EFFECTSOFRHEUMATOIDARTHRITISONNUTRITIONALSTAT

RHEUMATOIDARTHRITIS
Definition

RA is an inflammatory disease of the synovial lining of the joint and results in pain, stiffness, swelling, jointdam age, and lossoffunction.Inflammationmostoftenaffectsjointsofthehandsand feet and tends to be symmetrical. This symmetry helps distinguish RA from other forms of the disease. Approximately 1% of the population has RA. Patients with RA may have excess death, radiographic deterioration of joints, and reduced functional status, despitediseasemodifying antirheumaticdrug(DMARD)treatment. MechanismsAffectingNutritionalStatus RA can affect nutritional status through several mechanisms. Joint swelling and tenderness can impairtheabilityto prepare food,involvement of thetemporomandibular joint canimpair chewing, and general joint involvement can impair selffeeding. In addition, patients may have xerostomia that can impair food intake. Many ofthe pharmacologic therapiesusedto treat RA alsohave side effects that further impair food intake, such as nausea with MTX orproteolysis with corticosteroid therapy. The catabolic and inflammatory aspects of thediseasealso affect nutritional status. Table91.3displaysmechanismsbywhichRAmayaffectnutritionalstatus. NutrientIntakesandVitaminConcentrationsinPatientswithRheumatoidArthritis In 1943, 31 patients with RA were evaluated to deter mine their dietary history for the year before onset. Although their dietary intakes were not substantially different from those of a crosssection offamiliesin theNorthAtlantic States,more than twothirdsofpatientshaddietsthat werelowin calcium,thiamine,and riboflavin,andapproximately50%hadlowintakeofvitaminC.In 1996, Kremer found that patients with RA had diets that were high in total fat, low in fiber, and deficient in micronutrients. Among 41 patients with active RA, diets were low in pyridoxine, zinc, magnesium,folate,andcopper. Morganetalevaluatedthenutrientintakeandstatusof32MTXtreatedadultswithRA. Intakes of pyridoxine, calcium, magnesium, and zincwerelessthan33%ofthe1989RDA.Thirty percent had deficient plasmafolate,and 23%haddeficient erythrocytefolatebeforestartingMTX therapy. In a subsequentstudy, 79 patients (meanage,53years mean disease duration,9 years) were followed for 1 year after starting MTX therapy. Based on theaverage offive24hourdietary recalls, the patients consumed less than 67% of the recommended dietary intake for folate, vitaminB12,vitaminE,calcium, iron,magnesium,copper,andzinc.BeforethestartofMTXtherapy, 47% of patients had deficient plasma folate and 11% had deficient erythrocyte folate concentrations.

TABLE91.3ADVERSE Increasednutrientrequirements

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Increasedmetabolismandnitrogenlossesincreaseproteinrequirements. Inflammationincreasesmicronutrientrequirements(i.e.,antioxidantvitamins).Diminishedintake Articulardiseasediminishestheabilitytoselffeed,shop,andpreparefoods. Morning stiffness may decrease morning appetite. Temporomandibular joint disease mayimpair theabilitytochew. Depression from chronic diseasemayimpair food intake.Sjgrensyndromeandxerostomiamay impairfoodintake. Diminishedabsorption Abnormalitiesofthesmallbowel,liver,andpancreasmaydecreaseabsorptionofnutrients. Drugtherapy(e.g.,salicylazosulfapyridine)mayinhibitnutrientabsorption. Inadequateutilization Drugtherapy (e.g., methotrexate, salicylazosulfapyridine,andnonsteroidalantiinflammatorydrugs) mayinhibitenzymesofintermediarymetabolism. VitaminB12deficiencycanreducefolateuptakeandretentionbythecells. Increasedexcretion Urinaryexcretion ofnutrientsmaybeincreasedinthecatabolicstateofactivediseaseandbysome drugtreatments(e.g.,prednisone). Chronicbloodlossfromnonsteroidalantiinflammatoryagentsmayincreasetheneedfor hematopoieticprecursors(e.g.,iron) Nutritional Statusof Patients with RheumatoidArthritisand Juvenile RheumatoidArthritis andBodyComposition ComorbiditiesofRAincludelossofleanbodymass, termedrheumatoidcachexia,whichistheend product of the hypermetabolism associated with this disease. Sir James Paget first described rheumatoid cachexia in1873.In patients withrheumatoid cachexia, theremaybean increase in fatmasswithcoexistinglossofleanbodymasscalledcachecticobesity. In1984,Helliwelletalevaluated50patientswithRAand50normalcontrols,usinganthropometric andbiochemicalmeasurements,includingserumalbumin,transferrin,retinolbindingprotein, thyroxinebindingprealbumin,zinc,andfolicacidconcentrations.Patientswereclassifiedasbeing malnourishediftheyhadareductioninoneanthropometricmeasurementwithtwoormore biochemicalabnormalities.Theupperarmmusclecircumferencewaslowin14%ofpatientsand mostofthebiochemicalmeasures(serumalbumin,transferrin,retinolbindingprotein, thyroxinebindingprealbumin,zinc,andfolicacid)werelowinthepatients.Thirteenoutof50 patients(26%)metthecriteriaformalnutrition(lowanthropometryplustwoormorebiochemical measures),versusnoneofthecontrols. Collins et alstudied 38 hospitalizedpatientswith RA.Alikelihood ofmalnutrition indexwascalcu lated for 38 hospitalizedpatients with RA that includedserum folate and vitaminC levels,triceps skin fold or a BMI calculation, arm muscle area correctedfor bone area,a totallymphocytecount, serum albumin and a hemato crit. Twentyseven of 38 patients (71%) had a high likeli hood of malnutrition,basedonthisindex. Mody et al assessed the nutritional status of220patients withRAusingtriceps skinfold,upper
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arm muscle circumference, BMI, percentage idealbodyweight, and serum albumin. Fortyfiveof 220 patients(20%) had a low value inone ormore anthropometricmeasures, and 6 (3%)hadlow albumin. Obesity, defined as a BMI greater than 30, was found in 10% of this popu lation. In contrast, Kalla et alcompared65patientswith RA with71matched controls usinganthropometric measurements and serum protein concentrations. Lean bodymasswas similarin the controls andpatients,andcorticosteroidtherapyhadnoeffectonanthropometricmeasurements. HernandezBeriain et al evaluated 75 outpatients with RA having variable functional class, radiologic stage, rheumatoid factor seropositivity status, presence of extraarticular disease, and disease duration. Nutritional status was evaluated by measurements of weight, height, midupper arm circumference, and triceps skinfold, and calculation of midarm muscle area and midarm fat area. Lean bodymass, as evaluatedbymidupper armcircumference, waslowerinpatients with lower RA functional class24%of 75RAoutpatients hadanthropometricmeasurements belowthe 10th percentile, and 14% were below the 5thpercentile. The authors concluded that patients with poorer functional class, more severe radio graphic disease, or with extraarticular disease had worsenutritionalstatusandlossofleanbodymassthanpatientswithlessseveredisease. Munro and Capell evaluated BMI, upper armfatmass(anestimateofbodyfatmass),andupper arm muscle area (an estimate of body somatic muscle mass) by anthropometric measurements. Similarly,greaterthanhalfofpatientswithRAhadvaluesinthelowest10thpercentileforupperarm musclearea reflecting a loss insomatic muscle storesand the catabolicnatureofthedisease.In addition, in female patients, there was a correlation between low fat mass and elevated erythrocyte sedimentation rates and Creactive protein levels. The wasted patients were also more limited in their ability to perform activities of daily living as assessed by the Health AssessmentQuestionnaire(HAQ)whichmeasuresfunctionalstatus. Roubenoff et al found that in 24 patients, 67% were cachectic, and their lean bodymass was inversely associated with numbers of swollen joints. This suggestedthatprotein catabolism and gluconeogenesismay berequired tomaintain a high level ofdiseaseactivity. Chronic caloric deficits were apparently not a cause of lower lean body mass. Elevated tumor necrosis factor (TNF) wasfound in3out of5patients withflaringjoints.TNFwasnotelevatedinpatientswith less active disease. A later study showed that lean body mass was 13% lower in patients considered to be in control (without change in medication over the past year) than in matched controls, indicating thatthere wasalossofapproximatelyonethirdofmobilizablemusclecellmass. Cytokine production from peripheral blood mononuclear cells was also increased in these patients, and higher interleukin (IL)1 and TNF production was associated with increased restingenergyexpenditure. Morgan et al measured BMIin 79patients starting MTX forRA. Sixty percent had BMI less than 25, and 4% were severely underweight (BMI less than 18) but 40% were overweightor obese. Roubenoff et al found that low physical activity by women with RA results in lower total energy expenditure. Although patients withRA are at risk for cachexia,poorfoodchoices andinactivity mayalsoputthematriskforobesity. A more recentstudyevaluated bodycomposition by dualenergyxray absorptiometry (DXA)in 60 patients hospitalizedfor RA.The mean BMIforwomen andmen, respectively, were24.4and26.9. However, by calculation of the fatfree mass index (fatfree mass/kg/m2), 52% of the women and 30% of themenwere malnourished.They alsoevaluated the SubjectiveGlobalAssessment(SGA) andMini Nutritional Assessment (MNA) malnutrition screening tools.The MNAhadpoorspecificity and good sensitivity, whereas the SGA had good specificity and poor sensitivity to detect malnutrition. The authors suggested that the MNA be used as a screening tool, followed by body
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composition analysis determined by DXA. In another study of 80 outpatients with RA, the same investigators completed DXA, bioelectrical impedance analysis (BIA), BMI, the MNA, and waist circumference. Twentysixpercent ofwomen and 21%ofmen hadlowfatfreemassindexand,in thiscohort,the MNAand waistcircumference werepoor predictors ofrheumatoid cachexia.DXA and BIA had good general agreement, but because limits of agreement were wide, they concludedthatBIAmaybeoflimitedusefulnessinclinicalpractice. Other investigations have generally confirmed the rela tionship betweenchronic inflammation and rheumatoid cachexia/cachectic obesity. A crosssectional study of 14 patients with RA and 14 patients with noninflammatory arthritis, using measured resting energy expenditure (REE), joint counts for tenderness and swelling and the modified Stanford HAQ (mHAQ) found that REE, adjusted for fatfree mass, was significantly higher inthepatientswith RAcomparedwith patients withnoninflammatoryarthritis(1498:162kcalversus1330 : 206 kcal p < .031). In addition, REE and IL6 concentrations were higher, and fatfree mass lower,in patientswithactivearthritis,suggestingthathypermetabolismandlossoffatfreemassare associatedwithactiveinflammatorydisease. Giles et al matched 189 men and women with RA to nonRA controls and used DXA to determine body composition. Women, but notmen, withRA, had higherlikelihood ofsarcopenia, obesity, and sarcopenic obesity than those without RA. Abnormal body composi tion was associated with higher selfreported disabilityscores(mHAQ), higherCreactiveprotein,greater joint deformity, rheumatoid factor seropositivity, and lack of current treatment with a DMARD.In another investi gation in 197 subjects, higher disability scores by mHAQ were predicted by increasing fat mass and lower lean body mass. The mHAQ score was 0.52 units higher for individuals in the highest versus lowest quartile of fat mass (p<.001) and 0.81 units higher for subjects in the lowestversushighest quartile of leanbody mass (p< .001). Various inflammatory mediators have beenassociated with disability and cachexia including lowIGF1/IGFBP1ratio (insulinlike growth factorI and its regulating binding protein insulinlike growth factorbinding proteinI). Toms et alevaluated 400patients with RAfor meta bolic syndrome. Older ageand high HAQ score were associated with higher prevalence ofmetabolic syndrome, whereas MTX therapywas associated with reduced likelihood of metabolic syndrome. In contrast, StavropoulosKalinoglou correlated physical activity, dietary intake from a 3day food diary, and inflammatory status (IL6, IL1, TNF levels) with BMI and body fat determined by bioelectrical impedance. Theyfoundno relationship between inflammatory markers and BMI or body fat. Instead, higher levels of activity hadthehighestassociationwithlowerbodyfatandlowBMI. Several strategieshave beenusedto tryto alter the det rimentaleffectsofchronicstressofRAon body composi tion (168, 169). Progressive resistance exercise has been shown to increase strength, but was not accompanied by changes in body composition (168, 169). Rall et al (170) showed thattreatment withMTXnormalizedleucinekinetics, probablyasaresultof a reductionin protein catabolism. In a study of obese patients with RA, a weight reduction program which emphasized caloric restriction, protein supplements and physical exercise for 12 weeks was demonstratedtomaintainleanbodycellmassandmaintainphysicalfunctioning. One intervention study used hydroxybutyric acid, glutamine, and arginine versus a placebo mixture ofalanine,glutamicacid,glycine,andserine for12weekstotreat thehypermetabolism in RA similar to the nutrition support ofstressed hospitalized patients. Thehydroxybutyric acid, glutamine, and arginine were not more effective than theplacebomixture inreversingcachexiain patientswithRA.
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DietTherapy ComplementaryandAlternativeNutritionalTherapies Theuse ofcomplementary/alternativedietapproaches fortreatment ofRAiscommon.Inasample of 296 patients,60.5%admitted totheuseof some sortof alternative therapy suchasherbs/algae or cartilagecomponents . Variouscompounds have beenstudied fortheir efficacy inRAalthough many have preliminary data, stronger human studies are necessary for most of them. Probiotic supplementshavenotbeenfoundtoimprovesymptomsinRA. EffectsofSpecificFoodsonRheumaticSymptoms In a study of 742 patients with RA, juvenile RA, ankylosing spondylitis, psoriatic arthropathy, primary fibromyalgia,andOA,onethirdofpatientswithRA reported aworseningofsymptomswith specific foods. Fortythree percent of patients with juvenile RA reported an exacerbation of symptoms with specific foods. The foods that were most frequently cited in worsening joint symptomsweremeat,wine,alcohol,coffee,sweets,sugar,chocolate,apples,andcitrusfruits. FoodAllergy That allergicresponses tofoodmaybe related toRAdisease activityis a relatively old idea. In the early 1900s, many reports of arthritis caused by specific foods appeared. Van de Laar et al reported circumstantial evidence for a relationship between RA and food allergy. The human gut containsimmunologically active cells inthePeyerpatches.Mechanismsthatmayalterthehandling of food antigens include atrophic gastritis, increased intestinal permeability, and alteration in gut flora. Thirtyfive patients who reported foodrelated gastro intestinal symptoms were evaluated to determine if there was a relationship between jointswellingand arthralgias andthepresenceof circulating immune complexes. The number of individualswith circulating immune complexeswas higher in patients with arthralgias thaninpatientswithoutarthralgias,andtherewerehigherlevelsof complexes in those with arthralgias. This supports the idea that foodrelated gastrointestinal symptoms might involve immunologic/allergic mechanisms. However, the success of elemental diets,whichdonotcontainantigenicproteins,hasbeenvariable. In a study of 704 patients relating food intakes toarthritissymptoms,28%feltthattherewasan association between a specific food and their disease activity . The foods that were thought to havean unfavorable effect on their arthritisincluded preservatives,beef, pork, food additives,milk, and sugar. Patients with a history of allergy, drug allergy, or a family history of allergy were more likelytoreportanassociationbetweenfoodsanddiseaseactivity. Panush etal described a patientwithaninflammatoryarthritiswhosejointsymptomsworsenedwith milk intake.The patient wasfasted forseveral days and then given an elemental diet for 33days followed by blinded food challenges. Placebo foods such as lettuce and carrots caused no exacerbations in joint symptoms. Four blinded milk challenges caused increases in morning stiffnessand swollenjoints. Immune studies suggested delayedandcutaneoushyperreactivityto milk. An additional case study documented a patient whose RA wasworsened by intakeof milk andcheese. The mucosal production of nitric oxide and release ofmyeloperoxidaseand eosinophilcationic protein were measured after rectal challenges with cowsmilk and gluten in 27 individuals with RAand 18 healthy controls, but no relationship between selfreported foodintolerance symptoms and mucosal reactivity was seen. In a study of60 childrenwith juvenile RA, 1out of 60 patientshadmilkintolerancewhichwasassociatedwithkneeswelling.
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In conclusion,althoughfoodallergymayaffectasmallpercentage ofpatients withRA,itisnotlikely a major factor in most. If patients indicate that they have an arthritis flareassociated with a food, a prudent course of action would be to avoid the offending food. Referral to a registered/licensed dietitian can be beneficial to make sure that the diet is nutritionally adequate andthatfoodgroupsarenotcompletelyexcluded. PopularDietsasTreatment Panush et al conducted a doubleblind, placebo controlled trial of diet therapy for patients with active RA who met the American College of Rheumatology criteria. The experimental diet was modeled after theDongDiet andwasfreeofadditives,preservatives,fruit,red meat, herbs, and dairy products. The placebo diet also excluded items from some major food groups so that it somewhat mimicked the experimental dietary intervention. Clinical evaluations occurred at entry andterminationof the 10weektrialshowednodifferencesbetween the experimental versus the placebo diet in patients global assessment of disease, examiners assessment of disease, duration of morning stiffness, 50ft walking time, gripstrength, numbers oftender or swollenjoints, anderythrocytesedimentation rates. However, twopatientsimprovedmarkedlyontheexperimental dietandelectedtocontinueit. Fifty patients withdocumented RA werefollowed ina24week double blind, randomized trialof a wellbalanced diet versus a diet low in saturated fat, high in polyun saturated fat, and with hypoallergenic foods. The caloric content of the experimental diet was set tofacilitateweight loss and achieve thepatients ideal bodyweight. Therewasasignificantreductioninthenumberof tender jointsand erythrocytesedimentation ratebetweentheexperimentaldietversusthebalanced diet. Noother measures ofdiseaseactivitydiffered. It was speculated thatweightlossduringthe protocolmayhavehadabeneficialeffectondiseaseactivity. FastingandVegetarianDiets Theuse offastingandvegetarian diets hasbeen extensively reviewed. The preliminary reports of improvements in disease activity withfastinghaveledtospeculationontherelationshipofRAto dietaryantigens,becausefastingwouldlowertheantigenstimulustothegutmucosa. In 1979, Skldstam et al randomized patients with RA toacontroldietortoa10dayfast,followed by a lacto vegetarian diet. Fasting subjects received 800 kcal/day from fruit and vegetable juices, were purged with castor oil, and received 5 waterenemas on the first day of thefast.After fasting, the subjects began a lactovegetarian diet for 1 week and then were discharged with instructionsto follow the diet foranadditional9weeks.Yogurtwasallowed,butotherdairyproducts were discouraged. Ten patients served as controls and consumed a more typical diet. When compared with controls, 5 of 15 patients had a 10% decreasein erythrocyte sedimentation rate anda5point ormore decrease inthe Ritchie articular indexofjointtenderness. However, only 1of 14inthe dietgrouphadpersistent improvement after9weeks.Fastingpatientslostameanof 3.5 kg during the fasting period, which could itself have altered disease activity. In an additional study by the same group,20inpatients werefollowedfor severalmonths on anordinarydiet and then, after fasting for 10 days, began a vegan diet. The vegan diet did not include refinedsugar, corn flour,salt, strong spices, preservatives,alcoholic beverages, tea, orcoffee.Patientsimproved in theirpainperception,buttherewerenosignificantchangesingripstrength,tenderjointcounts, or an index of joint tenderness compared with the control period. Because improvements in disease activity in trials have frequently beenaccompaniedbyweightloss,theauthorscompleteda followup study usingdatafromclinicaltrials thatevaluatedtheeffectsofvegan,lactovegetarian,or
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Mediterraneandiets.Lossofbodyweightdidnotsignificantlycontributetodiseaseimprovement. KjeldsenKragh etal completedarandomized,singleblindcontrolledtrialofpatientswhostayedat ahealth farm for 4 weeks.Afteran initial10dayfast, patients werechangedto aglutenfreevegan diet for 3.5 months and then a lactovegetarian diet for the remainder ofthe trial. A control group stayed ataconvalescenthomeandateageneraldiet.Comparedwiththecontrolgroup,at1month, there was a significant improvement in number of tender joints, Ritchie articular index, and the number of swollen joints the pain score and the duration of morning stiffness, grip strength, erythrocyte sedimentationrate,Creactiveprotein,andHAQscore.Thesubjectsintheconvalescent home hadadecrease onlyin the painscore. At 13 months, therewasapersistentimprovement in the diet group compared with the control group in most of the indices. The radiographic score deteriorated slightly inbothgroupsat the end of thetrial.Although foodallergywassuspected,the authors stated thatitprobablydidnotexplaintheresults.Theyspeculatedthatchangesinfattyacids in the diet or weight loss could have affected disease activity. The BMI and triceps skin fold significantlydecreased inthe dietgroupversus control group however, the upperarmmusclearea was notdifferent. Therewere no significant differencesinserumalbumin,hemoglobin,ferritin, zinc, or copper concentrations betweenthe twogroups, suggestingthat thefastingandvegetariandiet had only a minor effect on nutritional status. Platelet counts, white blood cell counts, total immunoglobulin (Ig) G, IgM rheumatoid factor, and complement factors C3 and C4 were significantly lower in the diet group after 1 month. At 1 year, only white blood cell count, IgM rheumatoid factor, and C3andC4weresignificantlydifferent.Thedietgroupwasfurther classified as diet responders and diet nonresponders, based on subjective improvement in joint disease activity. There were greater decreases in platelet count, C3, and C4 in the responders versus nonresponders. Fecal flora changedmarkedlywhenthepatientschangedfromtheomnivorousdiet to the vegan diet and differed markedly between patients with high and low response. The authors speculated that changes in gut flora might be beneficial to disease activity by reducing intestinalinflammationandreducingabsorptionofbacterialanddietaryantigens. Differencesin psychologic factorsbetween the subjectswhovolunteered forthetrialversusother patients withoutRA notinthe trialanddietresponders versusnonresponders wereevaluated.The study patients had stronger belief in their ability to influence theirhealth status, lower belief that chance affects their health, and greater belief in the efficacy of alternative forms of treatment. When the diet group was classified as responders and nonresponders, responders had a significantly lowerbeliefin the effectivenessof traditionalmedicalcarethan nonresponders. This suggested thatpatientswith specificpsychologic characteristics were selectedfor theclinical trial and that the expectations concerning the efficacy of alternative therapies could have contributed to the effect ofthe vegetarian diet.A2yearfollowupofthepatients foundthatallof the diet responders andhalfofthedietnonresponders werestillfollowingamodifieddiet.Nofood item was identified that worsened joint disease. There was also a significant differencein the pain score, duration of morning stiffness, number of tenderjoints,Ritchiearticular index, and the number of swollen joints between diet responders versus the control patients. Thissuggeststhat some subgroupof patients withRAcanbenefitfromavegetariandietandthattheeffectsofthe diet canbesustainedinasubgroupofpatients. Nenonen et al randomized 43 patients to a control diet or to an uncooked vegan diet rich in lactobacilli. One half of the dietary group experienced nausea or diarrhea during the dietary intervention and stopped the diet pre maturely.The HAQscore, duration ofmorning stiffness and pain atrest and with movement,theRitchiearticularindex,andCreactiveproteinwere notdifferent between thecontrolanddietgroupsat 2months.However,acompositeDiseaseActivityScorethat measured subjective changes in arthritis was significantly improved in the dietary intervention
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group, compared with the control group. There was a significant difference in fecal florabetween patientswithimprovementversuslittleimprovementafter1monthofthediet. Hafstrom et alrandomized 66patients withRAtoaglutenfreevegandietoranonvegandietfor1 year (22 inthe glutenfree vegan group and25 inthe nonvegan diet group completed 9months of therapy) 40.5% ofthe vegangrouphad an ACR20(ameasureof jointimprovement) improvement in symptoms compared with 4% in the nonvegan group. Although antibodies against gliadin and lactoglobulin decreased in the glutenfree vegan group, there was no change in radiologic progressionineithergroup. McDougallet al reported ona4week,verylowfat(10%oftotalcalories)vegandiet interventionin free living patients with RA. After 4 weeks, there was a significant loss in body weight, but erythrocyte sedimentation rate, Creactive protein, and rheumatoid factor levels did not change. Thejointtenderness score,thejointswellingscore,andtheseverityofmorningstiffnessdecreased significantly, but therewas no significant changein duration of morning stiffness. Patients withthe largest degree of improvementhad themost active disease atthebeginningofthestudysubjects with longstanding disease showed little improvement. The authors concluded thatavegan diet could improve symptoms and speculated that changes in intestinal permeability to antigens and levelsoffoodandbacterialantigenscouldbemechanisms. A Cochrane review on dietary interventions for RAconcludedthat it wasdifficultto pool data from separate studies, but noted that two randomized controlled trials related to fasting and Mediterranean diet improvedpain. Theyandanotherreviewconcludedthattheeffectsofveganand elimination diets were uncertain and that many ofthedietsevaluated hadahighdropout rateand weightlossasunexpectedsideeffects. In conclusion, fasting and a vegetarian type of diet may have beneficial effects in a subset of patients. Food allergy may be related to disease activity in a minority of patients. Fasting is obviouslynotalongtermtherapeuticapproachtothemanagementofRA. Omega3FattyAcidsasTherapy Theantiinflammatory effects ofomega3fatty acids in RA are due to its replacement ofomega6 fatty acids (primarily arachidonic acid) at enzymes that metabolize omega6 to proinflammatory mediators.This, ineffect, inhibits omega6 metabolism. Omega3 fattyacidsmayalsoinhibitthe production of cytokines and reactive oxygen species. The typical dose is 2 to 5 g/day of eicosapentaenoicacidand1to3g/dayofdocosahexaenoicacid,usuallyoral,althoughintravenous infusion as anemulsionwas alsoeffectiveinthetreatmentofadjuvantarthritis.Adietrelativelylow in arachidonic acid along with omega3 fatty acid supple ments was shown to produce better clinical results, along with lower amounts of leukotriene, thromboxanes, and prostaglandin metabolismwhencomparedwithaWesterndiet. Inadoubleblind, placebocontrolled crossoverstudy,patientswithRAreceiveddairyproductswith or without added omega3 supplements. Biomarkers for DNA damage andoxidativestress were not changed. However, excretion of hydroxypyridinium crosslinks was reduced by this treatment indicatingprotectionofboneandcartilagecollagen. The addition of olive oil(containsoleicacid, an omega9 monounsaturated fatty acid)to omega3 supplements was reported to produce better clinicalchanges in patientswithRA.Theomega9 seriesof fatty acidsmaybemetabolizedtocompoundsthatinhibitthesynthesisofproinflammatory mediators from the omega6 series offattyacids.AreportfromSwedensuggeststhatmoderate intake of oily fish may prevent RA. This is in agree ment with the low prevalence of RA in the fisheatingGreenlandEskimos.
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Summary Reduced capacity for food preparation and poor intake results in poor nutritional status for some patients. In recent decades, both overweight and underweight patients with arthritis have appeared. For the overweightpatient, itisespeciallyimportanttoloseweightandnormalizeinsulin sensitivity,whichmayalleviatesomesymptomsofgout,OA,andpossiblyRA. The hypermetabolic state of RA leads to loss of lean body mass. The removal of specific foods from the diet andfastingfollowedbyavegetariandietmayhelpasmallsubsetofpatients.Specific diets and glucosamine and chondroitin sulfate supplements remain unproven thera pies for the treatment of RA or OA. Conversely, omega3 fatty acid supplements have some benefit in the treatmentof RA.Medical foodsthat interfere withomega6fattyacidmetabolismmaybeusefulin the treatmentof OA.An exampleof a preventable adversedrugnutrientinterac tion istheuseof folicacidsupplementstopreventMTXtoxicityinpatientswithRA.

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