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Liv.52® – Unparalleled in liver care

EditorialEating disorders are

characterized by abnormal eating habits of either insufficient or excessive intake of food that may be detrimental to the physical and mental health of an individual. Anorexia, a pathological form of satiety, is characterized by persistent loss of appetite that leads to a reduced food intake resulting in a progressive weakening of the body. Long-term anorexia associated with significant loss of weight requires medical intervention.

The Research update section of this issue features an article on eating disorders in children and adolescents highlighting the pathogenesis, etiology, screening, and treatment guidelines for these disorders.

It has been observed that a majority of cases of anorexia are due to loss of the basic rhythm of appetite and satiety. The probable mode of action of majority of conventional medications for anorexia is through either stimulation of appetite center or suppression of hyperactive satiety center; however, Liv.52 drops acts by renormalizing the appetite-satiety rhythm. The Clinical review section highlights the beneficial effects of Liv.52 drops in clinical practice with focus on anorexia.

In Expert comments section, Dr  Prithvirajsinh Zala discusses various aspects of anorexia in children and the efficacy of Liv.52 drops in treating these children.

The issue also features articles related to alcoholic liver disease (ALD)—a major cause of morbidity and mortality worldwide. In Herb facts section, we feature an article showing the hepatoprotective activity of Solanum nigrum, one of the major ingredients of Liv.52 formulation.

Do write in to us with your valuable feedbacks and suggestions at publications@himalayahealthcare.com.

Happy reading!– Editor

Risk Factors for the Development of an Eating Disorder• Familyhistoryofeatingdisorderorobesity• Affectiveillnessoralcoholisminfirst-degreerelatives• Ballet,gymnastics,modeling,“visualsports”• Personalitytraits(eg,perfectionism)• Parentaleatingbehaviorandweight• Physicalorsexualabuse• Lowself-esteem• Body-imagedissatisfaction• Historyofexcessivedieting,frequentlyskippedmeals,

compulsiveexercise

• C l i n i c a l r e v i e w

• D r u g a l e r t

• N e w s w i s e

• E x p e r t c o m m e n t s

• H e r b f a c t s

• N e w s f l a s h

• L a u g h l i n e s

• L i v - w i s e

Vol. 6 • No. 2 • Oct–Dec 2011

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Anorexia

Eating Disorders in Children and AdolescentsRome ES, et al.

Pediatrics. 2003;111(1):e98-e108.

IntroductionEatingdisorders in childrenandadolescents continue tobe a serious

problem and may result in premature death or lifelong medical andpsychosocial morbidity.This article provides an update on pathogenesisandetiology,riskfactors,screening,andaspectsofcarefromaprimarycareclinician’sperspective.

Pathogenesis and EtiologyDespite increasing awareness of themajor eatingdisorders, a specific

etiologyforthepathogenesisofanorexianervosa(AN)andbulimianervosa(BN) remains unclear. Rather than single-factor causal theories, eatingdisorders are now viewed as multifactorial disorders with the symptompatternrepresentingafinalcommonpathway.Interesthasfocusedvariouslyon the contribution of environmental and social factors, psychologicalpredisposition,andbiologicalvulnerability,withrecentfamilialaggregationstudiesrenewinginterestinthecontributionofgeneticpredisposition.

TheprominentphysiologicdisturbancesinANhaveledtospeculationthat abnormalbehaviors are causedby aprimarybiological abnormality.Disruptionsofthepituitary,hypothalamus,andvariousneurotransmittershavebeenpostulatedtobecausalfactorsinthedevelopmentofAN.

However,recentstudiesofserotonininparticularhavebroughtrenewedinterest in this area. The neurotransmitter serotonin is known to affectappetite control, sexual and social behavior, stress responses, and mood.Serotonin modulates feeding by producing the sensation of fullness orsatiety.Serotoninantagoniststhatdecreaseserotonergicneurotransmissionor block receptor activation increase food consumption and promoteweight gain. Decreases in brain serotonin function are associated withdepression,impulsivity,andaggressivebehavior.IthasbeenspeculatedthatapremorbiddisturbanceinserotonergicfunctionmightbeariskfactorforthedevelopmentofbothANandBN.

Clinical and population studies of women have consistentlydemonstratedanincreasedassociationbetweenmajordepressionandAN,withdepressionasariskfactorfordevelopmentofincidenteatingdisordersinadolescence.First-degreerelativesofwomenwithANhaveelevatedratesofmajordepression.Although ithasbeen suggested thatANandmajordepressionshareacommonetiology,ithasalsobeensuggestedthattheriskforANisdistinctfromthatofotheraffectivedisorders.However,manyoftheclinicalfeaturesofdepressioncanalsoresultsecondarilyfromstarvationandimprovewithweightrestoration.

Familial transmission of risk has emerged as an increasing focus ofresearchattention.Therearenowmultiplecase-controlstudiesdesignedtoinvestigatethefamilialityofeatingdisorders,whichdemonstrateahigherrateofANinrelativesofprobandswithAN.

Theincreased incidenceofANandBNinfamilies isconsistentwitharangeofobservations,including(i)thecoexistenceofbingeeatingwithAN; (ii) development of both AN and BN that has been demonstratedin longitudinal studies; (iii) overwhelming predominance of commonpatternsofgenderandpersonalitytraits;and(iv)comorbiditywithmoodandanxietydisorders.

providers. Simple screeningquestions related todietarypractices,weighthistory,menstrualcyclepatterns,exercisehistory,psychologicalsymptoms,and family/social history can help to determine whether additionalevaluationisrequired.

When symptoms of disordered eating are recognized, a carefuldiagnostic interview should follow. It should establish the presence orabsence of formal criteria for eating disorders including loss of weight,fearofweightgain,fatphobia,preoccupationwithfood,restrictiveeatingpatterns,purgingbehaviors,bodyimagedistortion,out-of-controleating,andmenstrualirregularity.

Some patients with eating disorders will be unable to describe theirbehavior accurately or truthfully, making assessment more difficult.Additional information from family and friends can sometimes berevealing.Other informationcanhelpsupportthepresumptivediagnosisofaneatingdisorder:Preference foreatingalone,extremely limited foodchoices,ritualizedeatinghabits(eg,preferenceforacertainplateorbowl,eating foods in particular order, unusual food combinations), excessivefluid intake, excessive chewing of ice or gum, or recent vegetarianism.All patients with eating disorders should be screened for risk of suicide.Suicidal ideationcanbepresent inanypatientwitheatingdisorders,butisespeciallycommoninpatientswithBN.Whenearlier identificationofdisorderedeatinghasresultedinappropriateintervention,betterprognosesareseen.Thus,concernovertheeatingbehaviorofapatientshouldquicklyleadtoacoordinatedplanthatspecificallyaddressestheproblem.

When an eating disorder is suspected, a careful medical andpsychosocialhistoryneedstobetakenandathoroughphysicalexaminationhastobeperformed.

Possible Physical Exam Findings in Patients with Eating DisorderGeneral appearance:Emaciated,sunkencheeks,sallowskin,andflataffectVital signs:Bradycardia,hypotension,hypothermia,andorthostasisSkin:Dryskin,lanugohair,lossofshineorbrittlehair,nailchanges,hypercarotenemic,andsubconjunctivalhemorrhage(fromvomiting)HEENT(indicatinghead,ear,eyes,nose,andthroat):Sunkeneyes,drylips,gingivitis,lossoftoothenamelonlingualandocclusolsurfaces,caries,andparotitisBreasts:AtrophyCardiac:Mitralvalveprolapse,clickand/ormurmur,andarrhythmiasAbdomen:Scaphoid,palpableloopsofstool,andtenderepigastrium(ifvomiting)Extremities:Edema,callusesondorsumofhand(Russellsign),acrocyanosis,andRaynaudphenomenonNeurological:Trousseau’signanddiminisheddeeptendonreflexes

Treatment Guidelines and Clinical Pathways

From a psychiatric perspective, the American Psychiatric Associationhasrecentlypublishedarevisionofits1993guideline.Asaguideline,itisaconsensusdocumentandassuchpresentsanoverallreviewratherthana specifically tailored approach. Interestingly, the American PsychiatricAssociationguidelineincludesrecommendationsformedicaltreatmentaswellasrecommendationsfortreatmentatdifferentlevelsofcare.Anotherguideline published by the Society for Adolescent Medicine, focused onthespecificmedicalproblemsofadolescentswitheatingdisorders.

By providing increasing detail and attention to treatment processes,clinicalpathwayscanbedeveloped.Clinicalpathwaysdescribetheoptimalsequencingandtimingofinterventionsbythetreatmentteam(eg,medical,nursing,nutrition,mentalhealth, andother staff ).As such, they shouldminimizedelaysincare,monitorresourceutilization,andmaximizequalityof care.Thereby, they should also reduce variation in the careprovided,improve outcomes, reduce inappropriate lengths of stay, and improvecost-effectiveness.

ScreeningFormal tools are available for the assessment of eating behavior and

eating attitudes; however, these are not typically used by primary care

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Liv.52 Drops in Clinical Practice: An UpdateExcerptedfrom:ParmarBJ.Perinatology. 2011;12(1):25-30.

Liv.52 DS Tablets in Alcoholic Liver CirrhosisAgal S, et al.

Med Update. 2007;15(6):25-32.

IntroductionAlcoholic liver disease is a major cause of morbidity and

mortalityworldwide.InWesterncountries,upto50%ofend-stageliverdiseasehasalcoholasthemainetiologicfactor.Themortality fromalcoholiccirrhosis ishigherthannonalcoholiccirrhosis,andsurvivalat5and10yearsisonly23%and7%in some studies, with 25% of patients dying within 1 year.Alcohol can cause liver damage in the form of steatosis orfatty liver, hepatitis, fibrosis, and liver cirrhosis. In general,the amount anddurationof alcohol abuse correlatewith thepresenceandseverityof liverdamage,at leastwithrespect totheinitialstageoffattyliver.ThepresentstudywasconductedtoevaluatetheclinicalefficacyandsafetyofLiv.52DStablet(apolyherbal formulation) inthemanagementofalcoholic livercirrhosis.

Materials and MethodsThestudyincluded50patients intheagegroupof28to

71years.AllthepatientsreceivedLiv.52DStabletatadosageof1tablettwiceadayfor6months.Thoroughsymptomaticevaluation and clinical examination were done for all thepatientsbeforethetreatmentandduringfollow-upvisits.Liver

function tests, hemogram, and other biochemical tests weredoneatbaseline andat the endof the study.Thepredefinedprimary end points were rapid relief from clinical symptomsand physical signs along with improvement in biochemicalparameters.Thepredefined secondaryendpointswere short-andlong-termsafetyandpatientcompliancetothetreatment.

ResultsA total of 40 patients completed the trial. The study

observed a significant reduction in the clinical symptomscoresofasthenia,easyfatigability,tiredness,nausea,anorexia,abdominal discomfort, abdominal pain, stool frequency,and muscle cramps; physical sign scores of muscle wasting,jaundice,anemia,edema,ascites,andhepatomegaly;andliverfunction test parameters of alanine transaminase, aspartatetransaminase, total bilirubin, alkaline phosphatase, albumin,and prothrombin time. There was no alteration in thehematologicalandotherbiochemicalparametersascomparedtothepretreatmentvalues.

ConclusionThisstudydocumentedasignificantrelieffromtheclinical

symptomsandphysicalsigns,andareductioninliverfunction

testparametersattheendofthe6-monththerapy,ascomparedto pretreatment values. There were no clinically significantadverse events, either reportedorobserved,during the entirestudy period. Thus Liv.52 DS tablet, directly or indirectly,influences the cellular and body metabolism and playsfavorable and protective role in maintaining liver integrityandrestoringitsfunction.Therefore,itcanbeconcludedthatLiv.52DStabletisclinicallysafeandeffectiveinthetreatmentandmanagementofalcoholiclivercirrhosis.

D r u g a l e r t

Chronic Hepatitis B Reactivation Following Infliximab Therapy in Patients with Crohn Disease Esteve M, et al.

Gut.2004;53(9):1363-1365.

There is little information about the effect ofinfliximab on the clinical course of liver diseasein patients with Crohn disease with concomitanthepatitis B virus (HBV) infection. Theoretically,immunosuppression induced by infliximab willfacilitate viral replication, which could be followedby a flare or exacerbation of disease when therapy isdiscontinued. There are no specific recommendationsonsurveillanceandtreatmentofHBVbeforeinfliximabinfusion.Two cases of severe hepatic failure related toinfliximab infusions have been described in patientswithrheumaticdiseases.

Hepatitismarkers(CandB)andliverfunctiontestswereprospectivelydeterminedin80patientswithCrohndisease requiring infliximab infusion in threehospitalsin Spain. Three patients with Crohn disease withchronic HBV infection were identified. Two of thethree patients with chronic HBV infection sufferedsevere reactivation of chronic hepatitis B afterwithdrawalofinfliximabtherapyandonedied.Athirdpatient, who was treated with lamivudine at the timeof infliximab therapy, had no clinical or biochemicalworseningofliverdiseaseduringoraftertherapy.Fromthe remaining 80 patients, six received the hepatitisB vaccine. Three patients had antibodies to bothhepatitis B surface antigen (anti-HBs) and hepatitis Bcoreprotein (anti-HBc)withnormal aminotransferaselevels, and one patient had positive anti-hepatitis Cvirus (HCV) antibodies, negative HCV RNA, andnormalaminotransferaselevels.ExceptforthepatientswithchronicHBVinfection,nosignificantchanges inhepaticfunctionweredetected.

Patients with Crohn disease, who are candidatesfor infliximabtherapy,shouldbetestedforhepatitisBserologicalmarkersbeforetreatmentandthenconsideredfor prophylaxis of reactivation using antiviral therapyifpositive.

IntroductionAnorexia, a persistent and pathological form of satiety, is

characterizedbyagradualonsetandprofoundandpersistentlossofappetitethatresultsinadecreaseinfoodintake,leadingto a progressive depletion of body energy stores. Anorexiareduces oral energy and protein intakes, thus contributingto the development of malnutrition and cachexia. Also,poor appetite is unequivocally associated with increasedhospitalizationrates,poorqualityoflife,andincreasedriskofmorbidityandmortality.

Several proinflammatory cytokines, most notably tumornecrosis factor-alpha (TNF-α), interleukin (IL)-1, andIL-6, induce anorexia and body weight loss. Drugs ofteninfluence appetite, for example, antibiotics increase appetitepresumably by controlling infection; however, prolonged usemaydecreaseappetitebydestroyingthenormalbacterialflora.Amphetamine, a psychostimulant drug, causes anorexia byacceleratingweightlossthroughtheinhibitionoffoodintake.

Anorexiamayleadtoreductioninfoodintake,weightloss,malnutrition, loss of muscle mass and strength, fatigue, andnegative emotions such as fear, anxiety, anger, sadness, anddepressivemood.Theimmediatephysicalsignsofanorexiaareconstipation,dizzinessandfaintness,abdominalpains,muscleweakness, cold, dry, and yellow skin, early morning waking,bloating, development of long, fine downy hair on face andbody,disruptedmenstrualcycles,orabsenceofmenstruation.

Role of Liv.52 Drops in the Management of Anorexia

Liv.52 drops, a hepatospecific formulation, restoresthe metabolic efficiency of liver by protecting the hepaticparenchyma andpromotinghepatocellular regeneration.As adaily health supplement, Liv.52 improves appetite, digestionand assimilationprocesses, andpromotesweight gain.Liv.52dropshasbeenfoundtopossesshepatoprotective,antioxidant,antimicrobial, and anti-inflammatory properties. Severalclinical and nonclinical studies conducted by The HimalayaDrugCompanyhaveshownthesafetyandefficacyofLiv.52invarioushepaticdisorders.

Mechanism of Anorexia and the Effect of Liv.52 on Food Intake

Aclinical studywas conducted to evaluate the safety andefficacyofLiv.52inpatientswithanorexia.Thestudyincluded

400 children (aged≤12 years) with various conditions, suchas cold, cough, fever, diarrhea, and respiratory infections,presenting anorexia as a major symptom.The children weredividedintotwogroups(Liv.52andcontrol).Amongthe400children,263receivedLiv.52and137receivedplacebo.Liv.52wasadministeredatadoseof10dropsTIDtoinfantsaged<2years,20dropsTIDtochildrenaged2to5years,and2tabletsTIDtochildrenaged>5years.Allchildrenwerefollowedupforaperiodof6months.

Resultsof the study showeda significant improvement inappetite in63.5%of children treatedwithLiv.52,whereas itwasonly22.7%inthecontrolgroup.Theappetite remainedsame in 31.2% of children in Liv.52 group and 70.5% incontrol group. A decrease in appetite was observed in only5.3%ofchildreninLiv.52groupascomparedto6.8%inthecontrol group. Results of the study also showed a significantimprovement in well-being, bowel movements, and weightgainalongwithanimprovementinappetiteinchildrentreatedwithLiv.52.

Effect of Liv.52 on Anorexia of Varied Etiology

Aclinical studywas conducted to evaluate the safety andefficacyofLiv.52inpatientswithanorexia.Thestudyincluded100 children with anorexia as a major symptom. Liv.52 wasadministeredforaperiodof1weekatadoseof10dropsBIDtoinfantsaged<1year,15dropsTIDtochildrenaged1to5years, and1 tabletTID to children aged>5 years.Thedrugwasdiscontinuedafteraperiodof1weektoobservewhetherthe improvement in appetite was reported during the courseof treatment or sustained even after the withdrawal of thetreatment.

Results of the study showed that the improvement inappetitewaspromptandfastwithinthefirstweekoftreatmentin 54 out of 100 children, indicating that the response toLiv.52was“good.”Improvementinappetitewasobservedafter2weeksof treatment in30 children, indicating “satisfactory”response.Improvementinappetitewasobservedwithin5daysin patients with various clinical types of tuberculosis of therespiratory system.Also, therewas a good response toLiv.52treatment in children with amebic dysentery. Among the 30children who reported loss of appetite as a major complaintwithout any recognizable disease, the response to Liv.52treatmentwasgoodin8andsatisfactoryin14children.

Discussion and ConclusionResultsof theabove-mentionedclinical trials showedthat

Liv.52dropsiseffectiveinimprovingappetiteinchildrenwithvariousconditionspresentinganorexiaasamajorsymptomandalsointhosewithanorexiaofunknownetiology.NosignificantadverseeffectwasobservedinanyofthepatientstreatedwithLiv.52drops.

The effect of Liv.52 drops against anorexia is due to thesynergistic activities of all herbs used in the formulation ofthe drug. Liv.52 promotes growth and improves appetite,digestion, and assimilation. Liv.52 restores liver function;improves clinical, biochemical, and histopathologicalparameters; and reduces SGPT and SGOT levels. It is safefor long-term use without any contraindications and adverseeffects.Therefore, it can be concluded that Liv.52 drops is asafe and effective therapeutic agent for the treatment andmanagementofchildrenwithanorexia.

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E x p e r t c o m m e n t s

Interview with Dr Prithvirajsinh Zala, MBBS, DCH, FRSH (London)

Anorexia in Children

Dr Prithvirajsinh Zala Consultant Pediatrician Shakti Children Hospital Khambhat, Gujarat

H e r b f a c t s

Solanum nigrum isusedinLiv.52®

The Etiology and Impact of Malnutrition in Pediatric Inflammatory Bowel DiseaseGerasimidis K, et al.

J Hum Nutr Diet. 2011;24(4):313-326.

Disease-associated undernutrition of all types is verycommon in pediatric inflammatory bowel disease (IBD).Recent weight loss remains one of the triad of clinicalmanifestationsandacornerstone for thediagnosisofCrohn’sdisease (CD), although significantly fewer patients nowpresent as being underweight. Recent evidence suggests thatthe introduction of medical treatment will quickly restorebody weight, although this does not reflect concomitantchanges in body composition. CD children present withfeatures of nutritional cachexia with normal fat stores butdepleted lean mass. Poor bone health, delayed puberty, andgrowth failure are additional features that further complicateclinical management. Suboptimal nutritional intake is amain determinant of undernutrition, although activationof the immune system and secretion of pro-inflammatorycytokines exert additional independent effects. Biochemicallylow concentrations of plasma micronutrients are commonlyreported in IBD patients, although their interpretationis difficult in the presence of an acute phase response andother indices of body stores adequacy are needed. Anemia isa common extraintestinal manifestation of the IBD child.Iron-deficient anemia is the predominant type, with anemiaof chronic disease being the second most common form.Decreaseddietaryintake,asaresultofdecreasedappetiteandfoodaversion,isthemajorcauseofundernutritioninpediatricIBD.Alteredenergyandnutrientrequirements,malabsorption,and increased gastrointestinal losses are additional factors,althoughtheircontributiontoundernutritioninpediatricCDneedstobestudiedfurther.

Feeding Disorders of Infancy: A Longitudinal Study to Middle ChildhoodAmmaniti M, et al.

Int J Eat Disord. 2011.

ObjectiveTo evaluate over time feeding behavior and emotional-

behavioralfunctioninginasampleofchildrendiagnosedwithinfantile anorexia (IA) and a group of typically developingchildren;andtoinvestigatetherelationshipbetweenmaternalpsychological functioning and the children’s feeding patternsandemotional-behavioralfunctioning.

MethodSeventy-twochildrendiagnosedwithIAand70childrenin

thecontrolgroupwereprospectivelyevaluatedthroughseveralmeasuresat2,5,and8yearsofage.

ResultsThe findings revealed partial improvement in the

nutritional status of the children with IA. However, theycontinuedtoshowongoingeatingproblemsand,inaddition,anxiety/depression, withdrawal, and rule-breaking behaviorsand social problems. There were significant correlationsbetween the children’s eating problems and their emotionaldifficultiesandtheirmothers’increasedemotionaldistressanddisturbedeatingattitudes.

DiscussionThislongitudinalstudypointsoutthatthenaturalcourse

ofuntreatedIAischaracterizedbythepersistenceofdifficultiesin eating behavior and emotional-behavioral adjustment inboth,thechildrenandtheirmothers.

Pathogenesis of Alcohol-induced Liver Disease: Classical Concepts and Recent AdvancesSeth D, et al.

J Gastroenterol Hepatol. 2011;26(7):1089-1105.

Alcoholicliverdisease(ALD)isaprimaryconsequenceofheavy and prolonged drinking. ALD contributes to the bulkof liver disease burden worldwide. Progression of ALD is amultifactorialandmultistepprocessthatincludesmanygeneticandenvironmentalriskfactors.ThemolecularpathogenesisofALDinvolvesalcoholmetabolismandsecondarymechanismssuch as oxidative stress, endotoxin, cytokines, and immuneregulators. The histopathological manifestation of ALDoccursasanoutcomeofcomplex,butcontrolled interactionsbetween hepatic cell types. Hepatic stellate cells are the keydrivers of fibrogenesis, but transformation of hepatocytes tomyofibroblastoids also implicate parenchymal cells as playingan active role in hepatic fibrogenesis. Recent discoveriesindicate that lipogenesis during the early stages of ALD is arisk for advancement to cirrhosis. Other recently identifiednovel molecules and physiological/cell signaling pathwaysinclude fibrinolysis, osteopontin, transforming growthfactor-SMAD, and hedgehog signaling, and involvementof novel cytokines in hepatic fibrogenesis. The observationthat ALD and nonalcoholic steatohepatitis share commonpathways and genetic polymorphisms suggests operation ofparallel pathogenic mechanisms. Future research involvinggenomics, epigenomics, deep sequencing, and noncodingregulatoryelementsholdspromisetoidentifynoveldiagnosticand therapeutic targets for ALD. There is also a need foradequate animal models to study pathogenic mechanisms atthemolecularlevelandtargetedtherapy.

Why is anorexia a common problem in pediatric practice?

Therearevariousreasonswhyanorexiaor lossofappetiteisacommonobservationinmanychildren.Thiscanbeduetotheirinclinationtowardjunkfoodthusreducingtherequirednutrientintake,naturaldisinterestineating,andtheirinabilityto communicate the initial symptoms of lack of appetite.Anorexiamayalsobearesultofreversibleconditionssuchasfatigue, constipation, depression, or chronic diseases such asdiabetes,hepatitis,andcancer.

Hereditaryfactors,feedingproblemsduringinfancy,acuteand chronic infections, hyperthyroidism, and medications(suchasamphetamines,sympathomimetics,antibiotics,coughand cold preparations, codeine, morphine, and medicines totreat attention deficit hyperactivity disorder) may also causelossofappetite.

Apart fromthese, childrenare at a risk fordevelopinganeating disorder if the parents themselves are too preoccupiedwiththeirappearanceandweight.Iftheparentsareconstantlydisliking and complaining about their own bodies, childrengetthemessagethatitisimportanttobethinandinordertomaintainthat,theystartself-starvation.

What is the role of cyproheptadine?Cyproheptadine is an antihistaminic and antiserotonergic

agentused for the treatmentof allergic reactions.Studieshaveshownsomeweightgaininpatientstreatedwithcyproheptadine.However,thedrughasbeenreportedtobeassociatedwithsomeadverse reactions suchasdrowsiness, excitation,hallucinations,ataxia, tachycardia, muscle twitching, gastric pain, dry mucussurfaces, acute urine retention, mydriasis, and rubeosis ofthe face. At therapeutic dosages, cyproheptadine reduces thesecretion of ACTH, cortisol, prolactin, and growth hormone,lowers blood glucose concentrations, and raises the levels ofunesterifiedfreefattyacids.

Cyproheptadineisalsofoundtocauseatropine-likeactions,which in turn may lead to sleep apnea, alteration of voice,dysphagia,dyspnea,aspiration,musclepain,andparesthesias.

What will happen if we do not treat anorexia?Untreated anorexia may lead to serious health problems

such as protein-energy malnutrition (eg, Marasmus and

Kwashiorkor),weightloss,anemia,severedehydration(whichmayleadtorenalfailure),fatigue,lanugogrowth,hyperactivity(as thebody relies on adrenaline insteadof food for energy),osteoporosis, muscle atrophy and weakness, and bradycardiaandlowbloodpressureleadingtoincreasedriskofheartfailure.

How does Liv.52 improve appetite?Studieshaveshownthat,unlikeothermedicationsavailable

for the treatment of anorexia, Liv.52 normalizes the basichunger-satiety rhythm rather than stimulating the appetitecenter or suppressing the satiety center. This helps in thelong-termmanagementofanorexia.Also,Liv.52improvesthedigestionassimilationprocessasadailyhealthsupplementandpromotesweightgain.

I have been prescribing Liv.52 from several years for themanagementofanorexiainchildrenandhavegotsatisfactoryresults. Liv.52 improves appetite and helps in weight gain inchildren,withoutanyadverseeffects.

Inhibitory Effect of Solanum nigrum on Thioacetamide-induced Liver Fibrosis in MiceHsieh CC, et al.

J Ethnopharmacol.2008;119(1):117-121.

Background and Aim

Solanum nigrum (Solanaceae) has beenused in traditionalfolk medicine as ahepatoprotectiveagent.

The purpose of thisstudy was to investigatethe effects of S nigrumextract (SNE) onthioacetamide (TAA)-induced liver fibrosis inmice.

Materials and Methods

HepaticfibrosiswasproducedinmicebyadministeringTAA(0.2g/kg,IP)threetimesaweekfor12weeks.Thesemice were treated daily with distilled water or SNE (0.2or1.0g/kg) viagastrogavage throughout the experimentalperiod.

Results

SNEreducedthehepatichydroxyprolineanda-smoothmuscle actin protein levels of TAA-treated mice. SNEinhibitedTAA-induced collagenea1 (I) and transforminggrowth factor-a1 (TGF-a1) mRNA levels in the liver.HistologicalexaminationalsoconfirmedthatSNEreducedthedegreeoffibrosiscausedbyTAAtreatment.

Conclusion

OraladministrationofSNEsignificantlyreducesTAA-induced hepatic fibrosis in mice, probably through thereductionofTGF-a1secretion.

Solanum nigrum

Livline • Vol. 6 • No. 2 • Oct–Dec 2011

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Edited and Published byDr Pralhad S Patki, MD

The Himalaya Drug Company, Bangalore

Printed atSri Sudhindra Offset Process

Bangalore

E-mailpublications@himalayahealthcare.com

Websitewww.himalayahealthcare.com

EDITORIAL TEAM

Editor in chiefDr Pralhad S Patki

Managing EditorDr Jayashree B Keshav

Editorial AssistantsPooja Sinha

Shruthi VB

Shahina KR

Rashmi Raj

Layout ArtistsDayananda Rao S

Santosh G

Believe with all of your heart that you will do what you were made to do.

– Orison Swett Marden

…contd from page 1 (Research update)

Liv-

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L a u g h l i n e s

Aflatoxins and Growth Impairment

Aflatoxins, fungal toxinsproducedbyAspergillus flavusandAspergillus parasiticus in a varietyof food crops, are well known aspotenthumanhepatocarcinogens.However,theassociationbetweenaflatoxin and growth impairmentin children is relatively lessdiscussed in literature. Exposureto foodborne aflatoxin, especiallythrough maize and groundnuts,is common in various regions ofAfrica and Asia where childhoodstuntingandunderweightarealsocommon,probablyduetovariousinteracting factors suchas entericdiseases, socioeconomic status,andsuboptimalnutrition.

The mechanism by whichaflatoxin may result in growthimpairment is not yet known;however,onepossibleexplanationmay be altered intestinalintegrity through cell toxicityor immunomodulation. Severalstudies showed that chronicexposure to aflatoxins in animalscan cause growth inhibition andimmunesuppression.

A recent review publishedin Critical Reviews in Toxicologyevaluated the effect of aflatoxinongrowthimpairmentinanimalsand human children followingexposure in utero and throughbreast-feeding. Findings of thereview suggested that aflatoxinexposure and its association withgrowth impairment in childrencouldresultinasignificantpublichealth burden in less developedcountries.

Khlangwiset P, et al.Crit Rev Toxicol. 2011;41(9):740-755.

OnedayinNewYorkCity,a banker was driving his newJaguar down the streets. Heparked it andopened thedoortogetout.Suddenlyataxiwentbyandrippedthedooroff.

Thedriverreportedthistoanearbypoliceofficer.

The officer saw the wholethingandsaid“Youbankersaresoinvolvedinyourpossessions.Youdidn’tevennoticethatyourarmwasrippedoffaswell!”

Thebanker staredatwherehisarmusedtobeandsaid“Ohno!MynewRolexisgonetoo!”

•••

A businessman draggedhimself home and barelymade it to his chair beforehe dropped exhausted.His sympathetic wife wasright there with a tall cool

drink and a comforting word.“My, you look tired,” she said.“You must have had a hardday today. What happenedto make you so exhausted?”“It was terrible,” her husbandsaid. “The computer brokedown and all of us had to doourownthinking.”

•••

Amanvisitingadoctorsays,“Doctor I just dropped in totellyouhowmuchIbenefittedfrom your treatment!”The doctor replied, “But youare not one of my patients.”The man said, “I know. ButmyuncleBillwas,andIamhisheir.”

•••

Judge: Why did you hityour husband with a chair?Wife:BecauseIcouldn’tliftthetable!

RecommendationsThe goal for practitioners working with eating disordered patients

aboveall is tohelpachieve thebestpossibleoutcomes,addressingbothshort-andlong-termhealthconsequences.Synthesizingtheinformationpresented, there seem to be three key elements that can help to attainpositiveoutcomes.

Early Detection

There is strongevidence that the longer thedurationof illness, theharder it is to achieve recovery. Eating disorders need to be diagnosedearly in thediseaseprocess inorder for treatment tobeas successfulaspossible.By the time a formaldiagnosis of an eatingdisorder ismade,the patient is already suffering from serious biopsychosocial problems.Practitionersneedtobesensitizedtothepossibilityofaneatingdisorderdevelopingevenatayoungage,andneedbettertrainingtoimprovetheirrecognition of the early stages of the disease process. Screening aboutbodyimage,dietarychangesanddietinghabits,andassessmentofgrowthpatternsshouldoccuryearly.

Early Intervention

Once an eating disorder is recognized, then families need to bewilling to seek treatment.The earlier the intervention, the more likelya patient will recover. Expert help should be sought if patients are notprogressingappropriately.Thiscanpotentiallypreventseriousmorbidityandmortalitythatpatientswitheatingdisordersexperience.

Restoration of Body Weight

Several studies indicate that weight restoration for patients withAN helps facilitate the recovery process. Premature discharge from thehospital below a healthy weight predicts poorer outcomes. In the daytreatment and outpatient settings, weight restoration goals should beclearly defined and monitored. If a patient is unable or unwilling toincrease weight as needed, more frequent visits and/or more intensiveintervention is warranted. In terms of preventing osteoporosis, weightrestorationisessential.

ConclusionEatingdisordersinchildrenandadolescentscanbeoflongduration,

potentially life-threatening depending on severity of illness, and withlikely relapse if adequate alternative coping skills are not developed.

A planned and skillful approach to treatment is necessary to obtain acost-effective, healthy outcome. Patients require ongoing monitoringandtreatmentwithabiopsychosocialperspectiveusingavariednumberof professionals, including a primary care clinician, therapist, dietitian,family therapist, and other team members as needed. Outcomes-basedresearchinthefieldcanfurtherclarifywaystodelivercost-effectivecareinavarietyofsettings.Cliniciansandfamiliesneedtoadvocateforadequatecoverage of both medical and mental health services for children andadolescentswitheatingdisorders,especiallybecausepathogenesis,medicaleffects, andnecessary treatments all demonstrate the interrelatednessofthemedicalandpsychologicalrelationsinthisdiseaseprocess.Ultimately,thegoalsincludeprimarypreventionandearlyrecognitionandtreatmenttopreventlong-termsequelae.

Aflatoxin B1

• Normalizesthebasicappetite-satietyrhythm• Restoresliverfunctionandcorrectsmetabolism• Improvesdigestionandassimilation• Doesnotcausedrowsinessunlikeconventional

preparations

Liv.52 – Unparalleled in liver care