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ATI (Amylase/trypsin-inhibitors) (Second part)

by luciano

Anti nutritional factors in cereals, especially amylase trypsin inhibitors, affecting digestibility.
“Anti nutritional factors (ANF) play an important role in cereals to protect against infestation and animal consumption. From an agronomic point of view these pest barriers are beneficial as the required pest control measures (chemical pesticides, storage facilities) is relatively limited.
From a health point of view a large group of ANF, the ATI are of special interest as they may impact digestion in multiple ways, e.g. they:
• can reduce digestibility of food directly by inhibition of enzymes from the digestive tract (human and microbiome; Weegels 1994),
• can increase the load of allergenic peptide presented to the small intestine, thus (così) increasing the allergenic and inflammation reactions (Junker et al. 2012; Zevallos et al 2014)
• complexation  behavior may strongly interact with the small intestine epithelium that can cause inflammation by itself (Zevallos et al 2014)
• are the not yet completely understood cause of Bakers asthma (asma), the major labour related allergy (Stobnicka and Górny, 2015)
• can increase the load of non digested peptides and carbohydrates especially of non-starch polysaccharides (FODMAPS) that are a major cause of Irritable Bowel Syndrome (IBS) which affects 7% to 21% of the general population (Chey et al 2015)
• may impact the microbiome itself. This is not established in detail
From a food processing point of view ATI’s play a negative role as they inhibit enzymes that are added as processing aids for improved processing and bread quality. This reduces processing effectiveness and quality control of cereal based products.
Understanding the role of ATI in cereals food processing and food digestion and mitigation of the negative effects is therefor (perciò) of prime importance for food safety, security and sustainability.
An interesting way to mitigate the effect of ATI could be by altering its molecular structure that is stabilised by the large number of disulphide bonds (5-6 on ca. 14 kDa; Buchanan et al 1997)”. “https://www.wur.nl/en/Research-Results/Chair-groups/Agrotechnology-and-Food-Sciences/Laboratory-of-Food-Chemistry/Research/Themes/Technology-of-cereal-foods-digestibility.htm”


Dietary Triggers in Irritable Bowel Syndrome: Is There a Role for Gluten?

by luciano

A very important study that highlights the superimposition of the symptoms of irritable bowel syndrome with those generated by the sensitivity to non-celiac gluten, by the ATI and by Fodmaps.

“A tight link exists between dietary factors and irritable bowel syndrome (IBS), one of the most common functional syndromes, characterized by abdominal pain/discomfort, bloating and alternating bowel habits. Amongst the variety of foods potentially evoking “food sensitivity”, gluten and other wheat proteins including amylase trypsin inhibitors represent the culprits that recently have drawn the attention of the scientific community. Therefore, a newly emerging condition termed non-celiac gluten sensitivity (NCGS) or nonceliac wheat sensitivity (NCWS) is now well established in the clinical practice. Notably, patients with NCGS/NCWS have symptoms that mimic those present in IBS. The mechanisms by which gluten or other wheat proteins trigger symptoms are poorly understood and the lack of specific biomarkers hampers diagnosis of this condition. The present review aimed at providing an update to physicians and scientists regarding the following main topics: the experimental and clinical evidence on the role of gluten/wheat in IBS; how to diagnose patients with functional symptoms attributable to gluten/wheat sensitivity; the importance of double-blind placebo controlled cross-over trials as confirmatory assays of gluten/wheat sensitivity; and finally, dietary measures for gluten/wheat sensitive patients. The analysis of current evidence proposes that gluten/wheat sensitivity can indeed represent a subset of the broad spectrum of patients with a clinical presentation of IBS. (J Neurogastroenterol Motil 2016;22:547-557). Umberto Volta, Maria Ines Pinto-Sanchez et al.

Extrac from the study:
…..omissis. Experimental Evidence for a Role of Wheat Components in Irritable Bowel Syndrome. Different mechanisms have been proposed to explain how gluten may trigger gastrointestinal symptoms in the absence of celiac disease (Figure).

In vitro studies have demonstrated that digests of gliadin increase the expression of co-stimulatory molecules and the production of proinflammatory cytokines in monocytes and dendritic cells (40,57,58). Certain “toxic” (that only stimulates the innate immune response) gliadin-derived peptides such as the 31-43mer, may evoke epithelial cell dysfunction, increased IL-15 production and enterocyte apoptosis (59). Recent studies have demonstrated increased expression of TLR-2 in the intestinal mucosa of non-celiac compared to celiac patients, suggesting a role of the innate immune system in the pathogenesis of non-celiac reactions to gluten or other wheat components (49). Other studies have shown that monocytes from HLA-DQ2+ non-celiac individuals spontaneously release 2-3 fold more IL-8 than monocytes from HLA-DQ2 negative patients. This suggests that patients without celiac disease (no enteropathy and negative specific serology), but with positive HLA-DQ2 status, may represent a subpopulation reacting mildly to gluten (60). In terms of gut dysfunction, gluten sensitization in mice has been shown to induce acetylcholine release, one of the main excitatory neurotransmitters in the gut, from the myenteric plexus (57).
This correlates with increased smooth muscle contractility and a hypersecretory status with increased ion transport and water movements (57). These functional effects induced by gluten were not accompanied by mucosal atrophy, and were not observed after sensitization with non-gluten proteins. Interestingly gluten-induced gut dysfunction was particularly notable in mice transgenic for the human celiac gene HLA-DQ8 (57).
ATIs, a group of wheat proteins that confer resistance of the grain to pests, are strong inducers of innate immune responses via TLR4 and via the myeloid differentiation factor 88-dependent and -independent pathway (40). This activation occurs both in vitro and in vivo after oral ingestion of purified ATIs or gluten, while gluten-free cereals display no or minimal activities (61). The role of ATIs in IBS is not yet known, however there is clear description of a mechanism that could be involved in the generation of gut dysfunction and symptoms. These mechanisms are different from those proposed for gluten and thus it is conceivable that they could co-exist in given patients or have a synergistic effect.

Adverse Reactions to Wheat or Wheat Components.

by luciano

The research we present is an excellent compendium of current knowledge on non-celiac gluten sensitivity

“Abstract: Wheat is an important staple food globally, providing a significant contribution to daily energy, fiber, and micronutrient intake. Observational evidence for health impacts of consuming more whole grains, among which wheat is a major contributor, points to significant risk reduction for diabetes, cardiovascular disease, and colon cancer. However, specific wheat components may also elicit adverse physical reactions in susceptible individuals such as celiac disease (CD) and wheat allergy (WA). Recently, broad coverage in the popular and social media has suggested that wheat consumption leads to a wide range of adverse health effects. This has motivated many consumers to avoid or reduce their consumption of foods that contain wheat/gluten, despite the absence of diagnosed CD or WA, raising questions about underlying mechanisms and possible nocebo effects. However, recent studies did show that some individuals may suffer from adverse reactions in absence of CD and WA. This condition is called non-celiac gluten sensitivity (NCGS) or non-celiac wheat sensitivity (NCWS). In addition to gluten, wheat and derived products contain many other components which may trigger symptoms, including inhibitors of α-amylase and trypsin (ATIs), lectins, and rapidly fermentable carbohydrates (FODMAPs). Furthermore, the way in which foods are being processed, such as the use of yeast or sourdough fermentation, fermentation time and baking conditions, may also affect the presence and bioactivity of these components. The present review systematically describes the characteristics of wheat-related intolerances, including their etiology, prevalence, the components responsible, diagnosis, and strategies to reduce adverse reactions.

Extract from the study:

Non-Celiac Gluten/Wheat Sensitivity
During recent years a third group of people has been classified who experience symptoms after eating wheat products, but have been diagnosed not to suffer from either WA or CD. Mostly these individuals are self diagnosed wheat intolerant/sensitive. In these individuals, irritable bowel syndrome (IBS)-like gastrointestinal symptoms and extra-intestinal complaints occur, which improve on a gluten-free diet. This group of patients is referred to as “non-celiac gluten sensitivity” (NCGS), or the more recently, “non-celiac wheat sensitivity” (NCWS). Di Sabatino emphasizes that NCWS is not a homogeneous disease syndrome (such as CD and WA), but rather a heterogeneous syndrome (Di Sabatino & Corazza, 2012). It is probable that the underlying causes and mechanisms are not the same for all people with NCWS and that reactions may be caused by different components of wheat or grain (products) and involving different host factors. Ludvigsson et al. (2013) defined NCGS as follows: one or more of a variety of immunological, morphological, or symptomatic manifestations that are precipitated by the ingestion of gluten in individuals in whom CD has been excluded. However, despite the word “gluten” in the currently most cited definition “NCGS,” it is far from certain that the gluten is the (main) cause of the symptoms observed. The more recent term “NCWS” was adopted since it was noted that gluten (NCGS) may not be the real cause (Biesiekierski, Peters, et al., 2013; Skodje et al., 2018). For that reason, we will use the term NCWS as most appropriate in the remainder of this article.

What are antinutrients?

by luciano

“Antinutritional or antinutrient compounds are natural or synthetic substances that interfere with the metabolism and absorption of nutrients. They are present both in plant organisms, where they perform structural, reserve or defense functions against any predators, and in animal organisms (e.g. toxins and biological amines present in molluscs or fish, in milk derivatives and in wine). They can also form from degradation, cooking (e.g. heterocyclic amines of cooked meats) or food preservation processes, or be present as environmental, microbial, fungal or xenobiotic contaminants (agrochemicals, hormones, etc.).

Gli antinutrienti possono essere classificati in base all’azione che svolgono:
• riducono la digestione proteica e l’utilizzazione delle proteine (es. inibitori della tripsina e della chimotripsina, lectine o emoagglutinine, composti fenolici, saponine);
• interferiscono con la digestione dei carboidrati (es. inibitori dell’amilasi, composti polifenolici, fattori di flautolenza);
• disturbano la digestione e l’azione dei sali minerali (glicosinolati, acido ossalico, acido fitico, gossipolo);
• inattivano le vitamine o causano un incremento del loro fabbisogno (antivitamine);
• producono un effetto tossico ( es. afla-tosine, nitrati).
• stimolano il sistema immunitario (istamina, antigeni).

Sensitivity to wheat, gluten and FODMAPs in IBS: facts or fiction?

by luciano


IBS is one of the most common types of functional bowel disorder. Increasing attention has been paid to the causative role of food in IBS. Food ingestion precipitates or exacerbates symptoms, such as abdominal pain and bloating in patients with IBS through different hypothesised mechanisms including immune and mast cell activation, mechanoreceptor stimulation and chemosensory activation. Wheat is regarded as one of the most relevant IBS triggers, although which component(s) of this cereal is/are involved remain(s) unknown. Gluten, other wheat proteins, for example, amylase-trypsin inhibitors, and fructans (the latter belonging to fermentable oligo-di-mono-saccharides and polyols (FODMAPs)), have been identified as possible factors for symptom generation/exacerbation. This uncertainty on the true culprit(s) opened a scenario of semantic definitions favoured by the discordant results of double-blind placebo-controlled trials, which have generated various terms ranging from non-coeliac gluten sensitivity to the broader one of non-coeliac wheat or wheat protein sensitivity or, even, FODMAP sensitivity. The role of FODMAPs in eliciting the clinical picture of IBS goes further since these short-chain carbohydrates are found in many other dietary components, including vegetables and fruits. In this review, we assessed current literature in order to unravel whether gluten/wheat/FODMAP sensitivity represent ‘facts’ and not ‘fiction’ in IBS symptoms. This knowledge is expected to promote standardisation in dietary strategies (gluten/wheat-free and low FODMAP) as effective measures for the management of IBS symptoms.

Extract from study:

Wheat is considered one of the foods known to evoke IBS symptoms. However, which component(s) of wheat is/are actually responsible for these clinical effects still remain(s) an unsettled issue. The two parts of wheat that are thought to have a mechanistic effect comprise proteins (primarily, but not exclusively, gluten) and carbohydrates (primarily indigestible short-chain components, FODMAPs). Two distinct views characterise the clinical debate: one line identifies wheat proteins as a precipitating/perpetuating factor leading to symptoms, while the other believes that FODMAPs are the major trigger for IBS.

The controversy over nomenclature
If gluten is a major trigger for IBS, it expands the gluten-related disorders by adding a new entity now referred to as non-coeliac gluten sensitivity (NCGS). Indeed, coeliac disease-like abnormalities were reported in a subgroup of patients with IBS many years ago. A recent expert group of researchers reached unanimous consensus attesting the existence of a syndrome triggered by gluten ingestion. This syndrome recognises a wide spectrum of symptoms and manifestations including an IBS-like phenotype, along with an extra-intestinal phenotype, that is, malaise, fatigue, headache, numbness, mental confusion (‘brain fog’), anxiety, sleep abnormalities, fibromyalgia-like symptoms and skin rash. In addition, other possible clinical features include gastroesophageal reflux disease, aphthous stomatitis, anaemia, depression, asthma and rhinitis. Symptoms or other manifestations occur shortly after gluten consumption and disappear or recur in a few hours (or days) after gluten withdrawal or challenge. A fundamental prerequisite for suspecting NCGS is to rule out all the established gluten/wheat disorders, comprising coeliac disease (CD), gluten ataxia, dermatitis herpetiformis and wheat allergy. The major issue not addressed by the consensus opinion was that gluten is only one protein contained within wheat. Other proteins, such as amylase-trypsin inhibitors (ATIs), are strong activators of innate immune responses in monocytes, macrophages and dendritic cells. Furthermore, wheat germ agglutinin, which has epithelial-damaging and immune effects at very low doses at least in vitro, might also contribute to both intestinal and extraintestinal manifestations of NCGS. Consequently, a further development of this research field led to suggestions of a broader term, non-coeliac wheat sensitivity (NCWS). The problems with this term are twofold. First, rye and barley may be inappropriately excluded. Second, the term will refer to any wheat component that might be causally related to induction of symptoms and, therefore, will also include fructans (FODMAPs). It will then have a very nonspecific connotation in IBS. A more correct term would then be non-coeliac wheat protein sensitivity (NCWPS) since this does not attribute effects to gluten without evidence of such specificity, eliminates the issue of fructan-induced symptoms and avoids the unknown contribution of rye and barley proteins to the symptoms. Both NCGS, the currently accepted term, and NCWPS will be used subsequently in this paper.