Food intolerance

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]

Food intolerances
SpecialtyGastroenterology, immunology

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]

  • Metabolic food reactions are due to inborn or acquired errors of metabolism of nutrients, such as in lactase deficiency, phenylketonuria and favism.
  • Pharmacological reactions are generally due to low-molecular-weight chemicals which occur either as natural compounds, such as salicylates, amines and glutamates or to food additives, such as preservatives, colouring, emulsifiers and flavour enhancers. These chemicals are capable of causing drug-like (biochemical) side effects in susceptible individuals.[5]
  • Gastro-intestinal (GI) reactions can be due to malabsorption or other GI tract abnormalities.
  • Immunological responses are mediated by non-IgE immunoglobulins, where the immune system recognises a particular food as a foreign body.
  • Toxins may either be present naturally in food, be released by bacteria, or be due to contamination of food products.[5] Toxic food reactions are caused by the direct action of a food or substance without immune involvement.[5]
  • Psychological reactions involve manifestation of clinical symptoms caused not by food but by emotions associated with food. These symptoms do not occur when the food is given in an unrecognisable form.[5]

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, 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.

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 not only aspirin and NSAIDs but also foods in which salicylates naturally occur, 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.

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. 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.

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. 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

References
  1. 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. 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. 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. 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. 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. 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.
  13. 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. 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. 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. 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. 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. 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.
  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.
  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. 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. 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. 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. 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.
  61. 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.
  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. 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. 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. 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. 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. 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. Nestle Nutr Workshop Ser Pediatr Program. 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. 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.
  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.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.