, and they induce the secretion of pro-inflammatory cytokines that disrupt tight junction proteins.

“Gut microbes do not directly disrupt the gut barrier, rather they alter butyrate availability for colonocytes that change colonic mucosal functions [100], and they induce the secretion of pro-inflammatory cytokines that disrupt tight junction proteins [101].”

• cites [100] Hamer, 2008, Review article: The role of butyrate on colonic function, Aliment. Pharmacol. Ther. sourceNot checked yet

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• cites [101] Turner, 2014, The role of molecular remodeling in differential regulation of tight junction permeability, Semin. Cell Dev. Biol. sourceNot checked yet

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The exact mechanisms by which purging behaviors affect gut microbes remain largely unclear, but are expected to be a consequence of structural and functional changes in the colon, such as damage to mucosal lining, electrolyte imbalance, and changes in transit time and intra-abdominal pressure, which collectively alter the gut environment for microbial colonization.

“The exact mechanisms by which these behaviors affect the gut microbes remain largely unclear, but are expected to be a consequence of structural and functional changes in the colon, e.g., damage to mucosal lining, electrolyte imbalance, as well as changes in transit time and intra-abdominal pressure, which collectively alter the gut environment for microbial colonization [81,82].”

• cites [81] Sato, 2015, Gastrointestinal symptoms and disorders in patients with eating disorders, Clin. J. Gastroenterol. sourceNot checked yet

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• cites [82] Forney, 2016, The medical complications associated with purging, Int. J. Eat. Disord. sourceNot checked yet

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In patients with anorexia nervosa following institutionalized nutritional rehabilitation programs, refeeding increases gut microbial diversity and shifts the composition towards, but remains significantly different from, that of healthy controls.

“There are some data on gut microbiota in patients with AN following institutionalized nutritional rehabilitation programs that suggest that refeeding increases gut microbial diversity and shifts the composition towards, but remains significantly different from that of healthy controls [30,32].”

• cites [30] Kleiman, 2015, The Intestinal Microbiota in Acute Anorexia Nervosa and During Renourishment: Relationship to Depression, Anxiety, and Eating Disorder Psychopathology, Psychosom. Med. sourceNot checked yet

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• cites [32] Mack, 2016, Weight gain in anorexia nervosa does not ameliorate the faecal microbiota, branched chain fatty acid profiles, and gastrointestinal complaints, Sci. Rep. sourceNot checked yet

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Morbidity and mortality of eating disorders are not always a direct consequence of malnutrition and/or psychiatric symptoms, but are often due to the deleterious metabolic sequelae of the illness, such as an increased risk of developing type 2 diabetes.

“Morbidity and mortality of eating disorders are not always a direct consequence of malnutrition and/or psychiatric symptoms, but are often due to the deleterious metabolic sequelae of the illness, e.g., an increased risk of developing type 2 diabetes [87].”

• cites [87] Raevuori, 2015, Highly increased risk of type 2 diabetes in patients with binge eating disorder and bulimia nervosa, Int. J. Eat. Disord. sourceNot checked yet

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An impaired gut barrier increases the translocation of microbial metabolites, or even the microbes themselves, from the lumen of the gastrointestinal tract into adjacent tissues, and these materials enter the portal and systemic circulation, a phenomenon known as endotoxemia, to trigger inflammatory responses at the tissue level.

“An impaired gut barrier (or a “leaky” gut) increases the translocation of microbial metabolites, or even the microbes themselves, from the lumen of the gastrointestinal tract into the adjacent tissues. These materials then enter the portal and systemic circulation, a phenomenon known as endotoxemia, to trigger inflammatory responses at the tissue level [97].”

• cites [97] Lam, 2011, Role of the gut in visceral fat inflammation and metabolic disorders, Obesity sourceNot checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

How the microbiota modulate innate immunity is less clear because the system lacks antigen specificity, but it is believed to respond broadly to the activity of microbes via tissue-level microbial sensing.

“How the microbiota modulate innate immunity is less clear as the system lacks antigen specificity, but is believed to respond broadly to the activity of microbes via tissue-level microbial sensing [90].”

• cites [90] Thaiss, 2016, The microbiome and innate immunity, Nature sourceNot checked yet

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Colonic gut permeability data are not available in patients with eating disorders, but a study by Monteleone et al. showed a significant decrease in small intestinal permeability in anorexia nervosa patients.

“Colonic gut permeability data are not available in patients with eating disorders, but a study by Monteleone et al. [103] showed a significant decrease in small intestinal permeability in AN patients.”

• cites [103] Monteleone, 2004, Intestinal permeability is decreased in anorexia nervosa, Mol. Psychiatry sourceNot checked yet

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Microbial fermentation is a key mechanism by which gut bacteria impact host metabolism; dietary fiber and undigested carbohydrates are the primary substrates for fermentation, with short-chain fatty acids, notably butyrate, acetate, and propionate, as the key end-products.

“Microbial fermentation is a key mechanism by which gut bacteria impact on host metabolism. Dietary fiber and undigested carbohydrates are the primary substrates for fermentation, with short-chain fatty acids (SCFAs), notably butyrate, acetate, and propionate, the key end-products generated in this process.”

May combine two claims.

Time-restricted feeding in mice and repeated prolonged cycles of feeding and withholding food in dogs cause a change in the overall gut microbiome that appears driven by changes in the abundance of species that differ by their preferred fermentable substrates.

“Time-restricted feeding in mice [79] and repeated prolonged cycles of feeding and withholding food in dogs [80] have all been shown to cause a change in the overall gut microbiome that appears to be driven by changes in the abundance of species that differ by their preferred fermentable substrates (e.g., host-vs. diet-derived glycans).”

• cites [79] Zarrinpar, 2014, Diet and feeding pattern affect the diurnal dynamics of the gut microbiome, Cell Metab. sourceNot checked yet

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• cites [80] Kasiraj, 2016, The effects of feeding and withholding food on the canine small intestinal microbiota, FEMS Microbiol. Ecol. sourceNot checked yet

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Mack et al. reported that the overall microbial structure was different between the two anorexia nervosa subtypes, but no specific species that drove this difference were identified, and they demonstrated a reduction in microbial diversity in those who reported using laxatives.

“Using constrained ordination techniques, Mack et al. [32] reported that the overall microbial structure (assessed using constrained ordination techniques) was different between the two AN subtypes, but no specific species that drove this difference were identified, and they further demonstrated a reduction in microbial diversity in those who reported using laxatives.”

• cites [32] Mack, 2016, Weight gain in anorexia nervosa does not ameliorate the faecal microbiota, branched chain fatty acid profiles, and gastrointestinal complaints, Sci. Rep. sourceNot checked yet

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Efficient attainment of a healthy body weight has been shown to predict recovery, and aggressive approaches including high caloric meals and/or enteral feeding are common, especially in institutionalized patients.

“Efficient attainment of a healthy body weight has been shown to predict recovery and thus aggressive approaches including high caloric meals and/or enteral feeding are common, especially in institutionalized patients [83].”

• cites [83] Garber, 2016, A systematic review of approaches to refeeding in patients with anorexia nervosa, Int. J. Eat. Disord. sourceNot checked yet

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Cross-feeding, in which microbes utilize metabolic end-products from one another, is another way by which fermentable substrate availability selects for particular microbial profiles.

“Cross-feeding, i.e., microbes utilizing metabolic end-products from one another, is another way by which fermentable substrate availability selects for particular microbial profiles [95].”

• cites [95] Margolles, 2016, Intestinal Short Chain Fatty Acids and their Link with Diet and Human Health, Front. Microbiol.Not checked yet

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Classified as probably not a substantial claim.

A lot of work is still required before microbiome-based treatments for eating disorders are ready to be developed.

“but a lot of work is still required before we get to the position where we are ready to develop microbiome-based treatments for these patients.”

• Also stated in: § 4. Therapeutic Potential of Microbiome-Based Treatments for Eating Disorders · plain

  “While we are still a long way from using strategies that restore a healthy gut microbiome to treat eating disorders”

Probably not a substantial claim: may not pass S3 (load-bearing).

Nutritional rehabilitation, also known as refeeding, is a key component of eating disorder treatment that aims to restore physiological functions by reversing malnutrition.

“Nutritional rehabilitation, also known as refeeding, is a key component of eating disorder treatment that aims to restore physiological functions by reversing malnutrition.”

May combine two claims.

Prebiotic supplementation has positive effects on the gut microbial profile and quality of life in tube-fed patients.

“the positive effects of prebiotic supplementation on the gut microbial profile and quality of life in tube-fed patients [107]”

• cites [107] Wierdsma, 2009, Fructo-oligosaccharides and fibre in enteral nutrition has a beneficial influence on microbiota and gastrointestinal quality of life, Scand. J. Gastroenterol. sourceNot checked yet

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Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.

Butyrate is locally consumed by colonocytes as an energy substrate that influences the physiology of the colon.

“Butyrate is locally consumed by colonocytes as an energy substrate that influences the physiology of the colon.”

Probably not a substantial claim: may not pass S1 (asserted), S2 (checkable).

It is logical to hypothesize a similar role of gut microbes in dysmetabolism associated with eating disorders.

“The molecular mechanisms by which dysbiosis induces metabolic dysfunctions are well-documented [28] and it is logical to hypothesize a similar role of gut microbes in dysmetabolism associated with eating disorders.”

• cites [28] Woting, A., and Blaut, M. (2016). The Intestinal Microbiota in Metabolic Disease. Nutrients, 8. sourceNot checked yet

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An animal-based diet shifted the gut microbial structure in humans such that the abundance of bile-tolerant microbes increased at the expense of those that metabolized dietary plant polysaccharides, an effect associated with concomitant changes in the proportion of short-chain fatty acids that originated from different macronutrients.

“David et al. [94] showed that an animal-based diet shifted the gut microbial structure in humans such that the abundance of bile-tolerant microbes increased at the expense of those that metabolized dietary plant polysaccharides, an effect associated with concomitant changes in the proportion of SCFAs that originated from different macronutrients.”

• cites [94] David, 2014, Diet rapidly and reproducibly alters the human gut microbiome, Nature sourceNot checked yet

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In obese rodents, antibiotics and prebiotics were able to restore gut barrier integrity and metabolic functions, providing evidence for the gut barrier as a mediator of microbiota-induced systemic inflammation.

“In obese rodents, antibiotics and prebiotics were able to restore gut barrier integrity and metabolic functions, providing evidence for the gut barrier as a mediator of microbiota-induced systemic inflammation [98,99].”

• cites [98] Cani, 2008, Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice, Diabetes sourceNot checked yet

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• cites [99] Cani, 2009, Interplay between obesity and associated metabolic disorders: New insights into the gut microbiota, Curr. Opin. Pharmacol. sourceNot checked yet

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The low content or even absence of fiber and resistant starch in feeding regimens limits energy substrate availability for gut microbes, and abnormal fluid secretion into the colon triggered by enteral formula infusion confers deleterious effects on the gut microbiota.

“The low content (or even absence) of fiber and resistant starch in these feeding regimens limits energy substrate availability for the gut microbes; abnormal fluid secretion into the colon triggered by enteral formula infusion also confers deleterious effects on the gut microbiota [84,85].”

• cites [84] Whelan, 2004, Enteral feeding: The effect on faecal output, the faecal microflora and SCFA concentrations, Proc. Nutr. Soc. sourceNot checked yet

  Not checked in the free run.

• cites [85] 2010, Tube feeding, the microbiota, and Clostridium difficile infection, World J. Gastroenterol. sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Prebiotic and probiotic supplementations relieve symptoms and improve gut functions in patients with functional and inflammatory bowel disorders.

“Prebiotic and probiotic supplementations have already been shown to relieve symptoms and improve gut functions in patients with functional and inflammatory bowel disorders [105,106].”

• cites [105] Ford, 2014, Efficacy of prebiotics, probiotics, and synbiotics in irritable bowel syndrome and chronic idiopathic constipation: Systematic review and meta-analysis, Am. J. Gastroenterol. sourceNot checked yet

  Not checked in the free run.

• cites [106] Curro, 2016, Probiotics, fibre and herbal medicinal products for functional and inflammatory bowel disorders, Br. J. Pharmacol. sourceNot checked yet

  Not checked in the free run.