Food intolerance

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Food intolerances
Specialty Gastroenterology, immunology

Food intolerance is a detrimental reaction, often delayed, to a food, beverage, food additive, or compound found in foods that produces symptoms in one or more body organs and systems, but generally refers to reactions other than food allergy. Food hypersensitivity is used to refer broadly to both food intolerances and food allergies. [1]

Contents

Food allergies are immune reactions, typically an IgE reaction caused by the release of histamine but also encompassing non-IgE immune responses. [1] This mechanism causes allergies to typically give immediate reaction (a few minutes to a few hours) to foods.

Food intolerances can be classified according to their mechanism. Intolerance can result from the absence of specific chemicals or enzymes needed to digest a food substance, as in hereditary fructose intolerance. It may be a result of an abnormality in the body's ability to absorb nutrients, as occurs in fructose malabsorption. Food intolerance reactions can occur to naturally occurring chemicals in foods, as in salicylate sensitivity. Drugs sourced from plants, such as aspirin, can also cause these kinds of reactions.

Definitions

Food hypersensitivity is used to refer broadly to both food intolerances and food allergies. [1] There are a variety of earlier terms which are no longer in use such as "pseudo-allergy". [2]

Food intolerance reactions can include pharmacologic, metabolic, and gastro-intestinal responses to foods or food compounds. Food intolerance does not include either psychological responses [3] or foodborne illness.

A non-allergic food hypersensitivity is an abnormal physiological response. It can be difficult to determine the poorly tolerated substance as reactions can be delayed, dose-dependent, and a particular reaction-causing compound may be found in many foods. [4]

Elimination diets are useful to assist in the diagnosis of food intolerance. There are specific diagnostic tests for certain food intolerances. [5] [6] [7]

Signs and symptoms

Food intolerance is more chronic, less acute, less obvious in its presentation, and often more difficult to diagnose than a food allergy. [8] Symptoms of food intolerance vary greatly, and can be mistaken for the symptoms of a food allergy. While true allergies are associated with fast-acting immunoglobulin IgE responses, it can be difficult to determine the offending food causing a food intolerance because the response generally takes place over a prolonged period of time. Thus, the causative agent and the response are separated in time, and may not be obviously related. Food intolerance symptoms usually begin about half an hour after eating or drinking the food in question, but sometimes symptoms may be delayed by up to 48 hours. [9]

Food intolerance can present with symptoms affecting the skin, respiratory tract, gastrointestinal tract (GIT) either individually or in combination. On the skin may include skin rashes, urticaria (hives), [10] angioedema, [11] dermatitis, [12] and eczema. [13] Respiratory tract symptoms can include nasal congestion, sinusitis, pharyngeal irritations, asthma and an unproductive cough. GIT symptoms include mouth ulcers, abdominal cramp, nausea, gas, intermittent diarrhea, constipation, irritable bowel syndrome (IBS), [6] [7] [9] and may include anaphylaxis. [13]

Food intolerance has been found associated with irritable bowel syndrome and inflammatory bowel disease, [14] chronic constipation, [15] chronic hepatitis C infection, [16] eczema, [17] NSAID intolerance, [18] respiratory complaints, [19] including asthma, [20] rhinitis and headache, [21] [22] functional dyspepsia, [23] eosinophilic esophagitis [9] and ear, nose and throat (ENT) illnesses. [21] [24]

Causes

Reactions to chemical components of the diet may be more common than true food allergies,[ citation needed ] although there is no evidence to support this. They are caused by various organic chemicals occurring naturally in a wide variety of foods, animal and vegetable, more often than to food additives, preservatives, colourings and flavourings, such as sulfites or dyes. [13] Both natural and artificial ingredients may cause adverse reactions in sensitive people if consumed in sufficient amounts, the degree of sensitivity varying between individuals.

Pharmacological responses to naturally occurring compounds in food, or chemical intolerance, can occur in individuals from both allergic and non-allergic family backgrounds. Symptoms may begin at any age, and may develop quickly or slowly. Triggers may range from a viral infection or illness to environmental chemical exposure. Chemical intolerance occurs more commonly in women, which may be because of hormone differences, as many food chemicals mimic hormones.[ citation needed ]

A deficiency in digestive enzymes can also cause some types of food intolerances. Lactose intolerance is a result of the body not producing sufficient lactase to digest the lactose in milk; [25] [26] dairy foods which are lower in lactose, such as cheese, are less likely to trigger a reaction in this case. Another carbohydrate intolerance caused by enzyme deficiency is hereditary fructose intolerance.

Celiac disease, an autoimmune disorder caused by an immune response to the protein gluten, results in gluten intolerance and can lead to temporary lactose intolerance. [27] [28]

The most widely distributed naturally occurring food chemical capable of provoking reactions is salicylate, [18] although tartrazine and benzoic acid are well recognised in susceptible individuals. [29] [30] [31] Benzoates and salicylates occur naturally in many foods, including fruits, juices, vegetables, spices, herbs, nuts, tea, wines, and coffee. Salicylate sensitivity causes reactions to aspirin and other NSAIDs, and also in foods which naturally contain salicylates, such as cherries.

Other natural chemicals which commonly cause reactions and cross reactivity include amines, nitrates, sulphites and some antioxidants. Chemicals involved in aroma and flavour are often suspect. [20] [32] [33] [34]

The classification or avoidance of foods based on botanical families bears no relationship to their chemical content and is not relevant in the management of food intolerance.[ citation needed ]

Salicylate-containing foods include apples, citrus fruits, strawberries, tomatoes, and wine, while reactions to chocolate, cheese, bananas, avocado, tomato or wine point to amines as the likely food chemical. Thus, exclusion of single foods does not necessarily identify the chemical responsible as several chemicals can be present in a food, the patient may be sensitive to multiple food chemicals and reaction more likely to occur when foods containing the triggering substance are eaten in a combined quantity that exceeds the patient's sensitivity thresholds. People with food sensitivities have different sensitivity thresholds, and so more sensitive people will react to much smaller amounts of the substance. [5] [9] [20] [33] [34] [35] [36] [37] [38] [39]

Pathogenesis

Food intolerance are all other adverse reactions to food. Subgroups include enzymatic (e.g. lactose intolerance due to lactase deficiency), pharmacological (e.g. reactions against biogenic amines, histamine intolerance), and undefined food intolerance (e.g. against some food additives). [40]

Food intolerances can be caused by enzymatic defects in the digestive system, can also result from pharmacological effects of vasoactive amines present in foods (e.g. histamine), [6] among other metabolic, pharmacological and digestive abnormalities.

Allergies and intolerances to a food group may coexist with separate pathologies; for example, cow's milk allergy (CMA) and lactose intolerance are two distinct pathologies.

Diagnosis

Diagnosis of food intolerance can include hydrogen breath testing for lactose intolerance and fructose malabsorption, professionally supervised elimination diets, and ELISA testing for IgG-mediated immune responses to specific foods. It is important to be able to distinguish between food allergy, food intolerance, and autoimmune disease in the management of these disorders. [41] Non-IgE-mediated intolerance is more chronic, less acute, less obvious in its clinical presentation, and often more difficult to diagnose than allergy, as skin tests and standard immunological studies are not helpful. [8] Elimination diets must remove all poorly tolerated foods, or all foods containing offending compounds. Clinical investigation is generally undertaken only for more serious cases, as for minor complaints which do not significantly limit the person's lifestyle the cure may be more inconvenient than the problem. [5]

Immunoglobulin (IgG) tests measure the types of food-specific antibodies present. There are four types of IgG, IgG1 makes up 60-70% of the total IgG, followed by IgG2 (20-30%), IgG3 (5-8%), and IgG4 (1-4%). Most commercially available tests only test for IgG4 antibodies, however some companies such as YorkTest Laboratories test for all four types. [42]

IgG4 only tests are debatably invalid; IgG4 presence indicates that the person has been repeatedly exposed to food proteins recognized as foreign by the immune system which is a normal physiological response of the immune system after exposure to food components. [43] [1] Although elimination of foods based on IgG-4 testing in IBS patients resulted in an improvement in symptoms, [44] the positive effects of food elimination were more likely due to wheat and milk elimination than IgG-4 test-determined factors. [45] The IgG-4 test specificity is questionable as healthy individuals with no symptoms of food intolerance also test positive for IgG-4 to several foods. [46]

Diagnosis is made using medical history and cutaneous and serological tests to exclude other causes, but to obtain final confirmation a double blind controlled food challenge must be performed. [6] Treatment can involve long-term avoidance, [47] or if possible re-establishing a level of tolerance.

Today there are many methods available such as cytotoxic testing, mediator release testing (MRT), enzyme-linked immunosorbent assay (ELISA) testing, microarray ELISA testing, and ELISA/ACT. Allergy US reviewed these methods and microarray technology appears to be the most reliable. [48] [49] [50] [51]

Prevention

There is emerging evidence from studies of cord blood that both sensitization and the acquisition of tolerance can begin in pregnancy, however, the window of main danger for sensitization to foods extends prenatally, remaining most critical during early infancy when the immune system and intestinal tract are still maturing.[ citation needed ] There is no conclusive evidence to support the restriction of dairy intake in the maternal diet during pregnancy, and this is generally not recommended since the drawbacks in terms of loss of nutrition can out-weigh the benefits. However, further randomised, controlled trials are required to examine if dietary exclusion by lactating mothers can truly minimize risk to a significant degree and if any reduction in risk is out-weighed by deleterious impacts on maternal nutrition. [52]

A Cochrane review has concluded feeding with a soy formula cannot be recommended for prevention of allergy or food intolerance in infants. Further research may be warranted to determine the role of soy formulas for prevention of allergy or food intolerance in infants unable to be breast fed with a strong family history of allergy or cow's milk protein intolerance. [53] In the case of allergy and celiac disease others recommend a dietary regimen that is effective in the prevention of allergic diseases in high-risk infants, particularly in early infancy. The most effective dietary regimen is exclusive breastfeeding for at least 4–6 months or, in absence of breast milk, formulas with documented reduced allergenicity for at least the first 4 months, combined with avoidance of solid food and cow's milk for the first 4 months. [54] [55]

Management

Individuals can try minor changes of diet to exclude foods causing obvious reactions, and for many this may be adequate without the need for professional assistance. For reasons mentioned above foods causing problems may not be so obvious since food sensitivities may not be noticed for hours or even days after one has digested food. Persons unable to isolate foods and those more sensitive or with disabling symptoms should seek expert medical and dietitian help. The dietetic department of a teaching hospital is a good start. (see links below)

Guidance can also be given to your general practitioner to assist in diagnosis and management. Food elimination diets have been designed to exclude food compounds likely to cause reactions and foods commonly causing true allergies and those foods where enzyme deficiency cause symptoms. These elimination diets are not everyday diets but intended to isolate problem foods and chemicals.

It takes around five days of total abstinence to unmask a food or chemical, during the first week on an elimination diet withdrawal symptoms can occur but it takes at least two weeks to remove residual traces. If symptoms have not subsided after six weeks, food intolerance is unlikely to be involved and a normal diet should be restarted. Withdrawals are often associated with a lowering of the threshold for sensitivity which assists in challenge testing, but in this period individuals can be ultra-sensitive even to food smells so care must be taken to avoid all exposures.[ citation needed ]

After two or more weeks if the symptoms have reduced considerably or gone for at least five days then challenge testing can begin. This can be carried out with selected foods containing only one food chemical, to isolate it if reactions occur. In Australia, purified food chemicals in capsule form are available to doctors for patient testing. These are often combined with placebo capsules for control purposes.[ citation needed ] This type of challenge is more definitive. New challenges should only be given after 48 hours if no reactions occur or after five days of no symptoms if reactions occur.

Once all food chemical sensitivities are identified a dietitian can prescribe an appropriate diet for the individual to avoid foods with those chemicals. Lists of suitable foods are available from various hospitals and patient support groups can give local food brand advice. A dietitian will ensure adequate nutrition is achieved with safe foods and supplements if need be.

Over a period of time it is possible for individuals avoiding food chemicals to build up a level of resistance by regular exposure to small amounts in a controlled way, but care must be taken, the aim being to build up a varied diet with adequate composition. [5] [14] [15] [41] [56] [57] [58]

Prognosis

The prognosis of children diagnosed with intolerance to milk is good: patients respond to diet which excludes cow's milk protein and the majority of patients succeed in forming tolerance. [59] Children with non-IgE-mediated cows milk intolerance have a good prognosis, whereas children with IgE-mediated cows milk allergy in early childhood have a significantly increased risk for persistent allergy, development of other food allergies, asthma and rhinoconjunctivitis. [60]

A study has demonstrated that identifying and appropriately addressing food sensitivity in IBS patients not previously responding to standard therapy results in a sustained clinical improvement and increased overall well-being and quality of life. [58]

Epidemiology

Estimates of the prevalence of food intolerance vary widely from 2% to over 20% of the population. [61] So far only three prevalence studies in Dutch and English adults have been based on double-blind, placebo-controlled food challenges. The reported prevalences of food allergy/intolerance (by questionnaires) were 12% to 19%, whereas the confirmed prevalences varied from 0.8% to 2.4%. For intolerance to food additives the prevalence varied between 0.01 and 0.23%. [62]

Food intolerance rates were found to be similar in the population in Norway. Out of 4,622 subjects with adequately filled-in questionnaires, 84 were included in the study (1.8%) Perceived food intolerance is a common problem with significant nutritional consequences in a population with IBS. Of these 59 (70%) had symptoms related to intake of food, 62% limited or excluded food items from the diet. Tests were performed for food allergy and malabsorption, but not for intolerance. There were no associations between the tests for food allergy and malabsorption and perceived food intolerance, among those with IBS. Perceived food intolerance was unrelated to musculoskeletal pain and mood disorders. [63]

According to the RACP working group, "Though not considered a "cause" of CFS, some patients with chronic fatigue report food intolerances that can exacerbate symptoms." [64]

History

In 1978 Australian researchers published details of an 'exclusion diet' to exclude specific food chemicals from the diet of patients. This provided a basis for challenge with these additives and natural chemicals. Using this approach the role played by dietary chemical factors in the pathogenesis of chronic idiopathic urticaria (CIU) was first established and set the stage for future DBPCT trials of such substances in food intolerance studies. [65] [66]

In 1995 the European Academy of Allergology and Clinical Immunology suggested a classification on the basis of the responsible pathogenetic mechanism; according to this classification, non-toxic reactions can be divided into 'food allergies' when they recognize immunological mechanisms, and 'food intolerances' when there are no immunological implications. Reactions secondary to food ingestion are defined generally as 'adverse reactions to food'. [67]

In 2003 the Nomenclature Review Committee of the World Allergy Organization issued a report of revised nomenclature for global use on food allergy and food intolerance, that has had general acceptance. Food intolerance is described as a 'non-allergic hypersensitivity' to food. [68]

Society and culture

In the UK, scepticism about food intolerance as a specific condition influenced doctors' perceptions of patients and of the patients' underlying problems. However, rather than risk damaging the doctor-patient relationship, general practitioners (GPs) chose - despite their scepticism and guided by an element of awareness of the limitations of modern medicine - to negotiate mutually acceptable ground with patients and with patients' beliefs. As a result, whether due to a placebo effect, a secondary benefit, or a biophysical result of excluding a food from the diet, the GPs acknowledge both personal and therapeutic benefits. [61]

In the Netherlands, patients and their doctors (GPs) have different perceptions of the efficacy of diagnostic and dietary interventions in IBS. Patients consider food intolerance and GPs regard lack of fibre as the main etiologic dietary factor. It has been suggested that Dutch GPs explore the patients' expectations and potentially incorporate these in their approach to IBS patients. [69]

New food labeling regulations were introduced into the US and Europe in 2006, [70] which are said to benefit people with intolerances. [71] In general, food-allergic consumers were not satisfied with the current labelling practices. [72] In the USA food companies propose distinguishing between food allergy and food intolerance and use a mechanism-based (i.e., immunoglobulin-E-mediated), acute life-threatening anaphylaxis that is standardized and measurable and reflects the severity of health risk, as the principal inclusion criterion for food allergen labeling. [73] Symptoms due to, or exacerbated by, food additives usually involve non-IgE-mediated mechanisms (food intolerance) and are usually less severe than those induced by food allergy, but can include anaphylaxis. [13]

Research directions

FODMAPs are fermentable oligo-, di-, monosaccharides and polyols, which are poorly absorbed in the small intestine and subsequently fermented by the bacteria in the distal small and proximal large intestine. This is a normal phenomenon, common to everyone. The resultant production of gas potentially results in bloating and flatulence. [74] Although FODMAPs can produce certain digestive discomfort in some people, not only do they not cause intestinal inflammation, but they avoid it, because they produce beneficial alterations in the intestinal flora that contribute to maintain the good health of the colon. [75] [76] [77] FODMAPs are not the cause of irritable bowel syndrome nor other functional gastrointestinal disorders, but rather a person develops symptoms when the underlying bowel response is exaggerated or abnormal. [74] A low-FODMAP diet might help to improve short-term digestive symptoms in adults with irritable bowel syndrome, [78] [79] [80] [81] but its long-term follow-up can have negative effects because it causes a detrimental impact on the gut microbiota and metabolome. [82] [79] [81] [83] It should only be used for short periods of time and under the advice of a specialist. [84] More studies are needed to assess the true impact of this diet on health. [79] [81]

Also, when a low FODMAP diet is used without a previous complete medical evaluation can cause serious health risks. It can ameliorate and mask the digestive symptoms of serious diseases, such as celiac disease, inflammatory bowel disease and colon cancer, avoiding their correct diagnosis and therapy. [85] [86] This is especially relevant in the case of celiac disease. Since the consumption of gluten is suppressed or reduced with a low-FODMAP diet, the improvement of the digestive symptoms with this diet may not be related to the withdrawal of the FODMAPs, but of gluten, indicating the presence of an unrecognized celiac disease, avoiding its diagnosis and correct treatment, with the consequent risk of several serious health complications, including various types of cancer. [86]

A three-month randomized, blinded, controlled trial on people with irritable bowel syndrome found that those who withdrew from the diet the foods to which they had shown an increased IgG antibody response experienced an improvement in their symptoms. [87] In individuals with Crohn's disease and ulcerative colitis food-specific-IgG-based elimination diets have been shown to be effective at reducing symptoms. [88] [89] [90] Significant presence of food-specific-IgG has also been detected jejunostomates, ileostomates, and in individuals with eosinophilic esophagitis or food malabsorption due to intolerance. [91]

Increased intestinal permeability, so called leaky gut, has been linked to food allergies [92] and some food intolerances. [93] [94] Research is currently focussing on specific conditions [95] [96] [97] and effects of certain food constituents. [98] [99] [100] At present there are a number of ways to limit the increased permeability, but additional studies are required to assess if this approach reduces the prevalence and severity of specific conditions. [94] [98]

See also

Related Research Articles

<span class="mw-page-title-main">Gluten</span> Group of cereal grain proteins

Gluten is a structural protein naturally found in certain cereal grains. The term gluten usually refers to the combination of prolamin and glutelin proteins that naturally occur in many cereal grains, and which can trigger celiac disease in some people. The types of grains that contain gluten include all species of wheat, and barley, rye, and some cultivars of oat; moreover, cross hybrids of any of these cereal grains also contain gluten, e.g. triticale. Gluten makes up 75–85% of the total protein in bread wheat.

<span class="mw-page-title-main">Coeliac disease</span> Autoimmune disorder that results in a reaction to gluten

Coeliac disease or celiac disease is a long-term autoimmune disorder, primarily affecting the small intestine, where individuals develop intolerance to gluten, present in foods such as wheat, rye and barley. Classic symptoms include gastrointestinal problems such as chronic diarrhoea, abdominal distention, malabsorption, loss of appetite, and among children failure to grow normally. Non-classic symptoms are more common, especially in people older than two years. There may be mild or absent gastrointestinal symptoms, a wide number of symptoms involving any part of the body, or no obvious symptoms. Coeliac disease was first described in childhood; however, it may develop at any age. It is associated with other autoimmune diseases, such as Type 1 diabetes mellitus and Hashimoto's thyroiditis, among others.

<span class="mw-page-title-main">Irritable bowel syndrome</span> Functional gastrointestinal disorder

Irritable bowel syndrome (IBS) is a "disorder of gut-brain interaction" characterized by a group of symptoms that commonly include abdominal pain, abdominal bloating and changes in the consistency of bowel movements. These symptoms may occur over a long time, sometimes for years. IBS can negatively affect quality of life and may result in missed school or work or reduced productivity at work. Disorders such as anxiety, major depression, and chronic fatigue syndrome are common among people with IBS.

<span class="mw-page-title-main">Gluten-free diet</span> Diet excluding proteins found in wheat, barley, and rye

A gluten-free diet (GFD) is a nutritional plan that strictly excludes gluten, which is a mixture of prolamin proteins found in wheat, as well as barley, rye, and oats. The inclusion of oats in a gluten-free diet remains controversial, and may depend on the oat cultivar and the frequent cross-contamination with other gluten-containing cereals.

<span class="mw-page-title-main">Fructose malabsorption</span> Medical condition

Fructose malabsorption, formerly named dietary fructose intolerance (DFI), is a digestive disorder in which absorption of fructose is impaired by deficient fructose carriers in the small intestine's enterocytes. This results in an increased concentration of fructose. Intolerance to fructose was first identified and reported in 1956.

Functional gastrointestinal disorders (FGID), also known as disorders of gut–brain interaction, include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and motility disturbances.

<span class="mw-page-title-main">Small intestinal bacterial overgrowth</span> Medical condition

Small intestinal bacterial overgrowth (SIBO), also termed bacterial overgrowth, or small bowel bacterial overgrowth syndrome (SBBOS), is a disorder of excessive bacterial growth in the small intestine. Unlike the colon, which is rich with bacteria, the small bowel usually has fewer than 100,000 organisms per millilitre. Patients with bacterial overgrowth typically develop symptoms which may include nausea, bloating, vomiting, diarrhea, malnutrition, weight loss and malabsorption, which is caused by a number of mechanisms.

Abdominal bloating is a short-term disease that affects the gastrointestinal tract. Bloating is generally characterized by an excess buildup of gas, air or fluids in the stomach. A person may have feelings of tightness, pressure or fullness in the stomach; it may or may not be accompanied by a visibly distended abdomen. Bloating can affect anyone of any age range and is usually self-diagnosed, in most cases does not require serious medical attention or treatment. Although this term is usually used interchangeably with abdominal distension, these symptoms probably have different pathophysiological processes, which are not fully understood.

<span class="mw-page-title-main">Milk allergy</span> Type of food allergy caused by milk

Milk allergy is an adverse immune reaction to one or more proteins in cow's milk. Symptoms may take hours to days to manifest, with symptoms including atopic dermatitis, inflammation of the esophagus, enteropathy involving the small intestine and proctocolitis involving the rectum and colon. However, rapid anaphylaxis is possible, a potentially life-threatening condition that requires treatment with epinephrine, among other measures.

<span class="mw-page-title-main">Wheat allergy</span> Medical condition

Wheat allergy is an allergy to wheat which typically presents itself as a food allergy, but can also be a contact allergy resulting from occupational exposure. Like all allergies, wheat allergy involves immunoglobulin E and mast cell response. Typically the allergy is limited to the seed storage proteins of wheat. Some reactions are restricted to wheat proteins, while others can react across many varieties of seeds and other plant tissues. Wheat allergy is rare. Prevalence in adults was found to be 0.21% in a 2012 study in Japan.

<span class="mw-page-title-main">Salicylate sensitivity</span> Medical condition

Salicylate sensitivity is any adverse effect that occurs when a usual amount of salicylate is ingested. People with salicylate intolerance are unable to consume a normal amount of salicylate without adverse effects.

<span class="mw-page-title-main">Gluten-related disorders</span> Set of diseases caused by gluten exposure

Gluten-related disorders is the term for the diseases triggered by gluten, including celiac disease (CD), non-celiac gluten sensitivity (NCGS), gluten ataxia, dermatitis herpetiformis (DH) and wheat allergy. The umbrella category has also been referred to as gluten intolerance, though a multi-disciplinary physician-led study, based in part on the 2011 International Coeliac Disease Symposium, concluded that the use of this term should be avoided due to a lack of specificity.

Gluten-sensitive enteropathy–associated conditions are comorbidities or complications of gluten-related gastrointestinal distress. GSE has key symptoms typically restricted to the bowel and associated tissues; however, there are a wide variety of associated conditions. These include bowel disorders, eosinophilic gastroenteritis and increase with coeliac disease (CD) severity. With some early onset and a large percentage of late onset disease, other disorders appear prior to the coeliac diagnosis or allergic-like responses markedly increased in GSE. Many of these disorders persist on a strict gluten-free diet, and are thus independent of coeliac disease after triggering. For example, autoimmune thyroiditis is a common finding with GSE.

An elimination diet, also known as exclusion diet, is a diagnostic procedure used to identify foods that an individual cannot consume without adverse effects. Adverse effects may be due to food allergy, food intolerance, other physiological mechanisms, or a combination of these. Elimination diets typically involve entirely removing a suspected food from the diet for a period of time from two weeks to two months, and waiting to determine whether symptoms resolve during that time period. In rare cases, a health professional may wish to use an elimination diet, also referred to as an oligoantigenic diet, to relieve a patient of symptoms they are experiencing.

The antigen leukocyte antibody test is one that claims to measure adverse reactions to dietary substances. It was created by American Medical Testing Laboratories and is now marketed by Cell Science Systems of Deerfield Beach, Florida. Researched conducted at Yale School of Medicine published in BMJ Open Gastroenterology in 2017 demonstrated improvement for those with irritable bowel syndrome

"These findings reject the null hypothesis and show that a diet guided by leucocyte activation testing results in demonstrable clinical improvement in IBS. These clinical results, associated with a reduction in plasma neutrophil elastase, have implications for better understanding the role of food intolerance and the pathophysiology of IBS."

FODMAPs or fermentable oligosaccharides, disaccharides, monosaccharides, and polyols are short-chain carbohydrates that are poorly absorbed in the small intestine and ferment in the colon. They include short-chain oligosaccharide polymers of fructose (fructans) and galactooligosaccharides, disaccharides (lactose), monosaccharides (fructose), and sugar alcohols (polyols), such as sorbitol, mannitol, xylitol, and maltitol. Most FODMAPs are naturally present in food and the human diet, but the polyols may be added artificially in commercially prepared foods and beverages.

Non-celiac gluten sensitivity (NCGS) or gluten sensitivity is a controversial disorder which can cause both gastrointestinal and other problems.

Serum-derived bovine immunoglobulin/protein isolate (SBI) is a medical food product derived from bovine serum obtained from adult cows in the United States. It is sold under the name EnteraGam.

<span class="mw-page-title-main">Intestinal mucosal barrier</span>

The intestinal mucosal barrier, also referred to as intestinal barrier, refers to the property of the intestinal mucosa that ensures adequate containment of undesirable luminal contents within the intestine while preserving the ability to absorb nutrients. The separation it provides between the body and the gut prevents the uncontrolled translocation of luminal contents into the body proper. Its role in protecting the mucosal tissues and circulatory system from exposure to pro-inflammatory molecules, such as microorganisms, toxins, and antigens is vital for the maintenance of health and well-being. Intestinal mucosal barrier dysfunction has been implicated in numerous health conditions such as: food allergies, microbial infections, irritable bowel syndrome, inflammatory bowel disease, celiac disease, metabolic syndrome, non-alcoholic fatty liver disease, diabetes, and septic shock.

A low-FODMAP diet is a person's global restriction of consumption of all fermentable carbohydrates (FODMAPs), recommended only for a short time. A low-FODMAP diet is recommended for managing patients with irritable bowel syndrome (IBS) and can reduce digestive symptoms of IBS including bloating and flatulence.

References

  1. 1 2 3 4 Lomer, M. C. E. (1 February 2015). "Review article: the aetiology, diagnosis, mechanisms and clinical evidence for food intolerance". Alimentary Pharmacology & Therapeutics. 41 (3): 262–275. doi:10.1111/apt.13041. ISSN   1365-2036. PMID   25471897. S2CID   8243181.
  2. ↑ Gerth van Wijk R, van Cauwenberge PB, Johansson SG (August 2003). "[Revised terminology for allergies and related conditions]". Ned Tijdschr Tandheelkd (in Dutch). 110 (8): 328–31. PMID   12953386.
  3. ↑ Johansson SG, Hourihane JO, Bousquet J, et al. (September 2001). "A revised nomenclature for allergy. An EAACI position statement from the EAACI nomenclature task force". Allergy. 56 (9): 813–24. doi:10.1034/j.1398-9995.2001.t01-1-00001.x. PMID   11551246. Archived from the original on 5 January 2013.
  4. ↑ "Food allergy and intolerance | Better Health Channel". betterhealth.vic.gov.au. Retrieved 27 June 2014.
  5. 1 2 3 4 5 6 7 8 Clarke L, McQueen J, et al. (1996). "The dietary management of food allergy and food intolerance in children and adults". Aust J Nutr Diet. 53 (3): 89–98. ISSN   1032-1322.
  6. 1 2 3 4 Ortolani C, Pastorello EA (2006). "Food allergies and food intolerances". Best Pract Res Clin Gastroenterol. 20 (3): 467–83. doi:10.1016/j.bpg.2005.11.010. PMID   16782524.
  7. 1 2 Pastar Z, Lipozencić J (2006). "Adverse reactions to food and clinical expressions of food allergy". Skinmed. 5 (3): 119–25, quiz 126–7. doi:10.1111/j.1540-9740.2006.04913.x. PMID   16687980.
  8. 1 2 Vanderhoof JA (1998). "Food hypersensitivity in children". Current Opinion in Clinical Nutrition and Metabolic Care. 1 (5): 419–22. doi:10.1097/00075197-199809000-00009. ISSN   1363-1950. PMID   10565387.
  9. 1 2 3 4 Ozdemir O, Mete E, Catal F, Ozol D (January 2009). "Food intolerances and eosinophilic esophagitis in childhood". Dig Dis Sci. 54 (1): 8–14. doi:10.1007/s10620-008-0331-x. PMID   18594978. S2CID   3076884.
  10. ↑ Maurer M, Hanau A, Metz M, Magerl M, Staubach P (February 2003). "[Relevance of food allergies and intolerance reactions as causes of urticaria]". Hautarzt (in German). 54 (2): 138–43. doi:10.1007/s00105-002-0481-2. PMID   12590308. S2CID   24220704.
  11. ↑ Moneret-Vautrin DA (May 2003). "[Allergic and pseudo-allergic reactions to foods in chronic urticaria]". Ann Dermatol Venereol (in French). 130 Spec No 1: 1S35–42. PMID   12843808.
  12. ↑ Novembre E, Vierucci A (2001). "Milk allergy/intolerance and atopic dermatitis in infancy and childhood". Allergy. 56 (Suppl 67): 105–8. doi:10.1111/j.1398-9995.2001.00931.x. PMID   11298023. S2CID   46144087.[ dead link ]
  13. 1 2 3 4 Cardinale F, Mangini F, Berardi M, et al. (December 2008). "[Intolerance to food additives: an update]". Minerva Pediatr. (in Italian). 60 (6): 1401–9. PMID   18971901.
  14. 1 2 MacDermott RP (2007). "Treatment of irritable bowel syndrome in outpatients with inflammatory bowel disease using a food and beverage intolerance, food and beverage avoidance diet". Inflamm Bowel Dis. 13 (1): 91–6. doi: 10.1002/ibd.20048 . PMID   17206644. S2CID   24307163.
  15. 1 2 Carroccio A, Di Prima L, Iacono G, et al. (2006). "Multiple food hypersensitivity as a cause of refractory chronic constipation in adults" (PDF). Scand J Gastroenterol. 41 (4): 498–504. doi:10.1080/00365520500367400. hdl: 10447/10104 . PMID   16635922. S2CID   24551094.
  16. ↑ Lang CA, Conrad S, Garrett L, et al. (April 2006). "Symptom prevalence and clustering of symptoms in people living with chronic hepatitis C infection". J Pain Symptom Manage. 31 (4): 335–44. doi: 10.1016/j.jpainsymman.2005.08.016 . PMID   16632081.
  17. ↑ Maintz L, Benfadal S, Allam JP, Hagemann T, Fimmers R, Novak N (May 2006). "Evidence for a reduced histamine degradation capacity in a subgroup of patients with atopic eczema". The Journal of Allergy and Clinical Immunology. 117 (5): 1106–12. doi: 10.1016/j.jaci.2005.11.041 . PMID   16675339.
  18. 1 2 Raithel M, Baenkler HW, Naegel A, et al. (September 2005). "Significance of salicylate intolerance in diseases of the lower gastrointestinal tract" (PDF). J. Physiol. Pharmacol. 56 (Suppl 5): 89–102. PMID   16247191. Archived from the original (PDF) on 26 March 2009. Retrieved 14 April 2009.
  19. ↑ Woods RK, Abramson M, Raven JM, Bailey M, Weiner JM, Walters EH (January 1998). "Reported food intolerance and respiratory symptoms in young adults". Eur. Respir. J. 11 (1): 151–5. doi: 10.1183/09031936.98.11010151 . PMID   9543285.
  20. 1 2 3 Maintz L, Novak N (2007). "Histamine and histamine intolerance". Am J Clin Nutr. 85 (5): 1185–96. doi: 10.1093/ajcn/85.5.1185 . PMID   17490952.
  21. 1 2 Böttcher I, Klimek L (August 2008). "[Histamine intolerance syndrome. Its significance for ENT medicine]". HNO (in German). 56 (8): 776–83. doi:10.1007/s00106-008-1793-z. PMID   18649066. S2CID   39347593.
  22. ↑ Götz M (1996). "[Pseudo-allergies are due to histamine intolerance]". Wien Med Wochenschr (in German). 146 (15): 426–30. PMID   9012205.
  23. ↑ Feinle-Bisset C, Horowitz M (August 2006). "Dietary factors in functional dyspepsia". Neurogastroenterol. Motil. 18 (8): 608–18. doi:10.1111/j.1365-2982.2006.00790.x. PMID   16918725. S2CID   22115920.
  24. ↑ Gordon BR (October 2003). "Approaches to testing for food and chemical sensitivities". Otolaryngol. Clin. North Am. 36 (5): 917–40. doi:10.1016/S0030-6665(03)00059-8. PMID   14743781.
  25. ↑ Heyman MB; Committee On, Nutrition (September 2006). "Lactose intolerance in infants, children, and adolescents". Pediatrics. 118 (3): 1279–86. doi:10.1542/peds.2006-1721. PMID   16951027. S2CID   2996092.
  26. ↑ Srinivasan R, Minocha A (September 1998). "When to suspect lactose intolerance. Symptomatic, ethnic, and laboratory clues". Postgrad Med. 104 (3): 109–11, 115–6, 122–3. doi:10.3810/pgm.1998.09.577. PMID   9742907.
  27. ↑ McGough N, Cummings JH (November 2005). "Coeliac disease: a diverse clinical syndrome caused by intolerance of wheat, barley and rye". Proc Nutr Soc. 64 (4): 434–50. doi: 10.1079/PNS2005461 . PMID   16313685.
  28. ↑ Rousset H (March 2004). "[A great imitator for the allergologist: intolerance to gluten]". Eur Ann Allergy Clin Immunol (in French). 36 (3): 96–100. PMID   15137480.
  29. ↑ Elhkim MO, Héraud F, Bemrah N, et al. (April 2007). "New considerations regarding the risk assessment on Tartrazine An update toxicological assessment, intolerance reactions and maximum theoretical daily intake in France". Regul. Toxicol. Pharmacol. 47 (3): 308–16. doi:10.1016/j.yrtph.2006.11.004. PMID   17218045.
  30. ↑ Nettis E, Colanardi MC, Ferrannini A, Tursi A (October 2004). "Sodium benzoate-induced repeated episodes of acute urticaria/angio-oedema: randomized controlled trial". Br. J. Dermatol. 151 (4): 898–902. doi:10.1111/j.1365-2133.2004.06095.x. PMID   15491435. S2CID   22547849.
  31. ↑ Worm M, Vieth W, Ehlers I, Sterry W, Zuberbier T (February 2001). "Increased leukotriene production by food additives in patients with atopic dermatitis and proven food intolerance". Clin. Exp. Allergy. 31 (2): 265–73. doi:10.1046/j.1365-2222.2001.00979.x. PMID   11251628. S2CID   33634326.
  32. ↑ Schnyder B, Pichler WJ (June 1999). "[Food intolerance and food allergy]". Schweiz Med Wochenschr (in German). 129 (24): 928–33. PMID   10413828.
  33. 1 2 Millichap JG, Yee MM (January 2003). "The diet factor in pediatric and adolescent migraine". Pediatr. Neurol. 28 (1): 9–15. doi:10.1016/S0887-8994(02)00466-6. PMID   12657413.
  34. 1 2 Hodge L, Yan KY, Loblay RL (August 1996). "Assessment of food chemical intolerance in adult asthmatic subjects". Thorax. 51 (8): 805–9. doi:10.1136/thx.51.8.805. PMC   472547 . PMID   8795668.
  35. ↑ Layer P, Keller J (2007). "[Therapy of functional bowel disorders]". Praxis (in German). 96 (9): 323–6. doi:10.1024/1661-8157.96.9.323. PMID   17361633.
  36. ↑ Parker G, Watkins T (2002). "Treatment-resistant depression: when antidepressant drug intolerance may indicate food intolerance". The Australian and New Zealand Journal of Psychiatry. 36 (2): 263–5. doi:10.1046/j.1440-1614.2002.00978.x. PMID   11982551. S2CID   46611658.
  37. ↑ Iacono G, Bonventre S, Scalici C, et al. (2006). "Food intolerance and chronic constipation: manometry and histology study". European Journal of Gastroenterology & Hepatology. 18 (2): 143–50. doi:10.1097/00042737-200602000-00006. hdl: 10447/4967 . PMID   16394795. S2CID   20007207.
  38. ↑ Asero R (2004). "Food additives intolerance: does it present as perennial rhinitis?". Current Opinion in Allergy and Clinical Immunology. 4 (1): 25–9. doi:10.1097/00130832-200402000-00006. PMID   15090915. S2CID   21383210.
  39. ↑ Semeniuk J, Kaczmarski M (2006). "Gastroesophageal reflux (GER) in children and adolescents with regard to food intolerance". Adv Med Sci. 51: 321–6. PMID   17357334.
  40. ↑ Wüthrich B (April 2009). "[Food allergy, food intolerance or functional disorder?]". Praxis (in German). 98 (7): 375–87. doi:10.1024/1661-8157.98.7.375. PMID   19340768.
  41. 1 2 Kitts D, Yuan Y, Joneja J, et al. (1997). "Adverse reactions to food constituents: allergy, intolerance, and autoimmunity". Can J Physiol Pharmacol . 75 (4): 241–54. doi:10.1139/cjpp-75-4-241. PMID   9196849.
  42. ↑ "What is the difference between IgG food intolerance tests?". YorkTest. Retrieved 9 July 2020.
  43. ↑ Stapel SO, Asero R, Ballmer-Weber BK, et al. (July 2008). "Testing for IgG4 against foods is not recommended as a diagnostic tool: EAACI Task Force Report" (PDF). Allergy. 63 (7): 793–6. doi:10.1111/j.1398-9995.2008.01705.x. PMID   18489614. S2CID   14061223.
  44. ↑ Atkinson, W; Sheldon, TA; Shaath, N; Whorwell, PJ (2004). "Food elimination based on IgG antibodies in irritable bowel syndrome: A randomised controlled trial". Gut. 53 (10): 1459–64. doi:10.1136/gut.2003.037697. PMC   1774223 . PMID   15361495.
  45. ↑ Hunter, JO (2005). "Food elimination in IBS: the case for IgG testing remains doubtful". Gut. 54 (8): 1203. PMC   1774875 . PMID   16009694.
  46. ↑ Kruszewski, J (1994). "High serum levels of allergen specific IgG-4 (asIgG-4) for common food allergens in healthy blood donors". Arch Immunol Ther Exp (Warsz). 42 (4): 259–61. PMID   7487363.
  47. ↑ Editorial Staff. "What's the difference between an allergy, an intolerance and a sensitivity?". Healthy Futures. Archived from the original on 16 November 2010. Retrieved 24 August 2010.
  48. ↑ "Intolerance tests." Allergy US
  49. ↑ Wüthrich B (2005). "Unproven techniques in allergy diagnosis" (PDF). J Investig Allergol Clin Immunol. 15 (2): 86–90. PMID   16047707.
  50. ↑ Gerez IF, Shek LP, Chng HH, Lee BW (January 2010). "Diagnostic tests for food allergy". Singapore Med J. 51 (1): 4–9. PMID   20200768.
  51. ↑ Mullins Raymond J; Heddle Robert J; Smith Pete (2005). "Non-conventional approaches to allergy testing: reconciling patient autonomy with medical practitioners' concerns". Med J Aust. 183 (4): 173–4. doi:10.5694/j.1326-5377.2005.tb06986.x. PMID   16097911. S2CID   30242205.
  52. ↑ Crittenden RG, Bennett LE (December 2005). "Cow's milk allergy: a complex disorder". J Am Coll Nutr. 24 (6 Suppl): 582S–91S. doi:10.1080/07315724.2005.10719507. PMID   16373958. S2CID   1325287.
  53. ↑ Osborn DA, Sinn J (2006). Sinn JK (ed.). "Soy formula for prevention of allergy and food intolerance in infants". Cochrane Database Syst Rev. 2010 (4): CD003741. doi:10.1002/14651858.CD003741.pub4. PMC   6885056 . PMID   17054183.
  54. ↑ Høst A, Halken S, Muraro A, et al. (February 2008). "Dietary prevention of allergic diseases in infants and small children". Pediatr Allergy Immunol. 19 (1): 1–4. doi:10.1111/j.1399-3038.2007.00680.x. PMID   18199086. S2CID   8831420.
  55. ↑ Chertok IR (2007). "The importance of exclusive breastfeeding in infants at risk for celiac disease". MCN Am J Matern Child Nurs. 32 (1): 50–4, quiz 55–6. doi:10.1097/00005721-200701000-00011. PMID   17308459. S2CID   25021206.
  56. ↑ Jacobsen MB, Aukrust P, Kittang E, et al. (2000). "Relation between food provocation and systemic immune activation in patients with food intolerance". Lancet. 356 (9227): 400–1. doi:10.1016/S0140-6736(00)02536-8. PMID   10972377. S2CID   24311710.
  57. ↑ Gaby AR (1998). "The role of hidden food allergy/intolerance in chronic disease". Alternative Medicine Review. 3 (2): 90–100. PMID   9577245.
  58. 1 2 Drisko J, Bischoff B, Hall M, McCallum R (2006). "Treating irritable bowel syndrome with a food elimination diet followed by food challenge and probiotics". J Am Coll Nutr. 25 (6): 514–22. doi:10.1080/07315724.2006.10719567. PMID   17229899. S2CID   9314332.
  59. ↑ Casado Dones MJ, Cruz Martín RM, Moreno González C, Oya Luis I, Martin Rodríguez M (September 2008). "[Children who are allergic to cow's milk. Nutritional treatment]". Rev Enferm (in Spanish). 31 (9): 51–8. ISSN   0210-5020. PMID   19007035.
  60. ↑ Høst A, Halken S, Jacobsen HP, Christensen AE, Herskind AM, Plesner K (2002). "Clinical course of cow's milk protein allergy/intolerance and atopic diseases in childhood". Pediatr Allergy Immunol. 13 (Suppl 15): 23–8. doi:10.1034/j.1399-3038.13.s.15.7.x. PMID   12688620. S2CID   536883.[ dead link ]
  61. 1 2 Nelson M, Ogden J (September 2008). "An exploration of food intolerance in the primary care setting: the general practitioner's experience" (PDF). Soc Sci Med. 67 (6): 1038–45. doi:10.1016/j.socscimed.2008.05.025. PMID   18584930.
  62. ↑ Wüthrich B (May 1996). "[Food allergy: definition, diagnosis, epidemiology, clinical aspects]". Schweiz Med Wochenschr (in German). 126 (18): 770–6. PMID   8693302.
  63. ↑ Monsbakken KW, Vandvik PO, Farup PG (May 2006). "Perceived food intolerance in subjects with irritable bowel syndrome-- etiology, prevalence and consequences". Eur J Clin Nutr. 60 (5): 667–72. doi:10.1038/sj.ejcn.1602367. PMID   16391571. S2CID   6382678.
  64. ↑ Working Group of the Royal Australasian College of Physicians (May 2002). "Chronic fatigue syndrome. Clinical practice guidelines—2002". Med. J. Aust. 176 Suppl (S9): S23–56. PMID   12056987.
  65. ↑ Gibson AR, Clancy RL (March 1978). "An Australian exclusion diet". Med J Aust. 1 (5): 290–2. doi:10.5694/j.1326-5377.1978.tb112553.x. PMID   661687. S2CID   8897411.
  66. ↑ Gibson A, Clancy R (November 1980). "Management of chronic idiopathic urticaria by the identification and exclusion of dietary factors". Clinical & Experimental Allergy. 10 (6): 699–704. doi:10.1111/j.1365-2222.1980.tb02154.x. PMID   7460264. S2CID   12346266.
  67. ↑ Montalto M, Santoro L, D'Onofrio F, et al. (2008). "Adverse reactions to food: allergies and intolerances". Dig Dis. 26 (2): 96–103. doi:10.1159/000116766. hdl: 11383/2076128 . PMID   18431058. S2CID   10055914.
  68. ↑ Johansson SG, Bieber T, Dahl R, et al. (May 2004). "Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization, October 2003". The Journal of Allergy and Clinical Immunology. 113 (5): 832–6. doi: 10.1016/j.jaci.2003.12.591 . PMID   15131563.
  69. ↑ Bijkerk CJ, de Wit NJ, Stalman WA, Knottnerus JA, Hoes AW, Muris JW (June 2003). "Irritable bowel syndrome in primary care: the patients' and doctors' views on symptoms, etiology and management". Can J Gastroenterol. 17 (6): 363–8, quiz 405–6. doi: 10.1155/2003/532138 . PMID   12813601.
  70. ↑ Taylor SL, Hefle SL (June 2006). "Food allergen labeling in the USA and Europe". Current Opinion in Allergy and Clinical Immunology. 6 (3): 186–90. doi:10.1097/01.all.0000225158.75521.ad. PMID   16670512. S2CID   25204657.
  71. ↑ MacDonald A (July 2005). "Better European food labelling laws to help people with food intolerances". Matern Child Nutr. 1 (3): 223–4. doi:10.1111/j.1740-8709.2005.00038.x. PMC   6860939 . PMID   16881903.
  72. ↑ Cornelisse-Vermaat JR, Voordouw J, Yiakoumaki V, Theodoridis G, Frewer LJ (April 2008). "Food-allergic consumers' labelling preferences: a cross-cultural comparison". Eur J Public Health. 18 (2): 115–20. doi: 10.1093/eurpub/ckm032 . PMID   17584733.
  73. ↑ Yeung JM, Applebaum RS, Hildwine R (July 2000). "Criteria to determine food allergen priority". J Food Prot. 63 (7): 982–6. doi: 10.4315/0362-028X-63.7.982 . PMID   10914674.
  74. 1 2 Peter R Gibson & Susan J Shepherd (2010). "Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach". Journal of Gastroenterology and Hepatology. 25 (2): 252–258. doi: 10.1111/j.1440-1746.2009.06149.x . PMID   20136989. S2CID   20666740.
  75. ↑ Makharia A, Catassi C, Makharia GK (2015). "The Overlap between Irritable Bowel Syndrome and Non-Celiac Gluten Sensitivity: A Clinical Dilemma". Nutrients (Review). 7 (12): 10417–26. doi: 10.3390/nu7125541 . PMC   4690093 . PMID   26690475.
  76. ↑ Greer JB, O'Keefe SJ (2011). "Microbial induction of immunity, inflammation, and cancer". Front Physiol (Review). 1: 168. doi: 10.3389/fphys.2010.00168 . PMC   3059938 . PMID   21423403.
  77. ↑ Andoh A, Tsujikawa T, Fujiyama Y (2003). "Role of dietary fiber and short-chain fatty acids in the colon". Curr Pharm Des (Review). 9 (4): 347–58. doi:10.2174/1381612033391973. PMID   12570825.
  78. ↑ Turco R, Salvatore S, Miele E, Romano C, Marseglia GL, Staiano A (2018). "Does a low-FODMAPs diet reduce symptoms of functional abdominal pain disorders? A systematic review in adult and paediatric population, on behalf of Italian Society of Pediatrics". Ital J Pediatr (Systematic Review). 44 (1): 53. doi: 10.1186/s13052-018-0495-8 . PMC   5952847 . PMID   29764491.
  79. 1 2 3 Staudacher HM, Irving PM, Lomer MC, Whelan K (April 2014). "Mechanisms and efficacy of dietary FODMAP restriction in IBS". Nat Rev Gastroenterol Hepatol (Review). 11 (4): 256–66. doi:10.1038/nrgastro.2013.259. PMID   24445613. S2CID   23001679. An emerging body of research now demonstrates the efficacy of fermentable carbohydrate restriction in IBS. [...] However, further work is urgently needed both to confirm clinical efficacy of fermentable carbohydrate restriction in a variety of clinical subgroups and to fully characterize the effect on the gut microbiota and the colonic environ¬ment. Whether the effect on luminal bifidobacteria is clinically relevant, preventable, or long lasting, needs to be investigated. The influence on nutrient intake, dietary diversity, which might also affect the gut microbiota,137 and quality of life also requires further exploration as does the possible economic effects due to reduced physician contact and need for medication. Although further work is required to confirm its place in IBS and functional bowel disorder clinical pathways, fermentable carbohydrate restriction is an important consideration for future national and international IBS guidelines.
  80. ↑ Marsh A, Eslick EM, Eslick GD (2015). "Does a diet low in FODMAPs reduce symptoms associated with functional gastrointestinal disorders? A comprehensive systematic review and meta-analysis". Eur J Nutr. 55 (3): 897–906. doi:10.1007/s00394-015-0922-1. PMID   25982757. S2CID   206969839.
  81. 1 2 3 Rao SS, Yu S, Fedewa A (2015). "Systematic review: dietary fibre and FODMAP-restricted diet in the management of constipation and irritable bowel syndrome". Aliment. Pharmacol. Ther. 41 (12): 1256–70. doi: 10.1111/apt.13167 . PMID   25903636. S2CID   27558785.
  82. ↑ Tuck, CJ; Muir, JG; Barrett, JS; Gibson, PR (2014). "Fermentable oligosaccharides, disaccharides, monosaccharides and polyols: role in irritable bowel syndrome". Expert Rev Gastroenterol Hepatol. 8 (7): 819–834. doi:10.1586/17474124.2014.917956. PMID   24830318. S2CID   28811344.
  83. ↑ Heiman ML, Greenway FL (2016). "A healthy gastrointestinal microbiome is dependent on dietary diversity". Mol Metab (Review). 5 (5): 317–320. doi:10.1016/j.molmet.2016.02.005. PMC   4837298 . PMID   27110483.
  84. ↑ Staudacher HM, Whelan K (2017). "The low FODMAP diet: recent advances in understanding its mechanisms and efficacy in IBS". Gut (Review). 66 (8): 1517–1527. doi:10.1136/gutjnl-2017-313750. PMID   28592442. S2CID   3492917.
  85. ↑ "Celiac disease". World Gastroenterology Organisation Global Guidelines. July 2016. Archived from the original on 17 March 2017. Retrieved 4 June 2018. Celiac disease (CD) is a chronic, multiple-organ autoimmune disease that affects the small intestine [...] Patients with (long-term untreated) celiac disease have an elevated risk for benign and malignant complications, and mortality. * Cancer – highest risk in the initial years after diagnosis, decreases to (near) normal risk by the fifth year [96], overall risk increment 1.35. * Malignant lymphomas * Small-bowel adenocarcinoma * Oropharyngeal tumors * Unexplained infertility (12%) * Impaired bone health and growth (osteoporosis 30–40%) * Bone fractures – increased risk 35% for classically symptomatic celiac disease patients [97,98] * The mortality risk is elevated in adult celiac patients, due to an increased risk for fatal malignancy (hazard ratio, 1.31; 95% confidence intervals, 1.13 to 1.51 in one study) [64] * Adverse pregnancy outcome [99] [...] Diagnostic tests [...] Biopsies must be taken when patients are on a gluten-containing diet.
  86. 1 2 Barrett JS (2017). "How to institute the low-FODMAP diet". J Gastroenterol Hepatol (Review). 32 (Suppl 1): 8–10. doi: 10.1111/jgh.13686 . PMID   28244669. Common symptoms of IBS are bloating, abdominal pain, excessive flatus, constipation, diarrhea, or alternating bowel habit. These symptoms, however, are also common in the presentation of coeliac disease, inflammatory bowel disease, defecatory disorders, and colon cancer. Confirming the diagnosis is crucial so that appropriate therapy can be undertaken. Unfortunately, even in these alternate diagnoses, a change in diet restricting FODMAPs may improve symptoms and mask the fact that the correct diagnosis has not been made. This is the case with coeliac disease where a low-FODMAP diet can concurrently reduce dietary gluten, improving symptoms, and also affecting coeliac diagnostic indices.3,4 Misdiagnosis of intestinal diseases can lead to secondary problems such as nutritional deficiencies, cancer risk, or even mortality in the case of colon cancer.
  87. ↑ Ikechi R, Fischer BD, DeSipio J, Phadtare S (2017). "Irritable Bowel Syndrome: Clinical Manifestations, Dietary Influences, and Management". Healthcare. 5 (2): 21. doi: 10.3390/healthcare5020021 . PMC   5492024 . PMID   28445436.
  88. ↑ Bentz, S.; Hausmann, M.; Piberger, H.; Kellermeier, S.; Paul, S.; Held, L.; Falk, W.; Obermeier, F.; Fried, M.; Schölmerich, J.; Rogler, G. (2010). "Clinical relevance of IgG antibodies against food antigens in Crohn's disease: a double-blind cross-over diet intervention study". Digestion. 81 (4): 252–264. doi:10.1159/000264649. ISSN   1421-9867. PMID   20130407. S2CID   9556315.
  89. ↑ Jian, Liu; Anqi, He; Gang, Liu; Litian, Wang; Yanyan, Xu; Mengdi, Wang; Tong, Liu (16 August 2018). "Food Exclusion Based on IgG Antibodies Alleviates Symptoms in Ulcerative Colitis: A Prospective Study". Inflammatory Bowel Diseases. 24 (9): 1918–1925. doi:10.1093/ibd/izy110. ISSN   1536-4844. PMID   29788288.
  90. ↑ Jones, V. A.; Dickinson, R. J.; Workman, E.; Wilson, A. J.; Freeman, A. H.; Hunter, J. O. (27 July 1985). "Crohn's disease: maintenance of remission by diet". Lancet. 2 (8448): 177–180. doi:10.1016/s0140-6736(85)91497-7. ISSN   0140-6736. PMID   2862371. S2CID   21174037.
  91. ↑ Carson, Walker K.; Baumert, Joseph L.; Clarke, Jennifer L.; Izard, Jacques (July 2022). "Small bowel stomas are associated with higher risk of circulating food-specific-IgG than patients with organic gastrointestinal conditions and colostomies". BMJ Open Gastroenterology. 9 (1): e000906. doi:10.1136/bmjgast-2022-000906. ISSN   2054-4774. PMC   9258506 . PMID   35790301.
  92. ↑ Heyman M (December 2005). "Gut barrier dysfunction in food allergy". Eur J Gastroenterol Hepatol. 17 (12): 1279–85. doi:10.1097/00042737-200512000-00003. PMID   16292078. S2CID   21021624.
  93. ↑ Baumgart DC, Dignass AU (November 2002). "Intestinal barrier function". Current Opinion in Clinical Nutrition and Metabolic Care. 5 (6): 685–94. doi:10.1097/00075197-200211000-00012. PMID   12394645. S2CID   2326543.
  94. 1 2 Bjarnason I, Takeuchi K (2009). "Intestinal permeability in the pathogenesis of NSAID-induced enteropathy". J. Gastroenterol. 44 (Suppl 19): 23–9. doi:10.1007/s00535-008-2266-6. PMID   19148789. S2CID   24383744.
  95. ↑ Fedorak RN (September 2008). "Understanding why probiotic therapies can be effective in treating IBD". J. Clin. Gastroenterol. 42 Suppl 3 Pt 1: S111–5. doi:10.1097/MCG.0b013e31816d922c. PMID   18806699. S2CID   6855166.
  96. ↑ Salvatore S, Hauser B, Devreker T, Arrigo S, Vandenplas Y (2008). "Chronic enteropathy and feeding in children: an update". Nutrition. 24 (11–12): 1205–16. doi:10.1016/j.nut.2008.04.011. PMID   18621505.
  97. ↑ Gibbons T, Fuchs GJ (2007). "Chronic Enteropathy: Clinical Aspects". Nutrition Support for Infants and Children at Risk. Series Set, 2007. Vol. 59. pp. 89–101, discussion 102–4. doi:10.1159/000098529. ISBN   978-3-8055-8194-3. PMID   17245093. S2CID   32663610.
  98. 1 2 Hamer HM, Jonkers D, Venema K, Vanhoutvin S, Troost FJ, Brummer RJ (January 2008). "Review article: the role of butyrate on colonic function". Aliment. Pharmacol. Ther. 27 (2): 104–19. doi:10.1111/j.1365-2036.2007.03562.x. PMID   17973645. S2CID   22698080.
  99. ↑ Veereman G (November 2007). "Pediatric applications of inulin and oligofructose". J. Nutr. 137 (11 Suppl): 2585S–2589S. doi: 10.1093/jn/137.11.2585S . PMID   17951508.
  100. ↑ Vanderhoof JA (November 2008). "Probiotics in allergy management". J. Pediatr. Gastroenterol. Nutr. 47 (Suppl 2): S38–40. doi: 10.1097/01.mpg.0000338810.74933.c1 . PMID   18931598. S2CID   9220248.
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