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Is veranderinge in koring verantwoordelik vir die styging in coeliakie?

Is veranderinge in koring verantwoordelik vir die styging in coeliakie?

Een kardioloog dink so, maar wetenskaplikes stem nie saam nie

Wikimedia Commons/ Bluemoose

Niemand is seker waarom daar 'n toename in coeliakie is nie.

As u van die skrywer William Davis, 'n kardioloog van Milwaukee, gehoor het, is dit waarskynlik as gevolg van sy gewilde boek Koringpens, wat die deugde van 'n koringvrye dieet verheerlik. Nadat Davis opgehou het om koring te eet, beweer hy dat 'n groot aantal siektes, insluitend diabetes, gemoedswisselings, gewrigspyn en suur terugvloei bedaar het. Davis het beweer dat die styging in coeliakie, 'n afkeer van koringluten, die afgelope 20 jaar grootliks te wyte is aan die feit dat nuwe koringvariëteite ingestel is, wat bedoel is om die graanopbrengs te verhoog. Maar hierdie week het 'n navorsingschemikus by die Amerikaanse departement van landbou bevindings gemaak van 'n studie wat hierdie bewering weerlê.

Volgens NPR, die apteker, Donald Kasarda, het die glutenvlakke in koring oor tyd dieselfde gebly, en coeliakie -deskundige Daniel Leffler stem saam dat die oorsaak van die siekte grootliks te wyte is aan 'n reeks faktore.

'Ek dink nie daar is 'n slegte kos wat die probleem in ons samelewing veroorsaak nie,' het Leffler aan NPR gesê. "Daar is goeie bewyse dat die oorgrote meerderheid mense eintlik net goed met koring vaar."

Hoewel coeliakie tot ongeveer 1 persent van die bevolking styg, is daar geen konsensus waarom dit die geval is nie. Of dit nou te wyte is aan die gebruik van antibiotika vroeg in die lewe, die sogenaamde "higiëne-hipotese", wat beweer dat ons omgewing so skoon is dat ons liggame nie-giftige dinge, soos grondboontjies, vind om allergies vir te word, of dat dit 'n ander proteïen is in koring heeltemal wat mense siek maak, sal dit waarskynlik lank duur voordat ons die gluten -onverdraagsaamheid bereik.


Die gruwels van glutenvrye kos

Dit gebeur steeds: ek loop mense raak wat vir my sê ek volg die koringstyl -leefstyl. Ek eet glutenvry! ” As ek hulle vra wat dit beteken, vertel hulle my dat hulle net glutenvrye brood, pasta, pizza, koekies, ens. Eet.

Ek is nie heeltemal seker hoekom hierdie verkeerde interpretasie van die boodskap van Wheat Belly so gereeld voorkom nie. Laat ons praat oor hierdie belangrike onderskeid, soos glutenvry wees kan 'n absolute gesondheids- en gewigramp wees, anders as die wonderlike gesondheid en gewigsverlies wat ons geniet op die Wheat Belly -leefstyl as dit reg gedoen word.

Dit is heeltemal goed om glutenvry te wees, dit wil sê om koring, rog en gars te vermy wat die gliadienproteïen bevat in gluten wat verantwoordelik is vir coeliakie en ander reaksies wat deur gliadien veroorsaak word. Mense met coeliakie argumenteer dikwels “Maar ek het Om glutenvry te wees! ” Maar die probleem kom as voedselvervaardigers probeer om 'n stukkie van die aksie te kry en glutenvrye brode, broodjies, pizzakors, ens. te herskep met behulp van een of meer van die vier bestanddele:

Koring en verwante korrels verhoog bloedsuiker tot hoë vlakke, hoër as tafelsuiker, as gevolg van die unieke verteerbaarheid van amylopektien A. Baie min voedsel verhoog bloedsuiker hoër as koring. So, watter voedsel verhoog bloedsuiker selfs hoër as suiker, hoër as koring? Yup: mieliestysel, rysmeel, tapioca -stysel en aartappelmeel. Eet glutenvrye kosse wat uit hierdie bestanddele bestaan, en u sal hoë bloedsuikers ervaar. Doen dit herhaaldelik en ontwikkel u insulienweerstandigheid, pre-diabetes en tipe 2-diabetes. Maar dit eindig nie daar nie.

Wat doen glutenvrye vervangingsbestanddele nog aan die ongelukkige verbruiker wat dit eet en dink dat dit gesond en veilig is? Baie. Onder die gevolge van glutenvrye voedsel is:

  • Glykasie reaksiesHoë bloedglukose verander die proteïene van die liggaam deur 'n proses genaamd glikasie, 'n onomkeerbare reaksie wat in wese sellulêre puin veroorsaak. Terwyl u die glikasie kan opspoor deur middel van die gewone HbA1c -toets (geglikateerde hemoglobien), sal u nie die glikasie van die proteïene in die ooglense opspoor totdat dit as katarak ophoop nie, of in die niere totdat u nierversaking ontwikkel, of die hart as klein geglyceerde LDL -deeltjies versamel as aterosklerotiese plaak en hartaanval, of in die brein wat bydra tot demensie van Alzheimer.
  • Zein -mielieproteïen boots gliadien naDie zeienproteïenreste in mielieblom kan in klein hoeveelhede soos gliadien optree by mense met coeliakie en gliadiengevoelighede (bv. Met ander woorde, glutenvrye voedsel kan coeliakie en ander toestande heraktiveer.
  • Koringkiem agglutinien in rysAlhoewel dit in rys is, word dit nog steeds koringagglutinien genoem omdat die struktuur identies is aan die struktuur in koring. Alhoewel dit in klein hoeveelhede voorkom, is daar genoeg om die dermvoering op coeliakagtige maniere te ontwrig (direkte toksisiteit, eerder as die indirekte immuungemiddelde pad van coeliakie).
  • Gewig optelDie hemelhoë bloedsuikers wat deur glutenvrye bestanddele gegenereer word, veroorsaak ook hoë insulien, wat weer insulienweerstandigheid veroorsaak, wat weer veroorsaak dat viscerale inflammatoriese vet ophoop. Dit is die rede waarom mense wat glutenvrye voedsel inneem, 'n ekstra band om hul middel groei, wat die ophoping van vet rondom buikorgane en hart weerspieël.
  • Steek ontsteking aanHoë insulienvlakke en opeenhoping van viscerale vet veroorsaak dat inflammasie toeneem, waarneembaar as verhoogde C-reaktiewe proteïene, Il-2, TNF-alfa en ander maatreëls. Inflammasie is onderliggend aan talle gesondheidstoestande soos hartsiektes, kanker en demensie.
  • Versteur hormonale statusNamate viscerale vet ophoop, ontwikkel 'n verskeidenheid hormonale ontwrigtings wat veroorsaak dat mans se borste vergroot en hul testosteroon daal. Dit veroorsaak dat vroue hoër estrogeenvlakke ontwikkel wat verband hou met 'n verhoogde risiko vir borskanker. By vroue met PCOS styg testosteroon, bloedsuiker en bloeddruk styg en onvrugbaarheid ontwikkel.
  • Dysbiose en dunderm bakteriële oorgroei (SIBO)Hoogverfynde koolhidraatryke meel, soos glutenvrye meel, is soos om 'n spoor broodkrummels vir eende uit te haal: dit sal die krummels se pad volg. Die inname van die hoogs verteerbare koolhidrate van glutenvrye voedsel is 'n opset om kolonmikrobes in die dunderm uit te nooi, die situasie wat SIBO definieer. Dit verander ook die samestelling van dermfloraspesies op ongesonde maniere.
  • TandbederfDie amylopektien A-koolhidrate van sommige glutenvrye meel, soos mielieblom, versterk die potensiaal vir tandbederf aansienlik, net soos koring.

Kry jy die idee? Glutenvrye voedsel gemaak met gewone glutenvrye meel moet nie eers verkoop word nie. Of moet ten minste erken word dat dit nie beter is as om suiker uit 'n bak te eet nie. Niemand in die Wheat Belly -leefstyl behoort sulke kosse te eet met die rampspoedige gevolge daarvan nie.

Regtig: kry die koringstyl reg, en u word beloon met 'n ongelooflike gesondheid, gewigsverlies en jeugdigheid.


Daar is meer koring as coeliakie

Ek wil hierdie kwessie met die hand vat, aangesien die gewilde “wisdom ” is dat probleme met die verbruik van koring en verwante korrels begin en eindig met coeliakie. The Wheat Lobby, byvoorbeeld, voer gereeld aan dat as u nie coeliakie het nie, u geen sake het om koring en verwante korrels te vermy nie.

Verdedigers van koring, soos dié in hierdie New York Times -artikel, voer aan dat coeliakie 1% van die menslike bevolking raak, maar dat die ander 99% van die mense kan koring nie net straffeloos verbruik nie, maar kan dit eintlik doen en gesondheidsvoordele kry as gevolg van vesel- en B -vitamieninhoud. Hulle sê dat die uitskakeling van koring en graan dus onnodig, ongesond, selfs gevaarlik is.

Laat ons dus ondersoek wat gesondheidstoestande kan ontwikkel by die 99% van die mense wat dit doen nie het coeliakie:

  • Serebellêre ataksieDit is 'n toestand waarin teenliggaampies teen gliadien (hoewel dit anders is as by coeliakie) die serebellum, die deel van die brein wat verantwoordelik is vir koördinasie, blaasbeheer en ander liggaamsfunksies, beskadig. Mense met hierdie toestand ontwikkel progressiewe koördinasie, begin struikel, verloor beheer oor hul blaas, beland dan in 'n rolstoel en ervaar voortydige dood. Hou op om koring en verwante korrels te eet, en die verloop van die siekte stop, en kan gedeeltelik omkeer (slegs gedeeltelik, aangesien die weefsel van die brein en die senuweestelsel swak genees).
  • Perifere neuropatieTerwyl die meeste gevalle van perifere neuropatie, of skade aan die senuwees van die bene en organe (bv. Die maag, wat 'n nie-funksionele maag of gastroparese tot gevolg het) die gevolg is van langdurige diabetes, is die oorblywende gevalle by mense sonder diabetes, 50% van die gevalle van nie-diabetiese perifere neuropatie word veroorsaak deur 'n outo-immuunreaksie wat veroorsaak word deur gliadien met hoë vlakke teen-gliadien teenliggaam. Soos met serebellêre ataksie, keer die inkoordinasie, beenpyn, selfs gastroparese, soms heeltemal, uit met koring/korrel eliminasie.
  • Ystertekort bloedarmoedeDie fytate van koring en korrels verminder ysteropname met tot 90%, wat koring/graanverbruik die tweede mees algemene oorsaak van ystertekortanemie in die wêreld maak na bloedverlies. Raak ontslae van die koring/korrels, ystertekort keer om.
  • GynekomastieDit is die “man boob ” kwessie – vergrote borste by mans, verleentheid, ontsierende, en nou verantwoordelik daarvoor dat manlike borsverminderingsoperasies een van die algemeenste elektiewe operasies by mans is. Onthou dat die A5-pentapeptied uit gedeeltelike vertering van die gliadienproteïen 'n kragtige stimulant is vir die vrystelling van pituïtêre prolaktien (pro- + laktien = verhoog laktasie), verwyder koring en korrels, verwyder alle bronne van gliadien, en prolaktienvlakke daal en borsgrootte neem af. Nog beter: verloor die koring en korrels, verloor die amylopektien A wat verantwoordelik is vir hoë bloedsuikers en insulien, inflammatoriese buikvet neem af, die aktiwiteit van die ensiem aromatase in buikvet daal, en testosteroonvlakke styg, estrogeenvlakke daal by mans (sedert ooraktief aromatase in maagvet omskep manlike testosteroon in estrogeen).
  • Vitamien B12 -tekortAbsorpsie van vitamien B12, noodsaaklik vir talle liggaamsprosesse, soos die produksie van bloedselle en funksionering van die senuweestelsel, word benadeel omdat koring en korrels 'n outo -immuunrespons veroorsaak teen die pariëtale selle van die maag wat 'n proteïen produseer (“intrinsic factor & #8221) benodig vir B12 -opname. Skade aan pariëtale selle benadeel die produksie van intrinsieke faktore, en B12 word nie geabsorbeer nie. Dit keer terug met die uitskakeling van koring/graan en gaan gepaard met 'n styging in B12 -vlakke en omkering van skadelike of makrocitiese anemie.
  • Hashimoto se tiroïeditisTot 50% van die mense met hierdie outo -immuun skildklier toestand het 'n hoë teenliggaampie teen die gliadien proteïen van koring en verwante korrels. Verwyder koring/korrels en die outo -immuun skildklierontsteking bedaar (veral as dit gekombineer word met vitamien D en die kweek van 'n gesonde dermflora), maar dit gaan ongelukkig gewoonlik nie gepaard met die volledige herstel van die produksie van tiroïedhormone nie, wat beteken dat skildklierhormone, T4 en T3, steeds nodig is geneem word om normale skildklierstatus te verkry.
  • Tipe 1 -diabetesDie bewyse is redelik duidelik: baie, indien nie die meeste, gevalle van outo -immuun vernietiging van pankreas -beta -selle wat insulien produseer, word geïnisieer deur die gliadienproteïen van koring en verwante korrels (sowel as die zeienproteïen van koring en die kaseïen beta A1 suiwelproteïen, hoewel minder algemeen), wat deur beide die mens sowel as die ervaring in twee eksperimentele modelle bewys word. Net soos met die vernietiging van die skildklier by Hashimoto, is beta-selle in die pankreas baie swak om te herstel en die oorgrote meerderheid van tipe 1-diabete is lewenslank insulienafhanklike diabete.
  • Rumatoïede artritisRumatoïede artritis dien as die prototipiese outo -immuun siekte, in hierdie geval 'n outo -immuun aanval op die gewrigte van die liggaam. Die outo -immuunproses word geïnisieer deur ongeskonde vorme van gliadienproteïen, die pad wat elegant deur Dr. Alessio Fasano en kollegas uitgewerk is aan die Universiteit van Maryland.
  • Hiperglukemie/tipe 2 -diabetesDie formule om 'n persoon diabeet te maak, is eenvoudig: eet voedsel wat bloedsuiker en insulien verhoog, weerstand teen insulien ontwikkel, viscerale vet groei wat bydra tot inflammasie wat insulien verder blokkeer, vetterige lewer ontwikkel (as gevolg van lewer De novo lipogenese) wat ook insulien verder blokkeer, en bloedsuikers styg tot by die diabetiese reeks. Die proses word dus begin deur voedsel wat die bloedsuiker die hoogste verhoog. Watter kosse het die hoogste glukemiese indeks (en glukemiese hoeveelhede) van alle voedsel? Korrels, selfs meer as wit tafelsuiker. Volg 'n dieet wat oorheers of ryk is aan korrels, wit of heel, en bloedsuikers styg baie keer per dag (aangesien daar feitlik geen verskil is met die oog op bloedsuiker nie): 'n perfekte opset vir tipe 2 -diabetes. Raak ontslae van alle koring en korrels, en die hele siklus draai af.
  • Ekseem, psoriase, seborrhea, rosaceaHierdie algemene outo -immuun veltoestande wat miljoene mense beïnvloed, kom voor by mense sonder coeliakie, en verdwyn of verdwyn in die meerderheid met koring-/graanuitskakeling.
  • Paranoia van skisofrenie, manie van bipolêre siekte, depressie'N Aansienlike deel van mense met elk van hierdie toestande ervaar 'n afname in die simptome van koring/graan uitskakeling. Skisofrenie word nie genees nie, maar verminder paranoia, verminderde ouditiewe hallusinasies (hoorstemme) en verhoogde kapasiteit vir sosiale betrokkenheid. Die mense wat die meeste geneig is om koring/graan uit te skakel, is gewoonlik mense met hoë teenliggaampies teen gliadien, maar daar is baie wat nie sulke teenliggaampies het nie, wat ook verbeter, waarskynlik as gevolg van die gedagte- en gedragsveranderende effek van die verwydering van gliadien. -afgeleide opioïede peptiede.

Ek kan aangaan, soos daar letterlik is honderde ander toestande wat veroorsaak word deur die verbruik van koring en graan by mense sonder coeliakie, alles gedokumenteer in die wetenskaplike literatuur (baie verwysings in die boek Wheat Belly Total Health) —it is nie 'n kort lys nie. U kan begin besef hoe absoluut absurd hierdie glutenvrye metode slegs is vir mense met coeliakie. Koring en verwante korrels (veral rog, gars en koring) het 'n verreikende uitwerking op die brein, skildklier, vel, lugweë en sinusse, gewrigte, pankreas, borste, maag, ens. Nie net die dunderm nie. Verstaan ​​hierdie basiese beginsel, erken dat die Wheat Lobby 'n gebrekkige versameling voedselprodukte met misleidende rookskerms verdedig, wat herinner aan die taktiek wat Big Tobacco 'n paar jaar terug gebruik het om sigarette te verdedig en dat u die sleutel gevind het tot 'n ongelooflike kragtige terugkeer na gesondheid: eet geen koring of korrels nie.


4 groot mites oor coeliakie ontbloot

Vir so baie van ons is die internet ons reddingsboei, wat ons toegang gee tot glutenvrye resepte en ons verbind met ander wat ons ervarings deel. Benewens hierdie magdom inligting, kom egter 'n magdom verkeerde inligting.

Dit is geen verrassing dat mites oor coeliakie op die internet versprei word nie. Hierdie mites laat mense egter hul eie beste raaiskote maak oor hoe hierdie inligting op hul lewens van toepassing is.

Die Beyond Celiac -span werk saam met navorsers van regoor die wêreld en hou tred met die nuutste navorsing oor coeliakie om mediese tydskrifte te bereik. Hier identifiseer ons vier algemene navorsingsmites wat tans in omloop is.

1. Mite: Koringteling het die voorkoms van coeliakie verhoog.

Navorsers weet nie hoekom coeliakie toeneem nie. Wat hulle wel weet, is dat koringteling waarskynlik nie daarvoor verantwoordelik is nie. In 2013 het die coeliakie -kenner Donald Kasarda, PhD, studie -resultate bekend gemaak wat toon dat koringteling nie bykomende glutenproteïen in die finale produk tot gevolg het nie.

Om dit te bepaal, bestudeer Kasarda data oor koring uit die 20ste en 21ste eeu. Hy het gevind dat koringteling nie die inhoud van gluten in koring verhoog nie. Wat hy wel gevind het, is dat daar 'n toenemende gebruik van 'vitale gluten' in voedsel is. Dit is 'n gekonsentreerde glutenproteïen wat bygevoeg kan word om die produkte donser te maak en hulle meer elastisiteit te gee.

Alhoewel dit nie die gevolg is van koringteling nie, val die toename in coeliakie saam met die toename in die gebruik van bykomende vitale gluten. Kasarda beklemtoon dat meer navorsing nodig is, en hoewel vitale gluten in meer produkte voorkom, is dit steeds nie 'n belangrike deel van die gemiddelde totale gluteninname as gevolg van die inname van produkte op koringmeel nie. Uiteindelik soek navorsers steeds antwoorde op die vraag waarom coeliakie vandag meer gereeld voorkom.

2. Mite: Vertraging van die bekendstelling van gluten in die dieet van 'n kind kan coeliakie voorkom.

In 2015 het 'n span navorsers 15 studies oor hierdie onderwerp ondersoek. Wat hulle gevind het, was dat kinders wat die eerste keer na ses maande gluten gekry het, 'n 25 persent groter kans het om coeliakie te ontwikkel. Tans sê pediatriese aanbevelings dat gluten -bekendstelling tussen die ouderdom van vier en ses maande moet plaasvind.

In 'n Beyond Celiac -onderhoud met deskundige dr.Stefano Guandalini, het hy voorgestel dat die beste venster tussen vyf en ses maande oud kan wees, en dat daar geen wetenskaplike bewyse is dat vroeë gluten -bekendstelling (die toevoeging van gluten aan die dieet voor of voor drie maande van ouderdom) verhoog die kans om coeliakie te voorkom.

3. Mite: Borsvoeding kan coeliakie voorkom.

Borsvoeding word deur dokters aanbeveel om babas wat met formule voed, om verskeie gesondheidsredes. Voorkoming van coeliakie is egter nie een daarvan nie.

In die studie van 2015 het navorsers bevind dat borsvoeding en nie -borsvoeding geen rol gespeel het in die ontwikkeling van coeliakie nie. Alhoewel dit nie coeliakie voorkom nie, word borsvoeding steeds deur dokters aanbeveel vir die vele voordele wat dit vir moeders en hul babas bied.

4. Mite: Kliniese proewe om nuwe behandelings vir coeliakie te bestudeer, is onnodig omdat die glutenvrye dieet die geneesmiddel is.

Die glutenvrye dieet is letterlik 'n lewensredder vir mense met coeliakie, maar dit is beslis nie 'n geneesmiddel nie. Volgens dr. Joseph Murray van die Mayo Clinic word tot 70 persent van mense met coeliakie steeds blootgestel aan gluten, ondanks hul beste pogings om streng glutenvry te bly. Die bewyse in die navorsing is duidelik: die glutenvrye dieet alleen is nie genoeg nie.

Daar is verskeie kliniese toetse aan die gang wat die glutenvrye dieet wil aanvul of vervang. Alhoewel hierdie vordering uiters opwindend is, is dit belangrik om te weet dat ander navorsing net so belangrik is. Alhoewel die betrokkenheid van mense met coeliakie van kritieke belang is vir geneesmiddelproewe, is deelname nog steeds nodig op ander gebiede van navorsing, soos: die ontwikkeling van nuwe bloedtoetse of ander diagnostiese hulpmiddels, of om meer te leer oor simptome en verwante toestande.

Geleenthede om deel te neem, kan opnames, fokusgroepe en ander deel van inligting insluit om navorsers te help om 'n verskeidenheid gebiede wat verband hou met coeliakie beter te verstaan.

Om deur die mites en feite te sorteer, kan skrikwekkend voel, veral as u onlangs met coeliakie gediagnoseer word. Beyond Celiac deel gereeld geloofwaardige, bewysgebaseerde inligting. Moenie enige van die navorsingsnuus misloop deur aan te meld by die Beyond Celiac -navorsingsnuusbrief nie.

Alice Bast is die uitvoerende hoof van Beyond Celiac, die nasionale organisasie wat namens die gemeenskap met coeliakie werk. Besoek Beyond Celiac vir meer inligting.


Simptome

Volgens Beyond Celiac is daar meer as 300 simptome van coeliakie wat van persoon tot persoon verskil. Die mees algemene sluit in:

  • Abdominale bloeding
  • Chroniese diarree
  • Hardlywigheid
  • Gas
  • Maagpyn
  • Naarheid
  • Braking
  • Laktose onverdraagsaamheid

By jong kinders en babas kan addisionele simptome insluit:

  • Versuim om te floreer
  • Onverklaarbare gewigsverlies
  • Vertraagde groei/vertraagde puberteit
  • Prikkelbaarheid of verandering in bui
  • Gekleurde tande

Bly gesond in die nuwe jaar met coeliakie

Elke nuwe jaar begin met die beste bedoelings. Lees verder vir gespesialiseerde inligting vir diegene op die glutenvrye dieet om u gesondheid in 2015 na 'n volgende vlak te neem (plus wenke om hierdie veranderinge te help vashou!)

Maksimeer u gesondheid met natuurlik glutenvrye voedsel

Daar is geen behoefte aan duur glutenvrye gesondheidsprodukte met aansprake wat te goed lyk om waar te wees nie. Profiteer van die positiewe aspekte van die coeliakie deur natuurlike glutenvrye voedsel te gebruik om u gesondheid te maksimeer:

Draai jou volgraan: die vitamien- en mineraalinhoud van elke graan wissel. As u dieet meestal vol glutenvrye produkte op grond van rys, mielies en aartappels is, kry u liggaam steeds dieselfde voedingstowwe (en mis u ongelooflike superkorrels!). Maak ook seker kies produkte wat op graan gebaseer is en glutenvry is om natuurlik GF-voedsel te vermy wat moontlik koringbesmet is met koring, gars of rog (lees meer hieroor). 'N Voorbeelddag wat GF -korrels maksimeer, kan soos volg daar uitsien:

  • Ontbyt: bokwiet (kasha) en hawermout van hawer, bedien met neute, bessies en 'n klomp jogurt
  • Middagete: gemengde groenslaai met witboontjies, gekookte quinoa en gierst
  • Aandete: gebraaide salm en gebakte boerenkool bedien met amarant en mielie -platbrood
  • Vind meer maklike, voedsame resepte HIER!

Instituut Vleislose Maandae en Vette Vis Vrydae:Die Amerikaanse dieet maak dikwels te sterk staat op dierlike vette en proteïene, wat beteken dat ons in die proses die hartgesonde voordele van plantproteïene en vette misloop. Plantgebaseerde proteïene (dws boontjies en peulgewasse, insluitend soja) lewer uitstekende omega-3 en omega-6-vetsure, bevat min versadigde vet, bevat natuurlik GEEN cholesterol nie en kan baie chroniese siektes voorkom. Om die gesondheid verder te versterk, toon studies aan dat slegs twee porsies vetterige vis per week noodsaaklike vetsure lewer wat inflammasie in die liggaam kalmeer, iets wat mense met coeliakie baie nodig het.

Kry ten minste een blaargroen per dag: Donker blaargroentes is 'n pragtige geskenk van die natuur. Onder die groen kleur is eintlik 'n magdom ander fitochemikalieë, soos dié wat in oranje, rooi en pers groente voorkom. Een porsie kale, chard, spinasie of mosterdgroente per dag gee u 'n hupstoot van vitamiene A, C, K en folaat om die oksidatiewe stres van die daaglikse lewe, plus baie noodsaaklike minerale, te bekamp. Maksimaliseer die opname van vitamiene en minerale deur liggies te kook en te bedien met 'n vetbron, soos gebraai in olyfolie. U kan dit ook in 'n slaai geniet vir 'n uitstekende tekstuur of dit by 'n smoothie voeg sonder dat die smaak verander (selfs u kinders sal dit nie agterkom nie!).

Varieer u kookolie en slaaisous: Net soos die verskillende voedingsinhoud in korrels, het die eienskappe en voordele van verskillende vette baie voordele vir die liggaam. Het u geweet dat elke sel in ons liggaam uit vetsure bestaan? Om die gesondheid van u vel, ingewande en kardiovaskulêre stelsel te verbeter, moet u verskillende olies byderhand hou vir warm en koue geregte. Vlasaad-, hennep-, pampoensaad en okkerneutolies is te delikaat vir hitte, maar voeg wonderlike geure by slaaie en ander koue disse. Olyfolie-, druiwe- en sesamolie is geskik vir vinnige sautering, en klapper-, avokado-, saffloer- en canola -olies is stabiel vir langer braai en bak. As u u vetbronne van die tipiese plantaardige olie en botter afwissel, kry u beslis 'n wonderlike balans van enkel -onversadigde, meer -onversadigde en versadigde vette in die beste verhoudings.

Gewigsbeheer na diagnose

As u nuwejaarsvoorneme 'n gewigsdoelwit insluit, moet u die volgende inligting in gedagte hou om 'n realistiese en gesonde plan te maak:

    Gewigstoename is tipies na die diagnose van coeliakie, selfs al is u reeds as normaal of oorgewig beskou. Die voedsel wat u geëet het, is slegs gedeeltelik geabsorbeer voor die diagnose, en dit kan nog 'n paar maande lank op die glutenvrye dieet bly totdat die dermswille heeltemal genees is. In hierdie opsig is gewigstoename 'n teken dat die liggaam goed genees en u slaag met die glutenvrye dieet.
  • As gevolg van bogenoemde eetlus, moet die porsiegroottes en algehele inname verminder word voordat die diagnose hoër as normaal was, aangesien daar nie aan die voedingsbehoeftes voldoen is nie. Dit kan 'n onaangename aanpassing wees wat gedoen moet word (benewens die groot lewensverandering van die uitskakeling van gluten!). Fokus op die bogenoemde wenke om gesondheid te maksimeer, en moenie sterk vertrou op verpakte glutenvrye produkte om gelyktydig gewigstoename te voorkom en u gesondheid te verbeter nie.
  • As u ondergewig was by die diagnose en gewigstoename nie na 'n paar maande begin nie, of as dit begin, maar dan tot stilstand kom voordat u na normaal terugkeer, raadpleeg u gastro -enteroloog vir meer inligting en 'n geregistreerde dieetkundige vir dieetberading. Die mees algemene oorsaak van voortgesette wanabsorpsie is blootstelling aan gluten. Ander algemene oorsake van wanabsorpsie op die GF-dieet sluit in: dunderm bakteriële oorgroei (SIBO), chroniese diarree en kolitis (lees meer oor coeliakie wat swak reageer)
  • Terwyl die gewig normaal moet word namate die ingewande genees, kan sommige baat by gewigstoename om die genesingsproses te versnel as hulle tydens die diagnose ernstig ondergewig is. Dit kan veral geld vir kinders wie se groei en ontwikkeling gestrem is, of wat afkeer daarvan om te eet as gevolg van chroniese negatiewe simptome nadat hulle geëet het.
  • Dit word gewoonlik nie aangeraai om die dieet van 'n kind kalorieë te beperk totdat hulle terugkeer na hul gewone groeikurwe nie, selfs al lyk die groei of inname baie. Raadpleeg 'n pediater en/of 'n geregistreerde dieetkundige wat spesialiseer in kindergeneeskunde om te verseker dat die groei van u kind met coeliakie op die regte pad is na die diagnose.

Gewigsbeheer by afwesigheid van coeliakie

  • Die glutenvrye dieet is nie 'n goeie gewigsverliesdieet nie, ondanks wat u van bekendes hoor.
  • Niks oor gluten self is “vettering ” of “ hoog in kalorieë nie ”. Daar bestaan ​​geen geloofwaardige navorsing wat bewys dat gluten of koring in Amerika verantwoordelik is vir oorgewig of vetsug nie.
  • Gewone gewigstoename lei gewoonlik tot die vervanging van gewone voedsel op basis van graan (brood, pasta, gebak) met glutenvrye verwerkte voedsel. Dit is omdat glutenvrye plaasvervangers gereeld meer suiker, vet en kalorieë bevat om die tekstuur van gluten na te boots, en minder vulling omdat hulle dikwels vesel laer is as hul eweknieë wat gluten bevat.
  • Daar is nie genoeg wetenskaplike navorsing oor gluten-sensitiwiteit nie-coeliakie (NCGS) om te weet hoe 'n glutenvrye dieet die gewig in NCGS beïnvloed.

Oorwin die “New Years Resolution ” Phenomenon

Maak positiewe doelwitte eerder as negatiewe. Gedrag word die suksesvolste verander as 'n ou gedrag vervang word deur 'n nuwe, in plaas van net iets uit te skakel:

Begin klein en realistiese drastiese veranderinge bly selde vas!

Kom weer op die wa, maak nie saak watter maand van die jaar die kalender sê nie. Gedrag verander met die praktyk en mettertyd moet u nie verwag dat u van oornag af sal verander nie, en dat u uself nie as 'n mislukking beskou as daar ups en downs in die proses is nie.

Vra die hulp van ander om die beste te bly as dit nie alleen gedoen word nie. Vir 'n individuele en kundige hulp, vind 'n geregistreerde dieetkundige in die CDF Healthcare Practitioner Directory!


Kan 'n glutenvrye dieet help met vitiligo?

Coeliakie en vitiligo, 'n velafwyking, hou albei verband met outo-immuun siektes, en 'n glutenvrye dieet kan nuttig wees om albei te behandel.

Vitiligo is 'n veltoestand wat veroorsaak dat die vel sy natuurlike kleur verloor, wat kolle ligter vel laat verskyn. Die toestand beïnvloed ongeveer 1 persent van die wêreld se bevolking en 2 tot 5 miljoen mense in die Verenigde State.

Volgens die American Academy of Dermatology ontwikkel vitiligo wanneer melanosiete, die selle wat die vel en hare kleur gee, sterf. Dit is nie heeltemal bekend waarom die selle sterf nie, hoewel vermoedelik nie-segmentele vitiligo 'n outo-immuun siekte is. Alhoewel vitiligo soms pyn of jeuk op die vel veroorsaak, het dit gewoonlik geen ander simptome nie. Verskeie behandelingsopsies is beskikbaar, insluitend ligterapie, aktuele medisyne en soms chirurgie.

Ons weet dat pasiënte met outo -immuun toestande oor die algemeen 'n groter risiko loop om sekere ander outo -immuun toestande te ontwikkel, en 'n paar klein studies het bevind dat pasiënte met vitiligo 'n effens hoër risiko het om coeliakie te ontwikkel in vergelyking met die normale bevolking, ” Dr Kristina Liu, direkteur van die Vitiligo -kliniek in die Brigham and Women ’s -hospitaal.

Volgens Mercola kan 'n glutenvrye dieet veroorsaak dat vitiligo verbeter.

Koring is een van die korrels in baie van die verwerkte voedsel in u kruidenierswinkel wat 'n gesonde gelaatskleur inmeng en bydra tot uitbrake van psoriase en ekseem. Proteïene in koring is verantwoordelik vir inflammasie en veranderinge in u spysverteringskanaal, senuweestelsel en kardiovaskulêre stelsel.

Aknee, atopiese dermatitis, psoriase, ekseem en vitiligo kan deur gluten in die dieet vererger word, veral vir diegene wat gluten onverdraagsaam is. Volgens Mercola is 'n 22-jarige pasiënt in 'n gevalverslag op 'n glutenvrye dieet geplaas nadat hy sonder sukses mediese terapie vir vitiligo ondergaan het. “ Gedeeltelike, maar vinnige repigmentasie het in die eerste maand plaasgevind en gestabiliseer na vier maande van glutenvryheid. ”

Dr Alessio Fasano, 'n wêreldbekende kenner van coeliakie en glutengevoeligheid in die Mass General Hospital for Children en direkteur van die Sentrum vir Coeliaknavorsing, het gesê dat dit nie gereeld voorkom dat pasiënte met coeliakie ook deur vitiligo geraak word nie. Maar soos met ander chroniese inflammatoriese siektes, is daar ook 'n beskrywing van hierdie co-morbiditeit van vitiligo met coeliakie, het Fasano gesê.

Die komponent wat in koring voorkom, is gekoppel aan inflammasie, wat die immuunstelsel kan aktiveer en u melanosiete kan aanval, verduidelik hierdie Mercola -artikel.

Aangesien vitiligo en coeliakie uit dieselfde familie van outo -immuunafwykings kom (daar is 14 bekende gene wat verband hou met vitiligo, en daar is gevind dat 13 daarvan ook 'n komponent in coeliakie is), kan die vermyding van gluten voordelig wees vir die behandeling van beide.

Fasano het gesê mediese kundiges weet nie seker of die gebruik van gluten die simptome van vitiligo vererger nie. Daar was verskeie anekdotiese verslae wat daarop dui dat kruisbesmetting met gluten beide gastro-intestinale simptome kan aansteek en vitiligo kan vererger by mense wat deur beide siektes geraak word, en hy het gesê.

Liu said a gluten-free diet is a “reasonable” option for those struggling with autoimmune conditions. “There has a few case reports of patients with vitiligo and celiac disease improving when they adhered to a strict gluten-free diet,” she said. “I think it’s reasonable for patients who have celiac disease, which was diagnosed by a physician, to adhere to a gluten-free diet, since this would be very beneficial for their celiac disease, and may be helpful with vitiligo if they also have this condition.”

Most medical experts agree that there has not been enough research done to determine whether a gluten-free diet can help with vitiligo. However, some small studies and anecdotal reports imply that it can help. Overall, in a patient with celiac, vitiligo or both, a healthy and balanced diet is essential.

“Just as in many other autoimmune diseases, it is intuitive that a nutritious, balanced diet that maintains the gut microbiome as a healthy ecosystem may mitigate the inflammatory process that characterizes this autoimmune process in vitiligo,” Fasano said.

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Are Changes in Wheat Responsible for the Rise in Celiac Disease? - Recipes

Here, I present my assessment of celiac disease in relation to cereal grains. What I have to say is based on many years of research in the area of gluten proteins as they relate to celiac disease, but because of the complexity of the subject, I do not claim definitive knowledge. My conclusions do not necessarily represent those of the Agricultural Research Service, United States Department of Agriculture (USDA), and are not intended to define USDA policy. There is much to be learned about celiac disease and some of my conclusions based on current knowledge may be modified as new information develops. In other words, some things I say here might turn out to be incorrect. Finally, I am a research chemist, not a physician, and do not intend this essay to be taken as medical advice in any legal sense.

Celiac disease (coeliac is the usual spelling in Europe and Australia) is a condition that may develop in certain genetically susceptible individuals. People with celiac disease cannot eat wheat, rye, or barley. Proteins in these grains (and peptides derived from the proteins during digestion) initiate pathophysiological processes that may eventually lead to severe damage to the absorptive epithelium lining the small intestine. It appears likely that celiac disease is initiated by a mechanism involving immune response, but this has not been proved beyond any question. Certainly, immune reactions become involved after initiation.

Because almost all nutrients, vitamins, minerals, amino acids, carbohydrates, and so on are absorbed by way of the small intestine, malabsorption resulting from damage to the absorptive lining of the small intestine can have wide ranging consequences weight loss, osteoporosis, neuropathy, and so on. There is a wide range in response among those with celiac disease-some may have only minimal changes in the intestinal epithelium and no obvious symptoms, others may have severe damage to the lining of the intestine and severe symptoms. Although poor digestion of food usually leads to diarrhea, one of the most common symptoms in celiac disease, patients presenting with constipation have been reported.

Although there is a definite genetic component, celiac disease is apparently a multigene disease, and its inheritance is not completely understood. It has been strongly associated with European populations and may be rare in African blacks or Asians of Chinese or Japanese descent. There is a strong correlation with certain histocompatibility antigens, but some people with the suspect antigens show no evidence of celiac disease.

Although some people manifest evidence of celiac disease in the first year of life shortly after the introduction of gluten into the diet, others experience the onset of disease manifestations later in life-even very late in life. Consequently, it has been hypothesized that some environmental factor is likely to be involved in triggering the disease. Candidates for this environmental factor are viral infection, parasite infection (Giardia?, Cryptosporidium? Eimeria?), surgery, childbirth, even the stress of giving up smoking-these suggestions are highly speculative.

The manifestations of celiac disease are initiated (and re-initiated) in susceptible individuals upon eating wheat, rye, or barley, or any products from these grains that contain the main storage proteins of these grains. Both the proteins themselves and relatively small peptides derived from the proteins by enzymatic digestion are active in celiac disease. Accordingly, testing for intact proteins rather than peptides derived from then will often be ineffective. Celiac disease may be signalled by the presence of antibodies to gliadins or to endomysium in the blood serum and there are a number of commercial testing centers that provide testing for these antibodies. These tests are valuable, but do not provide complete certainty-either in indicating celiac disease or in indicating its absence.

The presence of antigliadin or anti-endomysium antibodies will frequently result in a recommendation by the diagnosing physician to proceed to the most generally accepted test, intestinal biopsy. In severe cases, the biopsy will show mucosal damage, indicated especially by a flattening of the surface and loss of villous structure. Even this latter test is not entirely specific. A flattened mucosa may be the consequence of a few other diseases and damage may be patchy. The tiny tissue sample excised from the intestine in the biopsy procedure might by chance be taken from a relatively normal patch. To eliminate false negative histological results, the latest recommendation is to obtain 4-5 biopsies from different spots in the small intestine. The earliest stages of the disease may be subtle, perhaps indicated only by lymphocyte infiltration of the epithelium.

Nevertheless, the finding of a flattened mucosa by way of the biopsy, followed by a marked improvement in symptoms and healing of the intestine upon initiation of a wheat, rye, and barley free diet are a pretty good indication of celiac disease. Because antibody levels decline and the intestinal mucosa recovers on such a diet, it is best for tests to be carried out before the potential celiac patient initiates the appropriate diet, thereby making testing impossible or difficult without a new challenge. This is especially so because the time for a challenge to take effect may vary considerably from person-to-person and too short a challenge might fail to bring about changes sufficient for diagnosis.

The only plants demonstrated to have proteins that damage the small intestines of people with celiac disease are those from wheat, rye, and barley, (and the man-made wheat-rye cross called triticale). Until recently, oats have been considered harmful on the basis of early studies. Several recent studies of very high quality involving testing approaches that were not available to earlier workers, indicate that oats are not harmful to celiac patients or to those with dermatitis herpetiformis, but these findings have not been accepted by all physicians. There is also a practical problem with oats in that they tend to be grown in rotation with wheat or in nearby fields, the same machinery and storage bins might be used for both. Consequently, oats can be contaminated with small amounts of wheat.

Wheat, rye, and barley are members of the grass family and are quite closely related to one another according to various schemes of plant classification (taxonomy). However, not all members of the grass family have proteins capable of damaging the intestines of celiac patients. Rice and corn, for example, are apparently harmless.

Many other grains have not been subjected to controlled testing or to the same scrutiny as wheat, rye, barley, oats, rice, and corn in relation to celiac disease. If we accept corn and rice as safe, then members of the grass family that are more closely related to these species (on the basis of taxonomy) than to wheat are likely to be safe. Such grasses include sorghum, millet, teff, ragi, and Job's tears, which appear to be reasonably closely related to corn, and wild rice, which is closely related to cultivated rice. In some cases, there are protein structure studies that support of this conclusion, although the studies are not sufficiently complete to provide more than guidance. Scientifically controlled feeding studies with celiac patients would provide a better answer. However, such studies are not likely to be carried out in the forseeable future because of high costs and the difficulty of obtaining patient participation (such studies would be very likely to involve intestinal biopsy and patients are reluctant to undergo challenge once they are well).

The scientific name for bread wheat is Triticum aestivum--the first part of the name defines the genus (Triticum) and the second part, the species (aestivum). Species falling in the genus Triticum are almost certain to be harmful to celiac patients. Grain proteins of these species include the various types characteristic of the gluten proteins found in bread wheats (including the alpha-gliadins) that cause damage to the small intestine in celiac disease. Some Triticum species of current concern include Triticum spelta (common names include spelt or spelta), Triticum polonicum (common names include Polish wheat, and, recently, Kamut), and Triticum monococcum (common names include einkorn and small spelt). I recommend that celiac patients avoid grain from these species.

Rye (Secale cereale) and barley (Hordeum vulgare) are also toxic in celiac disease even though these two species are less closely related to bread wheat than spelta and Kamut. They belong to different genera, Secale en Hordeum, respectively, and lack alpha-gliadins, which may be an especially toxic fraction. There have been anecdotal reports suggesting a lack of toxicity in celiac disease for spelta and Kamut. Controlled tests would be necessary to draw a firm conclusion, but I don't consider anecdotal reports as reliable for the following reasons.

The diagnosis, sometimes self-diagnosis, of celiac disease is occasionally made without benefit of reasonably rigorous medical or clinical tests, especially intestinal biopsy. Individuals who are "diagnosed" in this way without rigorous testing may not actually have celiac disease. Claims that particular foods cause this latter group no problems in relation to their celiac disease could cause confusion.

Furthermore, celiac patients who report no problems in the short run with spelta or Kamut will very likely relapse later. There is now adequate evidence that when celiac patients on a "gluten-free" diet (that is, a diet free of any proteins or peptides from wheat, rye, barley, and oats) have wheat reintroduced to their diets, times-to-relapse vary enormously among individuals, ranging from hours to months, or even years. And this is for wheat, presumably the most toxic of all cereal grains to celiac patients.

Additionally, the relapse may not be accompanied by obvious symptoms, but could be recognized only by physicians through observation of characteristic changes in the small intestinal tissues obtained by biopsy. The reasons for the enormous variability of response times are not known. It may be speculated that they have something to do with the degree of recovery of the lining of the small intestine on a gluten-free diet, the degree of stress that the patient had been experiencing (including infections), and individual genetic differences.

As I have indicated, all known grain species that cause problems for celiac patients are members of the grass family. In plant taxonomy, the grass family belongs to the Plant Kingdom Subclass known as monocotyledonous plants (monocots). The only other grouping at the Subclass level is that of dicotyledonous plants (dicots). Some other species about which celiac patients have questions actually are dicots, which places them in very distant relationship to the grass family. Such species include buckwheat, amaranth, quinoa, and rape. The seed of the last plant listed, rape, is not eaten, but an oil is pressed from the seeds that is becoming commonly used in cooking. This oil is being marketed as canola oil.

Because of their very distant relationship to the grass family and to wheat, it is highly unlikely that dicots will contain the same type of protein sequence found in wheat proteins that causes problems for celiac patients. Of course, some quirk of evolution could have given rise in these dicot plants to proteins with the harmful amino acid sequence found in wheat proteins. But if such concerns were carried to a logical conclusion, celiac patients would have to exclude all plant foods from their diets.

It may be in order to caution celiac patients that they may have undesirable reactions to any of these foods--reactions that are not related to celiac disease. Allergic reactions may occur to almost any protein, but there is a great deal of individual variation in allergic reactions, and there are possibly non-allergic food reactions, such as to the sulfites used to preserve certain foods, which further complicates the situation. Also, buckwheat, for example, has been claimed to contain a photosensitizing agent that will cause some people who have just eaten it to develop a skin rash when they are exposed to sunlight. Such reactions, apparently rare, should be looked for, but for most people, buckwheat eaten in moderation apparently does not cause a problem. (Buckwheat is sometimes found in mixture with wheat, which of course would cause a problem for celiac patients.) It seems no more necessary for all people with celiac disease to exclude buckwheat from their diets because some celiac patients react to it than it would be for all celiac patients to exclude milk from their diets because some celiac patients have a problem with digestion of milk sugar (lactose) or are allergic to milk proteins, such as lactalbumin. Buckwheat, quinoa, and amaranth have been reported to have relatively high levels of oxalic acid, almost as much as in spinach, and may not be suitable for very young children because the oxalic acid may cause gatrointestinal problems.

Some celiac patients may exhibit allergic reactions to gluten proteins or non-gluten proteins of wheat (and rye and barley), the alpha-amylase inhibitors being an example of the non-gluten proteins that can cause allergic reactions. Related inhibitor proteins can be found in rice as well. Alpha-amylase inhibitors might also interfere with starch digestion, causing symptoms similar to lactose intolerance in people with a weakened digestive capability. Celiac disease is thought to involve delayed immunoreaction and patients would not generally be expected to have an immediate and violent reaction to eating wheat whereas allergic reactions of the immediate hypersensitivity type might be both immediate and violent. It is also possible that both immediate hypersensitivity and delayed reactions might be present in the same person. There is a considerable potential then for confusion between allergy and celiac disease. It may be difficult to distinguish immediate hypersensitivity reactions or allergies from celiac disease as traditionally defined, but more research on this problem is needed.

In conclusion, scientific knowledge of celiac disease, including knowledge of the proteins that cause the problem, and the grains that contain these proteins, is in a continuing state of development. There is much that remains to be done. Nevertheless, steady progress has been made over the years. As far as I know, the following statements regarding various grains are a valid discrimination of the state of our knowledge:

  • Spelt or Spelta and Kamut are wheats. They have proteins toxic to celiac patients and should be avoided just as bread wheat, durum wheat, rye, barley, and triticale should be avoided.
  • Rice and corn (maize) are not toxic to celiac patients.
  • Certain cereal grains, such as various millets, sorghum, teff, ragi, and Job's tears are close enough in their genetic relationship to corn to make it likely that these grains are safe for celiac patients to eat. American wild rice is sufficiently closely related to normal rice that it is likely also to be safe. Significant scientific studies with celiac patients have not been carried out, however, for these grains.
  • There is no reason for celiac patients to avoid plant foods that are very distantly related to wheat. These include buckwheat, quinoa, amaranth, and rapeseed oil (canola). Some celiac patients might suffer allergies or other adverse reactions to these grains or foodstuffs made from them, but there is currently no scientific basis for saying that these allergies or adverse reactions have anything to do with celiac disease. A celiac patient may be lactose intolerant or have an allergy to milk proteins, but that does not mean that all celiac patients will have an adverse reaction to milk.

A list of my publications with pertinence to celiac disease follows. Cross-references to the literature for most of the points discussed above can be found in these publications.


Who Has the Guts for Gluten?

WE know that the proteins called gluten, found in wheat and other grains, provoke celiac disease. And we know how to treat the illness: a gluten-free diet. But the rapidly increasing prevalence of celiac disease, which has quadrupled in the United States in just 50 years, is still mystifying.

Scientists are pursuing some intriguing possibilities. One is that breast-feeding may protect against the disease. Another is that we have neglected the teeming ecosystem of microbes in the gut — bacteria that may determine whether the immune system treats gluten as food or as a deadly invader.

Celiac disease is generally considered an autoimmune disorder. The name celiac derives from the Greek word for “hollow,” as in bowels. Gluten proteins in wheat, barley and rye prompt the body to turn on itself and attack the small intestine. Complications range from diarrhea and anemia to osteoporosis and, in extreme cases, lymphoma. Some important exceptions notwithstanding, the prevalence of celiac disease is estimated to range between 0.6 and 1 percent of the world’s population.

Nearly everyone with celiac disease has one of two versions of a cellular receptor called the human leukocyte antigen, or H.L.A. These receptors, the thinking goes, naturally increase carriers’ immune response to gluten.

This detailed understanding makes celiac disease unique among autoimmune disorders. Two factors — one a protein, another genetic — are clearly defined and in most cases, eliminating gluten from the patient’s diet turns off the disease.

Yet the more scientists study celiac disease, the more some crucial component appears in need of identification. Roughly 30 percent of people with European ancestry carry predisposing genes, for example. Yet more than 95 percent of the carriers tolerate gluten just fine. So while these genes (plus gluten) are necessary to produce the disease, they’re evidently insufficient to cause it.

Animal studies have reinforced that impression. In mice engineered to express those H.L.A.’s, tolerance to gluten must be deliberately “broken.” Without an immunological trigger of some kind, the rodents happily tolerate the protein.

A recent study, which analyzed blood serum from more than 3,500 Americans who were followed since 1974, suggested that such a trigger could strike adults at any time. By 1989, the prevalence of celiac disease in this cohort had doubled.

“You’re talking about an autoimmune disease in which we thought we had all the dots connected,” says Alessio Fasano, head of the Center for Celiac Research and Treatment at the Massachusetts General Hospital for Children in Boston, and the senior author of the study. “Then we start to accumulate evidence that there was something else.”

Identifying that “something else” has gained some urgency. In the United States, improved diagnosis doesn’t seem to explain the rising prevalence. Scientists use the presence of certain self-directed antibodies to predict celiac disease. They have analyzed serum stored since the mid-20th century and compared it to serum from Americans today. Today’s serum is more than four times as likely to carry those antibodies.

BLAME for the increase of celiac disease sometimes falls on gluten-rich, modern wheat varietals increased consumption of wheat, and the ubiquity of gluten in processed foods.

Yet the epidemiology of celiac disease doesn’t always support this idea. One comparative study involving some 5,500 subjects yielded a prevalence of roughly one in 100 among Finnish children, but using the same diagnostic methods, just one in 500 among their Russian counterparts.

Beeld

Differing wheat consumption patterns can’t explain this disparity. If anything, Russians consume more wheat than Finns, and of similar varieties.

Neither can genetics. Although now bisected by the Finno-Russian border, Karelia, as the study region is known, was historically a single province. The two study populations are culturally, linguistically and genetically related. The predisposing gene variants are similarly prevalent in both groups.

Maybe more telling, this disparity holds for other autoimmune and allergic diseases. Finland ranks first in the world for Type 1 autoimmune diabetes. But among Russian Karelians, the disease is nearly six times less frequent. Antibodies indicative of autoimmune thyroiditis are also less prevalent, and the risk of developing allergies, as gauged by skin-prick tests, is one-fourth as common.

What’s the Russians’ secret?

“It’s a remote territory of Russia,” says Heikki Hyoty, a scientist at the University of Tampere in Finland. “They live like Finns 50 years ago.”

At the time of this research, roughly a decade ago, Russia’s per-capita income was one-fifteenth of Finland’s. Analysis of house dust and potable water suggests that the Russian Karelians encountered a greater variety and quantity of microbes, including many that were absent in Finland.

Not surprisingly, they also suffered from more fecal-oral infections. For example, three of four Russian Karelian children harbored Helicobacter pylori, a corkscrew-shaped bacterium, while just one in 20 Finnish children did. The bacterium can cause ulcers and stomach cancer, but mounting evidence suggests that it may also protect against asthma.

Professor Hyoty suspects that Russian Karelians’ microbial wealth protects them from autoimmune and allergic diseases by, essentially, strengthening the arm of the immune system that guards against such illnesses.

Meanwhile, Yolanda Sanz, a researcher at the Institute of Agrochemistry and Food Technology in Valencia, Spain, makes a compelling case for the importance of intestinal microbes.

Years ago, Dr. Sanz noted that a group of bacteria native to the intestine known as bifidobacteria were relatively depleted in children with celiac disease compared with healthy controls. Other microbes, including native E. coli strains, were overly abundant and oddly virulent.

How to determine cause or consequence?

In a test tube, she found that those E. coli amplified the inflammatory response of human intestinal cells to gluten. But bifidobacteria switched the response from inflammation to tolerance.

In rats, the E. coli again intensified inflammation to gluten, prompting what’s sometimes called a “leaky gut” — the milieu suspected of contributing to celiac disease. Conversely, bifidobacteria protected the intestinal barrier. Microbes, it seemed, could influence the immune response to gluten.

Bifidobacteria occur naturally in breast milk, which, along with protective antibodies and immune-signaling proteins, conveys hundreds of prebiotic sugars. These sugars selectively feed certain microbes in the infant gut, particularly bifidobacteria. Breast-fed infants tend to harbor more bifidobacteria than formula-fed ones.

All of which may explain a curious historical phenomenon — an “epidemic” of celiac disease that struck Sweden some 30 years ago. Anneli Ivarsson, a pediatrician at Umea University, recalled a sudden wave of “terribly sick” infants.

Sleuthing revealed that, just before the spike, official guidelines on infant feeding had changed. In an effort to prevent celiac disease, paradoxically, parents were instructed to delay the introduction of gluten until their babies were six months old. That also happened to be when many Swedish mothers weaned their children. Coincidentally, companies had increased the amount of gluten in baby food.

This confluence produced an unwitting “experiment with a whole population,” says Dr. Ivarsson — a large quantity of gluten introduced suddenly after weaning. Among Swedes born between 1984 and 1996, the prevalence of celiac disease tripled to 3 percent. The epidemic ebbed only when authorities again revised infant-feeding guidelines: keep breast-feeding, they urged, while simultaneously introducing small amounts of gluten. Food manufacturers also reduced the gluten content of infant foodstuffs. Dr. Ivarsson found that, during the epidemic, the longer children breast-fed after their first exposure to gluten, the more protected they were.

Not all subsequent studies have found nursing protective, but partly as a result of Sweden’s experience, the American Academy of Pediatrics now recommends that infants start consuming gluten while still breast-feeding.

Research by Dr. Sanz of Spain again illuminates how this may work. Some years back, she began following a cohort of 164 newborns with celiac disease in the immediate family. By four months, children with celiac-associated genotypes — 117 of them — had accrued a microbial community with fewer bifidobacteria compared to those without. If bifidobacteria help us tolerate gluten, these children appeared to be edging toward intolerance.

There was one notable exception: Breast-feeding “normalized” the microbes of at-risk children somewhat, boosting bifidobacterial counts.

Dr. Fasano of Boston has made another potentially important find. He followed 47 at-risk newborns, regularly collecting microbes from 16 of them, which he analyzed after two years. Like Dr. Sanz, he found these genetically at-risk children to accumulate a relatively impoverished, unstable microbial community.

But it’s a secondary observation that has Dr. Fasano particularly excited. Two of these children developed autoimmune disease: one celiac disease, another Type 1 diabetes, which shares genetic susceptibility with celiac disease. In both cases, a decline of lactobacilli preceded disease onset.

Assuming that the pattern holds in larger studies, “imagine what would be the unbelievable consequences of this finding,” he says. “Keep the lactobacilli high enough in the guts of these kids, and you prevent autoimmunity.”

The caveats here are numerous: the tiny sample size in Dr. Fasano’s study Dr. Sanz hasn’t yet revealed who actually developed celiac disease in her cohort and even if these microbial shifts reliably precede disease onset — as they do in larger studies on allergic disease — they’re still bedeviled by the old “chicken or the egg” question: Which comes first, the aberrant microbial community, or the aberrant immune response?

Bana Jabri, director of research at the University of Chicago Celiac Disease Center, notes that immune disturbances change the microbial ecosystem. But here’s the catch: Even if the chicken comes first, she says, the egg can contribute. Rodent experiments show that intestinal inflammation can select for unfriendly bacteria that further inflame. “You can have a positive feedback loop,” she says.

SO your microbes change you, but your genes also shape your microbes — as do environment, breast milk, diet and antibiotics, among many other factors.

Such complexity both confounds notions of one-way causality and suggests different paths to the same disease. “You have the same endpoint,” Dr. Jabri says, “but how you get there may be variable.”

The intricacies don’t stop there.

Not all breast milk is the same. It varies according to diet and other factors. One study found that milk from overweight mothers had fewer of those bifidobacteria than milk from thinner mothers. Another observed that breast milk from farming mothers, who inhabit a microbially enriched environment, carried more anti-inflammatory proteins compared with urban mothers’ milk. “All these things are going to matter,” Dr. Jabri says. And they’re all potential nudge points in the quest to prevent disease.

The tangled web of possibilities should not, however, distract us from the facts on the ground. In a far-flung corner of Europe, people develop celiac disease and other autoimmune diseases as infrequently as Americans and Finns did a half-century ago. The same genes exposed to the same quantity of gluten do not, in that environment, produce the same frequency of disease.

“We could probably prevent celiac disease if we just give the same environment to the Finnish children as they have in Karelia,” says Dr. Hyoty. “But there’s no way to do it now, except to move the babies there.”


Should you go gluten-free?

If you feel you might be suffering from some of the above mentioned symptoms of gluten intolerance, it might help to take a break from gluten for a little while. At Parsley Health, to assess your tolerance to gluten we recommend a four to six week elimination of gluten and other commonly inflammatory foods from the diet to be followed by a reintroduction to “challenge” how you react.

To eliminate gluten, remove all refined grains and processed foods from the diet including bread, baked goods and pastas along with processed foods that sneakily contain gluten such as salad dressings, cheese, soy sauce and most beer. It’s important to remember that new fad foods labelled ‘gluten-free’ tend to be processed and usually incredibly high in sugar and carbs, which could make inflammation worse so it’s best to stick to naturally gluten-free foods such as fresh fruit, vegetables, beans, legumes, nuts, seeds, fish, seafood, meat and poultry. After the elimination period, talk to your doctor and a health coach about reintroduction and the right balance of gluten in your diet for overall health.

Even if you do not think you have an intolerance, there is some evidence to suggest that the gluten component gliadin increases inflammation in the digestive tract that can contribute to intestinal permeability or “leaky gut.” This can cause bacteria and other toxins to seep through the intestine into the rest of the body. If the tight junctions that seal the intestine are chronically opened, it can contribute to long-term issues like brain fog, bloating, and joint pain.

Test tube studies have shown that when intestinal cells are exposed to gluten, intestinal permeability occurs in all samples — not just those with a known sensitivity. This study suggests that gluten may promote inflammation and leaky gut in everyone. In clinical studies, gluten was shown to increase leaky gut in patients with irritable bowel syndrome (IBS) while other research found that intestinal permeability only occurred in those with CD, NCGS or IBS but not others.

While individuals with Celiac disease, non-Celiac gluten sensitivity and irritable bowel syndrome clearly have a greater extent of intestinal permeability that occurs when consuming gluten, because there is some evidence to suggest gluten is generally inflammatory it’s worth considering how much, how often and what types of gluten you’re consuming to ensure optimal gut and overall health. The truth is that everyone’s body is different and that’s exactly why we practice personalized medicine and do high-tech speciality testing here at Parsley Health to figure out what works best for you.

Credentials: Internal Medicine Physician • Institute for Functional Medicine Practitioner Training Institutions: Summa Cum Laude Graduate of the University of Pennsylvania • Columbia University’s College of Physicians and Surgeons • Internal Medicine Residency at Mount Sinai Hospital in New York City • Institute for Functional Medicine Clinical Interests: Thyroid & Adrenal Health • Autoimmune Disorders • Gastrointestinal Health • Biology of Stress • Cancer Prevention • Fertility Optimization Previous and Additional Positions: Founder and CEO of Parsley Health. Co-founded the&hellip

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Kyk die video: COELIAKIE, HELP! GLUTEN BINNEN GEKREGEN?! . VLOG #12. Aniek Vogel (Januarie 2022).