Shari Lieberman, Ph.D., C.N.S., F.A.C.N.

Gluten sensitivity (GS) is often used interchangeably orconfused with celiac disease (CD). Celiac disease(gluten-sensitive enteropathy), also known as celiac

sprue, is increasingly viewed as a subcategory of gluten insensi-tivity, along with other subcategories with a large degree of over-lap, such as rheumatologic, endocrinologic, dermatologic, andneuropsychiatric problems.

In early childhood, CD symptoms include chronic diarrhea,abdominal distension, and failure to thrive.1 Patients diagnosedlater in life have anemia, fatigue, weight loss, diarrhea, and neu-rologic symptoms.2 When the microscopic villi in the smallintestines are destroyed and flattened, large molecules such asantigliadin antibodies, the endomysial antibody, and antitissuetransglutaminase (anti-tTG) can be passed through the intestinalbarrier into the bloodstream. Currently, measurement of any twoor more of these molecules is used as a diagnostic tool for CD.

In addition, a positive result on an intestinal biopsy will onlyoccur when the villi are destroyed. Even if inflammation isseen in a biopsy, unless the villi are destroyed and flattened,the biopsy result will be considered either negative or incon-clusive.

A survey of nine commercial laboratories across the UnitedStates revealed that testing for the endomysial antibody yieldedpositive results in only 77 percent of cases with total villous atro-phy as confirmed by biopsy.

In patients with partial villous atrophy, positive cases droppedto 33 percent. These diagnostic tools are the “gold standard” fordiagnosing CD. There are numerous problems with these diag-nostic methods such as:3

1. CD does not occur quickly. It takes weeks, months, or years fortotal villous destruction to happen. Therefore, without totalvillous destruction, the “gold standard” of testing will yieldnegative results.

2. The inability to diagnose CD early (e.g., before villi destruc-tion) can result in irreparable damage to the patient.

3. CD is a disease only limited to the small intestines. However,the degree of symptomatology does not correspond to whetheror not one has a positive CD test result. A person can havesevere symptoms but not have enough destruction of the villi

to yield a positive test.4–18 More mild gastrointestinal (GI)symptoms rarely cause doctors to order any testing for CD.

4. GS occurs before diagnosis of CD. In patients who are sensitiveto gliadin, gluten should be removed from the diet immediately.However, this will rarely occur unless there is a positive testresult for CD.

5. GS can be associated with other serious conditions, such asautoimmune disease, autism, and neurologic illness withoutCD or any GI symptoms.

6. More than 90 percent of patients who develop CD carry theHLA DQ2 haplotype with virtually all remaining patients withCD carrying the HLA DQ8 haplotype. Surprisingly, 20–30 per-cent of the background populations will be either HLA DQ2and/or HLA DQ8 positive.This genetic screening is readily available and should be donepreferably at birth. It is a simple screening measure that isavailable for everyone and is rarely used unless CD is diag-nosed first or a family member is diagnosed with CD.

7. In a recent study on patients with CD whose biopsy specimenswere positive for serum antibodies, 35 percent had total villousatrophy, 25 percent had severe villous atrophy, and 25 percenthad mild atrophy. None of the patients with CD biopsy specimens that were nega-tive for serum antibodies had total or severe villous atrophy. Theauthors concluded that anti-tTG assay of the culture medium ofbiopsy specimens can increase the accuracy of a diagnosis of CDin patients who test negative for serum antibodies.19

8. CD prevalence is estimated to be 1 in every 100 people. Therehas been a dramatic increase in the rate of new cases in theUnited States. Women in their 40s, 50s, and 60s are most likelyto be affected.4 This suggests that environmental factors (e.g.,food, medications, pollutants) rather than simply genetics areplaying a role.

For someone to develop full-blown CD, she or he must haveGS. GS is not picked up via standard laboratory and biopsy anal-ysis but is presumed to occur if going on a gluten-free dietrelieves symptoms. Even with food allergy panels, GS may bemissed because it does not necessarily result in a classicimmunoglobulin (Ig)E or IgG reaction.

GS can result in activation or suppression of the immune sys-tem and can cause inflammation that can destroy tissue and cells.In fact, the immune dysregulation that occurs as a result of GS is

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Gluten SensitivityThe Hidden Epidemic

poorly understood2 and largely overlooked. GS produces anautoimmune reaction. This article reviews the literature examin-ing the roles of CD and GS in numerous conditions, some ofwhich, if left untreated, could be disabling and/or fatal.

Autism

The mechanisms behind the autoimmune reaction to nervous-system antigens in autism are not understood. In a study on 50patients who had autism and 50 controls (without autism) thereactivity to gliadin peptides was assessed. A significant percent-age of patients with autism (greater than 60 percent) showed ele-vations in antibodies against gliadin and cerebellar peptidessimultaneously.

Certain dietary proteins formpeptides, including casomorphinsfrom casein and gluteomorphinsfrom gluten, which are consideredto be opioid peptides. These opioidpeptides can st imulate T-cells ,induce pept ide-speci f ic T-ce l lresponses, and produce abnormallevels of cytokine production, whichmay result in inflammation, autoim-mune reactions, and disruption ofneuroimmune communications.

Peptides from inadequate digestion of casein and gluten areapparently absorbed in excess by autistic children; this is mani-fested in their very high levels of urinary peptides.5

In a study, data were collected from more than 23,700 parentsof autistic children who completed questionnaires from theAutistic Research Institute.6 The parents rated the children’sresponses to various types of treatment, including drug treat-ment, dietary supplementation, and dietary modification. Theratings, which were on a six-point scale, were combined intothree categories: “made worse” (ratings 1 and 2), “no effect” (rat-ings 3 and 4), and “made better” (ratings 5 and 6).

The highest rating of any diet in the “Special Diet” categorywas for gluten-casein free. Sixty-five (65) percent of parents whoresponded said that children “got better” when both gluten andcasein were removed from their diets.6 To put this in perspective,use of Ritalin resulted in 29 percent of parents rating their chil-dren with autism as “got better.” Removal of gluten and caseinresulted in a higher response rate (65 percent!) than any otherknown therapy for autism.

Neurologic Illness

A systematic screening of 143 patients with idiopathic ataxiashowed that 41 percent had gluten sensitivity as defined by the pres-ence of antigliadin antibodies in their blood.7 The mean age onset ofthe ataxia was 54 but the researchers have also seen this disorder inpatients under 20 years of age, although much less frequently.

Ataxia tends to progress slowly but, in some cases, it can take avery rapid course. If gluten is not removed from the diet quickly,a patient may have permanent neurologic damage from gluten

although the disease will generally stop progressing, accordingto the researchers. Other manifestations of gluten sensitivity,including peripheral neuropathy and myopathy, were also docu-mented. The authors of the study clearly stated that gluten sensi-tivity may not have any bowel involvement and the fact that it isregarded principally as a disease of the small intestine is a “his-torical” misconception.7

The study authors recognized the limitations of testing forendomysium and transglutaminase antibodies as well as intesti-nal biopsies, and suggested screening patients with neurologicdisease for antigliadin antibodies.7

Once again, many patients will be missed because these largepeptides only pass through the intestinal barrier if the villi havebeen severely compromised. However, the authors did suggest

trying a gluten-free diet in any caseand a lso descr ibed a group ofpatients that may still be hypersen-sitive to minute amounts of glutenin “gluten-free” products.7

F o r t h e s e h i g h l y s e n s i t i v epatients, the authors suggestedstaying on the diet longer andremoving gluten from the dietcompletely. They also reviewed35 papers of single or multiplecase reports from 1964 to 2000

that showed ataxia and peripheral neuropathy as the mostcommon neurologic manifestations seen in patients withestablished CD.

Multiple Sclerosis

Multiple sclerosis (MS) is a debilitating neurologic diseasewithout a known cause. However, immunologic changes foundin this disease are thought to reflect an autoimmune reaction ingenetically susceptible individuals. Antibodies that bind to thebrain’s basic myelin protein have been detected, and peptidesfrom myelin basic protein can induce experimental demyelinat-ing encephalitis in animal models.

Antibodies in serum against gliadin and gluten have a highaffinity for the brain barrier vasculature. IgA antibodies in serumagainst gliadin have been found in patients with ataxia andperipheral neuropathy.

In a study, researchers measured IgA antibodies to somecommon food antigens in 36 patients with MS as well as IgGagainst gliadin and gluten and compared them to controlpatients without MS.8 There was a highly significant increasein serum IgA and IgG antibodies against gliadin and gluten inp a t i e n t s w h o h a d M S c o m p a r e d t o t h e c o n t r o l s . T h eresearchers also found a significant increase in IgA and IgGantibodies against casein in the patients with MS compared tocontrols.

The study authors wrote that the longer a person is exposed togluten in CD, the greater that person will have a risk of develop-ing an autoimmune disorder. The authors also discussed otherneurologic diseases, such as gluten–gliadin related epilepsy, and

152 ALTERNATIVE & COMPLEMENTARY THERAPIES—AUGUST 2006

Removal of gluten and casein in the

diet resulted in a higher response rate

(65 percent!) than any other known

therapy for autism.

stated how important it is to remove gluten from the diet. Noneof these patients who had MS were diagnosed with CD.8

Reports of MS, demyelination (D), and optic neuritis (ON)associated with anti-tumor necrosis factor–α (TNF-α) therapyresulted in warnings on prescribing instructions for infliximab,etanercept, and adalimumab. However, the underlying relation-ship between irritable bowel disease (IBD) and these neurologicconditions has not been established.

Researchers performed a retrospective cohort study and a ret-rospective cross-sectional study using 1988 to 1997 data from theGeneral Practice Research Database.9 A total of 7988 patientswith Crohn’s disease and 12,185 patients with ulcerative colitiswere matched for age, gender, and primary care practice to80,666 randomly selected controls.

In the cohort study, incident cases of MS, demyelination,and/or ON (MS/D/ON) had to occur at least 1 year after regis-tration with the physician and after the diagnosis of IBD. In thecross-sectional study, the diagnosis of MS/D/ON could eitherprecede or follow the IBD diagnosis.

In the cohort study, the incidence of MS/D/ON was higher inpatients with Crohn’s disease and ulcerative colitis compared totheir matched controls, reaching statistical significance for ulcera-tive colitis (ulcerative colitis incidence rate ratio [IRR], 2.63; 95percent confidence interval [CI], 1.29–5.15; Crohn’s disease IRR,2.12; 95 percent CI, 0.94–4.50).

In the cross-sectional study, MS/D/ON was more prevalent inpatients with Crohn’s disease and ulcerative colitis comparedwith their matched controls (Crohn’s disease odds ratio [OR],1.54; 95% CI, 1.03–2.32; ulcerative colitis OR, 1.75; 95% CI,1.28–2.39).

The authors concluded that demyelinating diseases occur morecommonly among patients with IBD than among patients whodo not have IBD. Future studies should clarify whether treatmentwith TNF-α blockers results in further increased incidence ofMS/D/ON among patients with IBD. However, there was nomention of CD or GS.9

Systemic Lupus Erythematosus

In a case report, 3 patients were described who were originallydiagnosed with systemic lupus erythematosus (SLE).10

Case 1A 20-month-old girl had poor weight gain, intermittent

malaise, and sweating. Her parents reported that she developeda facial rash upon exposure to the sun. Her erythrocyte sedimen-tation rate (ESR) and antinuclear antibodies (ANA) were elevat-ed; she had an IgA deficiency, and she tested positive forsmooth-muscle antibodies and raised cardiolipin antibodies.

She was diagnosed with SLE and immediately started onsteroids. By age 4, she had poor enamel on her teeth and requiredteeth extractions. By age 6, she developed more side-effects fromthe steroids, and she was given another drug (azathioprine). Byage 17, she was referred to an adult SLE clinic. She tested positivefor antigliadin antibodies and a biopsy confirmed gluten-sensi-tive enteropathy (CD).

She started a gluten-free diet, stopped her medications, and,after 6 months, she was completely asymptomatic and her labo-ratory values returned to normal.

Case 2A 53-year-old woman had developed early symptoms of blurred

vision, headache, and generalized weakness at the age of 20. Sheimproved spontaneously but then developed the same symptoms 1year later and was treated with adrenocorticotropic hormone.Three (3) years later she was admitted to a hospital with heavinessof her legs, asthenia, and recurrent severe headaches. A computedtomography (CT) scan of her brain yielded normal results, her anti-cardiolipin antibodies were slightly raised, her rheumatoid factorwas raised, and magnetic resonance imaging of her brain showedextensive white matter abnormalities not typical of MS.

In view of her immunologic picture and the presence of circu-lating anticardiolipin antibodies, she was diagnosed with SLEwith an associated antiphospholipid syndrome. She was givenaspirin for her headaches and asthenia.

A few years later, she reported that she had generalizedarthralgia. She was treated with steroids and methotrexate. Shecontinued to experience severe headaches and fatigue. She tested

ALTERNATIVE & COMPLEMENTARY THERAPIES—AUGUST 2006 153

Wheat is one of the grains that should be removed in a gluten-free diet.

positive for antigliadin antibodies and had a positive intestinalbiopsy. She also tested positive for HLA DQ2.

After 6 months on a gluten-free diet, she was in completeremission and was able to stop taking all of her medications.

Case 3A 54-year-old woman had originally presented at age 40 with

persistent headaches. She had a raised erythrocytes sedimenta-tion rate (ESR) and mild neutropenia. The results of a temporalartery biopsy were normal as washer CT brain scan. Two (2) yearslater, she developed epigastric pain.Her abdominal ultrasound and gas-troscopy tests had normal results.She had a raised ESR, high globu-lins, a negative antinuclear factor(ANF), and abnormal liver transam-inases. Her abdominal CT scan results were normal.

Nine (9) years later, she was diagnosed with urticaria. Her lab-oratory findings were: elevated ESR; elevated double-strandedDNA; negative ANF; positive rheumatoid factor; neutropenia;and raised anticardiolipin levels. Her main complaints wereheadache and abdominal discomfort.

She was diagnosed with SLE based on the findings of thisextensive battery of testing and she was treated with aspirin. One(1) year later, her colonoscopy results were normal. She receivedanother battery of tests, which included testing for antigliadinantibodies. The test result was positive as was her test for HLADQ2. She refused a biopsy.

Several months after starting a gluten-free diet, her symptomscompletely subsided. Her ESR returned to normal.

Researchers’ Conclusions on the Three Case StudiesThe authors concluded that these patients were misdiagnosed

with SLE. While the researchers recognized that GS does nothave to manifest with GI symptoms, they sti l l rel ied onantigliadin antibodies to make their diagnoses.10

Systemic Lupus Erythematosus and Celiac DiseaseA similar paper11 documented 5 patients with SLE who were

diagnosed with CD. All 5 patients had positive biopsy results,while only 4 patients had positive results on serologic tests forCD and 3 patients had abdominal symptoms. The researchersnoted further that the SLE–CD combination is infrequent. Theycited a study from Texas on the prevalence of CD among patientswith SLE. Of 103 patients, only 24 had antibodies to gliadin andnone had antibodies to endomysium. These authors also report-ed that the patients had poor compliance with a gluten-free diet.

Psoriasis

Researchers observed a few patients with psoriasis who hadIgA antibodies to gliadin and normal duodenal biopsy resultsexperienced a marked improvement of their psoriasis when theyadhered to a gluten-free diet and a worsening of symptoms whentheir normal diets were resumed.

In a previous screening study, 16 percent of 302 patients withpsoriasis had IgA and/or IgG antibodies to gliadin (AGA). Theaim of the newer study12 was to evaluate the effect of a gluten-free diet in 33 AGA-positive and 6 AGA-negative patients withpsoriasis. Of the 33 AGA-positive patients, two had IgA antibod-ies to endomysium (EmA) and 15 had an increased number oflymphocytes in the duodenal epithelium, but in some patientsthis increase was slight. Two patients had villous atrophy.

A 3-month period on a gluten-free diet was followed by 3months on the patients’ ordinarydiets. The severity of psoriasis wasevaluated with the Psoriasis Areaand Severity Index (PASI). Theexamining dermatologists wereunaware of the EmA and duodenalbiopsy results throughout thestudy.

Thirty (30) of the 33 patients with AGA completed the gluten-free diet period, after which they had a highly significantdecrease in mean PASI. This included a significant decrease inthe 16 AGA-positive patients with normal routine histology induodenal biopsy specimens. The AGA-negative patients did notexperience any improvement. After the gluten-free diet, the AGAvalues were lower in 82 percent of the patients who improved.There was a highly significant decrease in serum eosinophilcationic protein in patients with elevated AGA.

When the ordinary diet was resumed, the psoriasis worsenedin 18 of the 30 patients with AGA who had completed the gluten-free diet period. In conclusion, patients with psoriasis who haveraised AGA might improve on a gluten-free diet even if theyhave no EmA or if the increase in duodenal intraepithelial lym-phocytes is slight or seemingly absent.12

Arthritis

Arthritis may be a presenting symptom in silent adult CD. It isconsidered to be “silent” because the patient does not have anyGI complaints. Researchers have documented 2 cases of persist-ing arthritis that were misdiagnosed and in which the patientsactually had silent CD.13 The authors have reported on othercases demonstrating rheumatoid arthritis, ankylosing spondyli-tis, and arthropathy associated with CD; the two case historiesare described below.

Case 1A 50-year-old man suffered from dermatitis on his legs for

some time. He experienced a 7-kg weight loss and did not haveany GI. He was admitted to a hospital with a slight fever and aswollen and tender knee. His synovial fluid revealed a fewleukocytes and his bacterial and blood cultures were negative.The patient’s fever subsided but his knee complaint persisted.

His C-reactive protein (CRP) was elevated and he had slightmacrocytic anemia. His folate, internal coagulation factors, andalbumin levels were low. Malabsorption resulting from silent CDwas suspected. Tests for his endomysium and IgA antigliadinantibodies were positive. His endoscopy showed flat mucosa and

154 ALTERNATIVE & COMPLEMENTARY THERAPIES—AUGUST 2006

Arthritis may be a presenting

symptom in silent adult CD.

a biopsy of the small intestine revealed lymphocytic infiltrationof the lamina propria and an absence of villi. He was diagnosedwith CD and a gluten-free diet was instituted.

Within a few months, his arthritis completely cleared with nor-malization of his laboratory test results and a complete disap-pearance of the dermatitis.

Case 2A 21-year-old female suffered from low-back pain for 3

months. She had had some GI symptoms since childhood andtenderness in her sacroiliac joint, which was relieved by a localintra-articular steroid injection. An X-ray and a CT scan revealedno abnormalities. Blood tests did not reveal inflammation. Hersymptoms persisted for 1 year.

She returned for laboratory testing and her results showedtransient leukopenia and a low vitamin B12 level. Her IgA anti-bodies to endomysium were positive and an intestinal biopsyshowed villous atrophy. A diagnosis of CD was made and thepatient followed a gluten-free diet for 1 year. Her low-back painsubsided in 1 month. On two occasions, when she ignored herdiet, she experienced abdominal discomfort and return of low-back pain.

Insulin-Dependent Diabetes

The association between CD and insulin-dependent diabetesmellitus (IDDM) is well-established. Rectal challenge has beenused in patients with CD as a tool to assess the mucosal responseto gluten.

In a study, rectal biopsies were obtained from 19 children withIDDM before and 6 hours after a rectal challenge with 2 g of pep-tic tryptic digest of gliadin. It was found that 20 percent of thesechildren reacted to rectal installation of gliadin. However, theresearchers did not follow up with a report on instituting agluten-free diet and the outcome.14

In another study,15 researchers examined the effect of a gluten-free diet on growth and diabetic control in 21 children with type1 diabetes and CD. A gluten-free diet resulted in a significantincrease in weight-for-age scores and body–mass index com-pared to control patients who had IDDM but did not have CD.

Insulin dosage at diagnosis was less in the patients with CDthan in the controls with IDDM without CD but was similar oncea gluten-free diet was established (the authors did not commenton why this happened). The authors concluded that identifica-tion and dietary treatment of CD in children with diabetesimproved growth and inf luenced diabet ic control . Theresearchers also cited other studies showing that a gluten-freediet improved growth and diabetic control.15

Other Conditions Associated with Celiac Disease

Other disorders associated with CD include dermatitis herpeti-formis, hyposplenism, bird fancier lung, Sjögren’s syndrome, pri-mary biliary cirrhosis, autoimmune thyroid disease, Addison’sdisease, recurrent apthous ulcers, autoimmune hepatitis, autoim-mune endocrine disease, microscopic colitis, dermatomyositis,

alopecia areata, asthma, chronic liver disease, osteoporosis,Down’s syndrome, and female infertility. Patients with CD havea significantly higher risk of autoimmune disease than the gener-al population.16–18

Discussion

There appears to be continuing confusion by practitioners andscientists about the difference between GS and CD. The distinc-tion is often blurred in published papers by referring to GS as thecause of an illness2–4,7–17 but only confirming its existence byusing the diagnostic criteria for CD. As previously stated, thediagnosis of CD can only be ascertained by positive antibodies togluten along with a positive endomysial antibody and/or posi-tive anti-tTG antibodies. It is generally necessary also to havepositive intestinal biopsy results although “silent CD” is referredto when the blood tests have positive results and the intestinalbiopsy has negative ones.13

ALTERNATIVE & COMPLEMENTARY THERAPIES—AUGUST 2006 155

Tell Your PatientsHow to Stay on a Gluten-Free Diet

AvoidDo not consume foods, beverages, or medications containing:

• Wheat• Barley• Rye• Oats (accept gluten-free oats).

Avoid all items made with flour (all-purpose, white, and wheat),including pasta, bread, pancakes, bagels, waffles, pizza, cakes, cookies,pie, croutons, most cereals, breaded foods, stuffing, gravies, crackers,most soups, and most convenience foods.

Less-obvious foods include communion host; soy, teriyaki, andmany other sauces and marinades; some salad dressings; beer; andsome candy.

Read all food labels to check for wheat and barley, which are bothused widely.

Beware of cross-contamination. Naturally gluten-free items maybecome contaminated by sharing transportation, a production line, afryer, or a grill with a grain such as wheat.

Special planning and calling ahead may become important mea-sures for eating at restaurants and social gatherings.

Food sourcesStaples of the gluten-free diet include:

• Fruits and vegetables • Meat• Milk-based items • Potatoes, rice, corn, and beans • Cereals made without wheat or barley malt • A wide variety of specialty foods (such as pasta, bread, pancakes,

and pastries) made with alternative grains (rice, tapioca, or cornflours and starches), purchased commercially or made fromscratch.

Source: http://www.nlm.nih.gov/medlineplus/ency/article/002443.htm#Recommendations

The problem is the complete lack of scientific reviewing andlack of understanding by the researchers themselves as manifest-ed by their not recognizing that GS and CD are two distinct con-ditions. While both share common disease associations, GSoccurs well before there is any manifestation of CD, as evidencedby older patients being diagnosed with CD rather than beingdiagnosed with CD as children.4,7–13

Unless someone at least tests positive for antigliadin antibod-ies, the diagnosis of GS will be ruled out. This is disturbing,given the fact that GS may, indeed, be present.1,2,18 As discussedin several of the papers reviewed,7,8,10,12–15,18 it is generallyaccepted that many patients with GS and those with “silent CD”do not have any GI symptoms or abnormal biopsy results.

Furthermore, it is clear from the available scientific evidencethat the intestine is not the only tissue targeted by the immunereaction to gluten.3,5,6–18 Given the statistics of 1 of every100Americans having CD, the number of individuals with GS couldpotentially be significantly higher.18 In addition, many patientswho are sensitive to gluten appear to have a cross-reactivity tocasein, so removal of dairy products from these patients’ dietsmay be prudent.5,7,18

Several researchers concluded that patients have had “incor-rect” diagnoses for many years, as evidenced in the case studieson SLE.10,11

I believe that all the patients described in this paper were diag-nosed correctly but the cause of their illness was GS. In my per-sonal clinical experience, I have witnessed, at first-hand,complete remissions of MS, SLE, attention-deficit disorder,autoimmune hepatitis, Darier’s disease, Crohn’s disease, andulcerative colitis—just to name a few conditions—when patientswere put on a gluten-free diet and adhered to it strictly.

I have also seen relapses in these patients when they went offthe gluten-free diet. In numerous patients, the relapse tookmonths or years to surface. This suggests further that theimmune reaction to gluten is not an overnight phenomenon.Many of these patients required dietary removal of casein also togain complete remissions.

There are no nutrients specific to wheat, rye, and barley thatrequire them to be part of a diet for balanced nutrition. Removal ofthese grains from the diet poses no danger to adults, adolescents,children, or infants. Oats can be contaminated with wheat, so onlygluten-free oats should be used. There is absolutely nothing to loseby trying a gluten-free diet with a patient for at least 3 months.

It is my opinion that, if a gluten-free diet is tried early when thereis a diagnosis of autoimmune disease, autism, and other severe dis-eases such as IDDM, permanent organ or tissue damage may beprevented or at least minimized and remission may be achieved. ■

References1. Kim CY, Quarsten H, Bergseng E, et al. Structural basis for HLA-DQ-2mediated presentation of gluten epitopes in celiac disease. PNAS2004;101:4175–4179.

2. Schuppan D, Hahn EG. Gluten and the gut—lessons for immune regu-lation. Science 2002;297:2218–2220.3. Howdle PD, Robins GG. Advances in celiac disease. Curr Opin Gas-troenterol 2005;21:152–161.4. Anonymous. Celiac disease: An intolerance to gluten. Mayo ClinicWomen’s Healthsource 2004;8:6.5. Vojdani A, O’Bryan T, Green JA, et al. Immune responses to dietaryproteins, gliadin and cerebellar peptides in children with autism. NutrNeurosci 2004;7:151–161. 6. Autism Research Institute. Parent ratings of behavioral effects of biomedi-cal interventions. Online document at: www.autismwebsite.com/ari/treatment/form34q.htm Accessed March 2005.7. Hadjivassiliou M, Grunewald RA, Davies-Jones GA. Gluten sensitivityas a neurological i l lness. J Neurol Neurosurg Psychiatry 2007;72:560–563.8. Reichelt KL, Jensen D. IgA antibodies against gliadin and gluten inmultiple sclerosis. Act Neurol Scan 2004;110:239–241.9. Gupta G, Gelfand JM, Lewis JD. Increased risk for demyelinating dis-eases in patients with inflammatory bowel disease. Gastroenterol2005;129:819–826.10. Hadjivassiliou M, Sanders DS, Grunewald RA, et al. Gluten sensitivitymasquerading as systemic lupus erythematosus. Ann Rheum Dis2004;63:1501–1503.11. Zitouni M, Daoud W, Kallel M, et al. Systemic lupus erythematosuswith celiac disease: A report of five cases. Joint Bone Spine 2004;71:344–346. 12. Michaelsson G, Gerden B, Hagforsen E, et al. Psoriasis patients withantibodies to gliadin can be improved by a gluten free diet. Br J Dermatol2000;142:44–51.13. Slot O, Locht H. Arthritis as presenting symptom in silent adult celiacdisease. Scan J Rheumatol 2000;29:260–263.14. Roncone R, Franzese A, Mazzarella G. Gluten sensitivity in a subset ofchildren with insulin dependent diabetes mellitus. Amer J Gastroenterol2003;98:592–595.15. Saadah OI, Zacharin M, O’Callaghan A, et al. Effect of gluten-free dietand adherence on growth and diabetic control in diabetics with celiac dis-ease. Arch Dis Child 2004;89:871–876.16. James MW, Scott BB. Coeliac disease: The cause of the various associ-ated disorders? Gastroenterol Hepatol 2001;13:1119–1121. 17. Viljamaa M, Kaukinen K, Huhtala H, et al. Coeliac disease, autoim-mune diseases and gluten exposure. Scand J Gastroenterol 2005;40:437–443.18. Fine K. Early diagnosis of gluten sensitivity: Before the villi are gone[transcript of talk given to Greater Louisville Celiac Sprue SupportGroup, June 2003]. Online document at: www.enterolab.com/StaticPages/EarlyDiagnosis.htm19. Carroccio A, Di Prima L, Pirrone G, et al. Anti-transglutaminase anti-body assay of the culture medium of intestinal biopsy specimens canimprove the accuracy of celiac disease diagnosis. Clin Chem 2006;52:1175–1780.

Shari Lieberman, Ph.D., C.N.S., F.A.C.N., is a research scientist, authorand industry consultant based in Pompano Beach, Florida. She is theFounding Dean of New York Chiropractic College’s (Seneca Falls, NewYork) M.S. Degree Program in Applied Clinical Nutrition.

To order reprints of this article, write to or call: Karen Ballen, ALTERNA-TIVE & COMPLEMENTARY THERAPIES, Mary Ann Liebert, Inc., 140Huguenot Street, 3rd Floor, New Rochelle NY 10801, (914) 740-2100.

156 ALTERNATIVE & COMPLEMENTARY THERAPIES—AUGUST 2006