β-Casomorphins-7 in infants on different type of feeding and different levels of psychomotor development

Кост, Н. В.; Sokolov, O. Yu.; Курасова, О. Б.; Дмитриев, А. Д.; Tarakanova, Yu. N.; Gabaeva, M. V.; Zolotarev, Yuriy A; Dadayan, A. K.; Grachev, S. A.; Korneeva, E. V.; Михеева, И Г; Zozulya, A. A.

doi:10.1016/j.peptides.2009.06.025

Cited by 88 publications

(63 citation statements)

References 34 publications

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Section: Mechanisms Of Brain Effects By Casein Derived Opioid Peptidementioning

confidence: 75%

“…After the formation of β-CM7 in the gut and if β-CM7 is able to cross the intestinal membrane, considerable concentrations of β-CM7 should be found in the blood and urine. Kost et al, [78] detected β-CM7 in blood plasma of 1 year olds after cow's milk ingestion, and this finding was confirmed by the study of Sokolov et al, [91] who investigated the urinary β-CM7 concentration.A significantly higher level of β-CM7 was found in the urine of children with ASD when compared to controls and an increase in β-CM7 urinary concentrations was measured when the severity of ASD increased [91]. In contrast, another study did not find an abnormally high β-CM7 level in the urine of ASD patient, probably due to the small sample size that was used [92].…”

mentioning

confidence: 75%

“…DPP4 is able to decrease opioid peptide levels in body fluids, including blood, urine and cerebrospinal fluid [65][66][67][68]78]. Consequently, if DPP4 is defective, opioid peptides will not be inactivated and opioid activity in the body rises [66][67][68].…”

Section: β-Cm7 Opioid Peptides and Dpp4 Activitymentioning

confidence: 99%

“…The mode of action through which β-CM7 elicits effects on the brain through the bloodstream starts with the digestion of cow's milk into β-CM7 in the gut [89] and subsequent crossing the intestinal membrane in rats [78,91]. No human studies were conducted that investigated if β-CM7 passed the BBB and induces opioid activity in the brain [11].…”

Section: Critical Appraisalmentioning

confidence: 99%

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Untitled

2015

HCIIN

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There is a rising interest in the use of dietary interventions to ameliorate prevalent brain diseases, including Autism Spectrum Disorder (ASD). Nowadays, the existence of communication between gut and brain is well accepted and thus diet can influence brain functioning. A well-known nutrition based intervention for ASD is the gluten-free and casein-free diet. However, only some of the patients experience a relief in symptoms and thus efficacy seems to be limited to certain phenotypes. However, not much is known about the mechanism of action through which this diet might work, or about interpersonal differences that could lead to variation in response to the diet. Current evidence for efficacy of the GFCF diet is poor. Large scale, good quality randomized controlled trials are needed. Genetic and environmentally induced interpersonal differences were found in intestinal membrane permeability and blood brain barrier integrity as well as in activity of peptidase enzymes. These differences probably affect responsiveness to the diet. In addition, age and duration of the dietary intervention play a role in the efficacy of the gluten-free and casein-free diet. This is the reason why all these factors need to be taken into account to give appropriate advice about whether or not to follow this diet.Keywords: Autism spectrum disorder; Casein-free; Casomorphin; Diet; Gluten-free; Intervention; Opioid; Peptides; Permeability Treating Autism Spectrum Disorder with Gluten-free and Casein-free Diet: The underlying Microbiota-Gut-Brain Axis MechanismsCitation: Cieślińska A, Kostyra E, Savelkoul HFJ (2017) Treating Autism Spectrum Disorder with • (GFCF) diet is strongly promoted while there are additional diets without salicylates and phenols, and anti-candida diets since many ASD patients are affected by this yeast [17]. However, so far it has been difficult to prove the effectiveness of this diet in all patients [10,18]. Limited information is available on the underlying mechanism as well as explanatory factors of differences in response to the GFCF diet. Here, we focus on the mechanism of action underlying this dietary intervention as well as the origin of differences in response to the GFCF diet. Gluten-Free and Casein-Free Diet Might Alleviate Autism Spectrum Disorder SymptomsPeople with ASD are often in need of intensive care and guidance, leading to loss of parental productivity and high emotional and economic costs [8,19]. Therefore it is important to investigate potential treatments that alleviate the symptoms or preferably cure the disease. So far, sometimes life long, educational and behavioral interventions are used, although these therapies have limited efficacy for ASD [6,20]. Currently, there is growing interest in nutritional interventions for this disorder and there are promising mechanisms underlying the putative success of such interventions [19].In 1983 it was suggested that gluten and casein containing products could cause autism-like symptoms by altering the functioning of the brain. It was propo...

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Section: Mechanisms Of Brain Effects By Casein Derived Opioid Peptidementioning

confidence: 75%

mentioning

confidence: 75%

Section: β-Cm7 Opioid Peptides and Dpp4 Activitymentioning

confidence: 99%

Section: Critical Appraisalmentioning

confidence: 99%

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Untitled

2015

HCIIN

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“…Exorphins are also released from pancreatic elastase digests [33]. They are probably absorbed since they have been measured in peripheral blood, at least in infants [34] and in patients with untreated coeliac disease [35]. …”

Section: Components Of Wheatmentioning

confidence: 99%

Other Dietary Confounders: FODMAPS et al.

Gibson

Muir

Newnham

2015

Dig Dis

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Background: While it is well documented and widely appreciated that ingestion of wheat (and less so rye and barley) is associated with gastrointestinal symptoms such as bloating or abdominal pain, the component of wheat to which such an effect is attributed is less well established. Key Messages: Wheat is a complex of proteins (80% gluten, 20% metabolic proteins), carbohydrates (starch, non-starch polysaccharides, fructans), lipids and other components. The majority of attention has focused on gluten as the culprit in triggering symptoms, but re-challenge studies have nearly all used wheat flour-related products (such as bread) as the stimulus. When carbohydrate-deplete gluten was used as the challenge agent, gluten-specific feelings of depression and not gut symptoms were observed in those who fulfilled strict criteria of ‘non-coeliac gluten sensitivity', thereby underlining the complexity of cereals and of undertaking research in this area. Candidate components other than gluten include poorly absorbed oligosaccharides (mainly fructans), non-gluten wheat proteins such as amylase-trypsin inhibitors or wheat germ agglutinin, and exorphins released during the digestion of gluten. Specific biological and/or clinical effects associated with gluten-free diets or wheat ingestion need to be carefully dissected before attribution to gluten can be claimed. Conclusions: Currently, coeliac disease is the only common condition that has been unequivocally linked to gluten. Inaccurate attribution will be associated with suboptimal therapeutic advice and at least partly underlies the current gluten-free epidemic gripping the Western world.

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