Matoverfølsomhet – et paradigmeskifte

Artikkel skrevet i 2011 som nevner mange viktige poenger. Blandt annet at vagus svekkes ved IBS og at det gir andre plager, spesielt hudplager.

http://www.naaf.no/Documents/Allergi%20i%20Praksis/matoverfoelsomhet_aip_1_2011w_v2.pdf

Dessuten hadde mange pasienter ekstra-intesti- nale symptomer og skåret høyt på «Subjective Health Complaints» (1). Påfallende mange anga at de hadde kronisk tretthet samt leddsmerter med morgenstivhet uten påvisbar artritt. Livskvaliteten var til dels be- tydelig redusert (2).

Over 50% av pasientene tilfreds- stilte kravene til en psykiatrisk diag- nose. Men hvor mye av de psykologiske problemene kan være sekundære? Inntil for knapt 20 år siden ble også magesårsykdommen regnet som en psykosomatisk sykdom. De psykolo- giske problemene vi så hos ulcuspasi- entene var ganske like de vi nå finner hos de matoverfølsomme, og vi har enda friskt i minnet hvordan alle pro- blemene hos ulcuspasientene, in- kludert de psykologiske, «blåste bort» etter fjerning av magesårbakterien Helicobacter pylori (4).

Kun sykdomspesifikk angst eller for- ventninger om plager var signifikante uavhengige prediktorer. Disse pre- diktorene forklarte dog til sammen ikke mer enn 10% av variansen i mageplagene, og alder var eneste signifikante prediktor av ekstra- intestinale plager. Det vil si at 90% av variansen i grad av somatiske plager ikke kunne forklares av psyko- logiske faktorer. Vi tror derfor nå at mange av de psykologiske problemene ved matoverfølsomhet er sekundære og at betydningen av psykologiske faktorer som årsak til matoverfølsomhet kan være betydelig overdrevet.

Vi kunne vise at et tungt fordøyelig, men fermenter- bart karbohydrat, som laktulose, ofte reproduserte pasientens plager (6). tester på klassisk IgE-sensitivisering mot spesifikke kostproteiner, deri- mot, var sjeldent positive. Det virker som om mageplagene først og fremst trigges av tungt fordøyelige karbo- hydrater og ikke spesielt av proteiner i kosten. Dessuten, at plagene kunne reproduseres av mat, viser at pasien- ten har rett – plagene kan skyldes maten! Det passer med at pasientene ikke har plager om natta, når de faster, etter tarm- skylling eller når de får tømt seg fullstendig.

Over 60% av pasientene hadde indikasjon på atopisk sykdom (Dette er hud- og slimhinnerelaterte sykdommer som allergi, tørr hud, kløe, m.m.)

Histamin øker sympatisk og redusert para- sympatisk (vagal) tonus, som også er karakteristisk for pasienter med funksjonelle mageplager (16, 17). Slik endret autonom aktivitet kan være et resultat av IgE-mediert histaminfrigjøring fra lokalt sensibili- serte mastceller (18).

Systemiske symptomer som kro- nisk tretthet og leddsmerter hos pasi- enter med IBS har tidligere ofte blitt forklart som somatisering av psykolo- giske problemer, men det finnes andre muligheter. For eksempel er det nylig rapportert at symptomer ved kronisk tretthetssyndrom kan behandles med en B-celle-antagonist (rituximab) (21). I likhet med de matoverfølsomme, har pasienter med kronisk tretthets- syndrom ofte IBS og endret mikro- flora som kan være av betydning for immunaktiveringen hos disse pasi- entene (22). Hos matoverfølsomme med IBS har vi nylig påvist økt nivå av B-celle aktiverende faktor (BAFF) i blod og tarmskyllevæske (23). BAFF er relatert til autoimmunitet og lokal immunaktivering i tarmen («lokal allergi») (24).

At karbohydrater kan reprodusere mageplagene hos pasienter med IBS og matoverfølsomhet, er verdt å merke seg, og mye tyder på at dette allerede nå bør få terapeutiske konsekvenser (27). Vi ser med andre ord for oss et paradigmeskifte når det gjelder utredning og behandling av pasienter med IBS og matoverfølsomhet.

Central sensitisation in visceral pain disorders

Nevner hvordan IBS skaper sentralsensitering og hyperalgesia andre steder enn bare tarmen, og bidrar til mange muskel- og ledd problemer. Nevner at dette spesielt skjer i korsryggen hvor sensoriske nerver fra tarmen treffer samme nerve i ryggmargen som de sensoriske nervene fra beina.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856337/

The concept of visceral hyperalgesia has been examined in a variety of functional gastrointestinal disorders (FGIDs), including oesophagitis, gastro‐oesophageal reflux disease, non‐ulcer dyspepsia, gastroparesis, and irritable bowel syndrome (IBS). Visceral hypersensitivity has also been demonstrated in non‐gastrointestinal disorders such as interstitial cystitis and ureteric colic.1 Although the pathophysiological mechanisms of pain and hypersensitivity in these disorders are still not well understood, exciting new developments in research have been made in the study of the brain‐gut interactions involved in the FGIDs.

In this issue of Gut, Sarkar and colleagues2 address the phenomenon of temporal summation of pain, termed “wind‐up”, and its relationship to central sensitisation and secondary visceral pain hyperalgesia caused by acidification of the oesophagus (see page 920). Also in this issue of Gut, Drewes and colleagues3 examine peripheral and central sensitisation using both mechanical and thermal stimuli in patients with oesophagitis compared with control subjects (see page 926). They found that in patients with oesophagitis, the interaction between central and peripheral nociceptive input may help explain patient symptoms. Understanding the implications of these two studies requires examining the concept of central sensitisation in visceral pain disorders. Both of these studies have important clinical and research ramifications for the study of FGIDs.

“Hypersensitivity in IBS patients is not just limited to the gut and more widespread alterations in central pain processing may be involved in this chronic pain disorder”

The most pronounced hyperalgesia appears to occur at the lumbosacral level at which colon and lower extremity nociceptive afferents are likely to converge onto common spinal segments, explaining why patients had higher thermal hypersensitivity in the foot than in the hand (see fig 11).14,15,19

Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related Disorders

Nyeste oppdateringen på gluten, som nevner at det ikke er glutenet i korn som er det største problemet, men FODMAPs. Ikke-cøliakisk glutenintoleranse er reell for noen, men ikke så mange som vi trodde. FODMAPs gjelder flere. Nevner også at dette kan gjelde opptil 30% av befolkningen. Beskriver symptomer på glutenintoleranse, og at pasienten ofte har oppdaget et fobindelse selv med sine symptomer når de kutter gluten-korn.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3820047/

Non Celiac Gluten sensitivity (NCGS) was originally described in the 1980s and recently a “re-discovered” disorder characterized by intestinal and extra-intestinal symptoms related to the ingestion of gluten-containing food, in subjects that are not affected with either celiac disease (CD) or wheat allergy (WA). Although NCGS frequency is still unclear, epidemiological data have been generated that can help establishing the magnitude of the problem. Clinical studies further defined the identity of NCGS and its implications in human disease. An overlap between the irritable bowel syndrome (IBS) and NCGS has been detected, requiring even more stringent diagnostic criteria. Several studies suggested a relationship between NCGS and neuropsychiatric disorders, particularly autism and schizophrenia. The first case reports of NCGS in children have been described. Lack of biomarkers is still a major limitation of clinical studies, making it difficult to differentiate NCGS from other gluten related disorders. Recent studies raised the possibility that, beside gluten, wheat amylase-trypsin inhibitors and low-fermentable, poorly-absorbed, short-chain carbohydrates can contribute to symptoms (at least those related to IBS) experienced by NCGS patients. In this paper we report the major advances and current trends on NCGS.

In order to develop a consensus on new nomenclature and classification of gluten-related disorders, a panel of experts first met in London, in February 2011. The panel proposed a series of definitions and developed a diagnostic algorithm that has been recently published [4].

After the 2011 London Meeting, many new papers have been published on GS. Although its frequency in the general population is still unclear, epidemiological data have been generated that can help establish the magnitude of the problem. Clinical studies further defined the identity of GS and its possible implications in human disease. An overlap between the irritable bowel syndrome (IBS) and GS has been suspected, requiring even more stringent diagnostic criteria. The first case reports of GS in children have been described. Lack of biomarkers is still a major limitation of clinical studies, making the differential diagnosis with other gluten related disorders, as well conditions independent to gluten exposure, difficult.

Evaluation and discussion of this new information was the aim of a Second Expert Meeting on GS that was held in Munich, November 30–December 2, 2012. In this paper we report the major advances and current trends on GS, as presented and debated at the Munich meeting.

According to recent population-based surveys performed in Northern Europe, the prevalence of IBS in the general adult population is 16%–25% [11,12]. In a selected (and, therefore, probably biased) series of adults with IBS, the frequency of NCGS, documented by a double-blind, placebo-controlled challenge, was 28% [13]. In the large study performed by Carroccio et al., 276 out of 920 (30%) subjects with IBS-like symptoms, according to the Rome II criteria, suffered from wheat sensitivity or multiple food hypersensitivity, including wheat sensitivity [14]. Should a consistent proportion of IBS patients be affected with NCGS, the prevalence of NCGS in the general population could well be higher than CD (1%).

NCGS is characterized by symptoms that usually occur soon after gluten ingestion, disappear with gluten withdrawal and relapse following gluten challenge, within hours or few days. The “classical” presentation of NCGS is a combination of IBS-like symptoms, including abdominal pain, bloating, bowel habit abnormalities (either diarrhea or constipation), and systemic manifestations such as “foggy mind”, headache, fatigue, joint and muscle pain, leg or arm numbness, dermatitis (eczema or skin rash), depression, and anemia [2,15]. When seen at the specialty clinic, many NCGS patients already report the causal relationship between the ingestion of gluten-containing food and worsening of symptoms. In children, NCGS manifests with typical gastrointestinal symptoms, such as abdominal pain and chronic diarrhea, while the extra-intestinal manifestations seem to be less frequent, the most common extra-intestinal symptom being tiredness [16].

In a second study, Biesiekirski et al. reported on 37 patients with IBS/self-reported NCGS investigated by a double-blind crossover trial. Patients were randomly assigned to a period of reduced low-fermentable, poorly-absorbed, short-chain carbohydrates (fermentable oligo-, di-, and mono-saccharides and polyols = FODMAPs) diet and then placed on either a gluten or whey proteins challenge. In all participants, gastrointestinal complaints consistently improved during reduced FODMAP intake, but significantly worsened to a similar degree when their diets included gluten or whey proteins [21].FODMAPS list includes fructans, galactans, fructose, and polyols that are contained in several foodstuffs, including wheat, vegetables, and milk derivatives. These results raise the possibility that the positive effect of the GFD in patients with IBS is an unspecific consequence of reducing FODMAPs intake, given that wheat is one of the possible sources of FODMAPs.

The pathophysiology of NCGS is under scrutiny. In the study conducted by Sapone et al. [2], NCGS subjects showed a normal intestinal permeability and claudin-1 and ZO-1 expression compared with celiac patients, and a significantly higher expression of claudin-4.

King Corn dokumentar

En av de første kommentarene i denne dokumentaren setter standarden:

«We recently learned that people who grew up the way we did are basicly made up of corn.

…what the heck!!!»

La oss gi dette litt tid synke inn. Du blir hva du spiser. I de aller fleste varene i butikken er korn/mel en viktig ingrediens. I tillegg anbefaler myndighetene oss at 3 av 4 måltider skal bestå av korn. Men ikke nok med det. Kyrne blir foret med korn også, hele 60% av deres diett består av korn. Det er så mye at om de må slaktes før de dør av acidose (lav pH i blod). Årsaken til at kyrne fores på så mye korn er at det øker deres vekt raskest, slik at de raskest mulig kan slaktes og komme ut på markedet. Om kyrne skulle fores på naturlig gress ville de brukt mer enn ekstra år før de ble store nok til å slaktes.

Denne dokumentaren er smekk full av viktige avsløringer som alle bør vite om.

Spectrum of gluten-related disorders: consensus on new nomenclature and classification

Oppdatert forhold til ikke-cøliakisk glutenintoleranse fra 14 eksperter i USA.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292448/

This review will summarize our current knowledge about the three main forms of gluten reactions: allergic (wheat allergy), autoimmune (celiac disease, dermatitis herpetiformis and gluten ataxia) and possibly immune-mediated (gluten sensitivity), and also outline pathogenic, clinical and epidemiological differences and propose new nomenclature and classifications.

It is now becoming apparent that reactions to gluten are not limited to CD, rather we now appreciate the existence of a spectrum of gluten-related disorders. The high frequency and wide range of adverse reactions to gluten raise the question as to why this dietary protein is toxic for so many individuals in the world. One possible explanation is that the selection of wheat varieties with higher gluten content has been a continuous process during the last 10,000 years, with changes dictated more by technological rather than nutritional reasons.

Additionally, gluten is one of the most abundant and diffusely spread dietary components for most populations, particularly those of European origin. In Europe, the mean consumption of gluten is 10 g to 20 g per day, with segments of the general population consuming as much as 50 g of daily gluten or more [6667] All individuals, even those with a low degree of risk, are therefore susceptible to some form of gluten reaction during their life span.

Does gluten sensitivity in the absence of coeliac disease exist?

Artikkel som nevner den fremadstormende forskningen som gjøre på ikke-cøliakisk glutensensitivitet.

http://www.bmj.com/content/345/bmj.e7907

However, the number of patients consuming a gluten-free diet seems greatly out of proportion to the projected number of patients with coeliac disease. Marketers have estimated that 15-25% of North American consumers want gluten-free foods,4 5

A third of patients (n=276) showed clinical and statistically significant sensitivity to wheat and not placebo, with worsening abdominal pain, bloating, and stool consistency. The evidence therefore suggests that, even in the absence of coeliac disease, gluten based products can induce abdominal symptoms which may present as irritable bowel syndrome.

For patients who report wheat intolerance or gluten sensitivity, exclude coeliac disease (with endomysial and/or tissue transglutaminase antibodies and duodenal biopsies on a gluten containing diet) and wheat allergy (IgE serum assay or skin prick test to wheat). Those patients with negative results should be diagnosed with non-coeliac gluten sensitivity. These patients benefit symptomatically from a gluten-free diet. They should be told that non-coeliac gluten sensitivity is a newly recognised clinical entity for which we do not yet fully understand the natural course or pathophysiology.