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Sthoulya kc009 gdg

  1. 1. 2000 EVALUATION OF THE EFFICACY OF PIPPALYADI GUGGULU IN MEDOROGA (WITH SPECIAL REFERENCE TO ITS HYPOLIPIDIMIC EFFECT) Thesis submitted to theRajiv Gandhi University of Health Sciences Karnataka,Bangalore In partial fulfillment of regulations for the Award of the degree of DOCTOR OF MEDICINE (AYURVEDA) By YASHODA. S. MUDIGOUDAR. Guide Dr. Ch. Ranga Rao. M.D. (Ayu) Professor and Head of the Department Post Graduate and Research Centre D.G.M.Ay. Medical College, Gadag. Co-Guide Dr. Siva Rama Prasad Ketamakka. M.D. (Ayu) Reader Post Graduate and Research Centre D.G.M.Ay. Medical College, Gadag. POST GRADUATE AND RESEARCH CENTRE DEPARTMENT OF KAYACHIKITSA D.G.M.AY. MEDICAL COLLEGE
  2. 2. Food is an entity with which we are associated from the first day ofour lives. We ignorantly consume many things in life, and probably foodis one out of them due to its own intimate association with us. In India, itseems that all functions, and social, spiritual, even corporate meetingseither begin or end with distribution of food. On all such occasions,including daily food ritual, major emphasis is on taste and only taste.Ignorant or otherwise, total neglect on the basic functions of food andbody needs, will allow our tongue to rule on entire body. These excess calories may “lengthen the waist line “ but shortensthe “life line” of the individual by imposing an extra burden. Thus obesityin humans is a health problem of appreciable magnitude, as it isassociated with an increased incidence of cardiovascular disease, gallbladder disease, diabetes and other conditions. And in which increasedmorbidity rate is witnessed 1 , survey shows 12-fold increase in the rate ofdeath form cardiovascular disease in men aged 25 – 34 with obesity. It is wisely told in Ayurveda, diet and drinks virtually constitute thevery life of all living beings. Those who take proper food and drinks willenjoy bliss without any disease during the present as well as future timesotherwise results into a premature death 2 . This properly utilised dietnourishes and supports the body like the pillars support the house 3Charaka has classified various articles of foods and drinks in the 1Introduction
  3. 3. following twelve groups VIZ; Shukadhanya, Shamidhanya, Mamsa, Shaka,Phala, Harita, Madya, Jala, Gorasa, Ikshuvikara, Kritanna, Aharayoga. It almost resembles the categorisation of food item done by Indiancouncil of medical research. It specifies the food requirement based onage, gender and physiological state, occupation or activity of a person.As a example, between 19 – 58 years of age group with sedentary typeof activity needs- Cereals 420g. Leafy vegetables 100g Other vegetables 100g Milk and Milk products 300g Sugars 25g Pulses 60g Roots and tubers 200g Fruits 100g Oil and fats 20gIf it is crossed gradually leads to obesity. In addition to the 2000 k cal / day necessary to meet basal needs,500 – 2500 or more k cal / day are required to meet the energy demandsof daily activities 4 . The caloric value of the dietary intake must equal the 2Introduction
  4. 4. energy expended as heat and work if body weight is to be maintained.When the intake is excessive, the obesity results. The word Medas is derived from “MID” dhatu that means snigdhadravya 5 . Thereby snigdha guna dravyas definitely increase Medodhatu.This excessive accumulation of Medas at udara, stana, sphik anddisproportionate growth (Ayatha upachaya) of the body is considered asMedoroga. Shleshmala and ama producing aharas induces madhurata toannarasa, which in turn causes increase of Medas by its snigdhaguna.This obstructs the nutrient channels of the remaining tissues deprivingthem of nutrition. Thus, only fat accumulates in large quantities in thebody. Because of obstruction only vayu comes to Kosta and begins to actfast inside the Kosta, increases the digestive activity, making forvoracious hunger and craving for large quantity of food. This excesshunger is the cause which make the treatment of the disease difficult. As it is virodhapakramaneeya for both Langhana and Brimhanatherapies, becomes kastasadhya. Along with Vata, kapha and Medohardravya, therapy needs strict diets and exercise. Treatment of obesity maysound like a strenuous program but it is really advantageous to come outof premature death. Increased mortality rate due to obesity andunsuccessful treatments for the disease attract the attention ofresearchers. 3Introduction
  5. 5. 6 The meaning of obesity is given as Medaswita and signs andsymptoms explained for obesity nearly resemble the sthoulya orMedoroga. Thus the comparison of Medoroga with obesity is justifiable. ITHIHAS Our ancient scripture Yajurveda quotes, “oh God! Give us a foodwhich will keep us away from diseases”. Charaka affirmed that in thebeginning of Kritayuga people were completely disease free and ojovanlike Devatas as they were getting foods rich in rasa, guna, veerya andvipaka. As days passed some become rich and habituated to eat more,which lead to increase in body weight. This increase in body weight leadthe disease free people of Kritayuga to the disease-full world. Thus,Medoroga is known since the times of Kritayuga and is one of the causesfor the disease to develop. Two thousand five hundred years ago Hippocratus, noted that fatmen “die suddenly 7. This suggests not only the disease but also he knewthe severity of the increased mortality rate due to obesity. 4Introduction
  6. 6. SAMHITA PERIODCharaka Samhita (Before1000 BC) 8 Incidence of disease may be high during that period, hence theywere able to study the disease clinically and mention the specific line oftreatment, and many single and compounds. Outstanding being theknowledge of genetic role in the etiopathogenesis.Sushruta Samhita (1000 – 1500 BC). 9 Increased incidences might have forced them to find the rootcause. So Sushruta clearly quotes Rasa is the cause for both obese andlean. 10Astanga Hridhaya (550C AD) Discussed sthoulya in dwividhopakramaneeya and included it underlanghan therapy. Treatment aspect of sthoulya is discussed but states asthere is no medicine for sthoulya. MEDIEVAL PERIODThis period of history of Indian medicine is known as a period ofcommentators. Hence most of the books of this period are collections ofthoughts of previous authors, commentaries of previous works. 5Introduction
  7. 7. Madhavakara (9C AD) 11 Madhavakara renamed sthoulya as Medoroga and compiled thedisease from the works of previous authors. But change of nomenclatureindicates, instead of considering anatomical change i.e. shareera sthulatahe wanted to consider physiological change in the disease condition.Chakrapani (11C AD) 12 The commentator of Charaka Samhita gives a critical commentaryover it but he has not emphasized much about the disease in his ownbook Chakradatta.Dalhana (12C AD) 13 A commentator of Sushruta Samhita, clarify important queries bygiving logical answers.Sharangadhara (13 C AD) 14 Even-though mentioned the disease in rogaganana prakarana, notconsidered in his explanations.Bhavamisra (16C AD) 15 He specifies profuse sweating due to excess Medas creates amedia for external germs on the skin. 6Introduction
  8. 8. Yoga Ratnakara (17C AD) 16 His views are almost similar to previous Acharyas.F ew rec ent w orks don e at d iffer en t re sear ch cen te rs ar e mentio ne d b elow 17 Effect of Turmeric extract on Lipid Profile by Deshapande U.R. and group, at Tata Memorial Hospital, Parel. Development of Hypolipidaemic agents from plants and Traditional remedies by Nityanand.S. at Central Drug Research institute, Lucknow. Hypolipidaemic effect of Fenugreek seeds, by Sharma.R.D. at P.G department S.N.Medical college, Agra Effect of purnus amygdalus seeds on lipid profile, by Sunita Teotia at Centre for Biomedical Engineering, IIT, Delhi. Hypolipidimic activity of Eleven different pectins, by Dept of Biochemestry,University of Kerala, Karivettam Hypocholesterolaemic action of three Guggulu preparations, by Nair R.B. RRI, Trivendrum. 7Introduction
  9. 9. Hypocholesterolaemic cffect of Terminalia Arjuna tree bark, by P. Gupta, at Dept of Pharmacology, SMS Medical college, Jaipur. Terminalia Arjuna : an ayurvedic cardiotonic, regualtes lipid metabolism in hyperlipaemic rates, by Kapoor N.K. at Div of Biochemistry, C.D.R.I Lacknow. Effect of boiled Barley rice feeding in hypercholesterolemic and Normolipidimic subjects, by Tomita, M at National Institute of Health and Nutrition. Tokyo. Preliminary screening of Hypocholesterolemic activity in solanium Indicum, by Badar, Y. at Pharmaceutical and Fine Chemical Research Centre, PCSIR Laboratories Complex, Karachi. Hypolipidemic effect of Coriander seeds, by Chitra, V at dept of Bio- Chemistry, University of Kerala, Kariavattom. Effect of agnimantha kwatha bhavita shilajita on Medoroga. By Murlikrishna.V at PG center Hydrabad. 8Introduction
  10. 10. REFERENCES1. Review of Medical Physiology – W. Ganong pp 2492. Charaka Sutrasthana 27 / 345,346,347 (chakrapani Commentary)3. Astanga Hridaya Sutrasthana 7 / 514. Review of Medical Physiology – W. Ganong pp 2945. Shabdha stoma maha nidi, vachaspathyam6. Dictionary English to Sanskrit by Sir Moniar Williams pp 647. your guide to health clifford .R.Anderson. pp 678. Ayurveda ka vigyanika ithihasa pp 189. Ibid pp 1910. Ibid pp 2111. Ibid pp 2312. Ibid pp 2513. Ibid pp 2614. Ibid pp 2715. Ibid pp 2916. Ibid pp 3017. Allied Ayurvedic Medical Research Abstracts (AAMRA) Research in ayurveda by Dr M.S.Baghel. 9Introduction
  11. 11. Basic knowledge about Anatomy and physiology concerned to thedisease is essential to study the pathophysiology of it. Some of theshareera aspects concerned to the Medoroga are explained here. AYURVEDIC VIEW It is essential to know the Medodhatu utpatti, transportation andalso about its place and function. The digestion of food commences as itenters into the mouth. Consumed food reaches the stomach with the helpof Pranavayu and Samanavayu stimulates the Jataragni to digest it.Even though the ingested food contains six Rasas, in Amashaya, aquiresfirst the Madhura paka at the influence of kapha. The partly digestedfood of Madhurabhavavastha moves into the Pachyamanashaya andenters into amlavasta. Pitta that is originally situated in this site, getsnourishment and support from this amlapakavasta. The partly digestedfood is then propelled from the Amashaya into pakvashaya 1 forcompletion of the digestion. The digested food after entering pakvashayabecomes dry due to the absorption of water and the waste material offood attains the form of solid mass with a little moisture. Thisavasthapaka is called katuavasthapaka and here Vata is increased 2. Eventhough the human body and the food are derived from thecombination of the five bhutas 3, the composition and the quality of their 9 Shareera
  12. 12. panchabhoutika constituents are different from each other there by it isknown as vijatiya. So transformation of vijatiya substances derived formthe food into the sajatiya nutrients which are to be incorporated in to thestructure of the dhatus is the function of bhutagnis, which follows afterthe completion of the action of jataragni. During this entire process the ahara gets divided into prasada andkittabhagas. The kitta bhagas of ahara excreted out as pureesh andmootra. The remaining prasada bhaga is again subjected to processingby dhatwagnis. Rasagni acts on it and forms rasa dhatu and does thenourishment of rakta dhatu. During this sthanya and arthava areproduced as upadhatus and malaroopi kapha as mala is formed.Similarly all the other dhatus can be explained. As Medoroga is mainlyconcerned with Medodhatu utpatti it can be explained as, mamsdhatwagniacts on mamsa and the nutrients of Medodhatu present in the mamsa-dhatu are transformed into Medodhatu getting an additional supply ofjalabhutamshas during paka, which make the dhatu snigdha and drawa 4.Probably vasa which is the sneha portion of mamsa is responsible for theproduction of Medas indirectly and partially. Medodhatu is 2 anjali in pramana and in its normal state does thesnehana, swedana, drudata and asthi pushti in the body. 10 Shareera
  13. 13. Srotas The internal transport system of the body is represented bysrotases and has been given a fundamental importance both in healthand disease. When the integrity of the srotases are impaired, both thesthanaga and margagha dhatus also become involved. The nutrients of aparticular dhatu pass through particular dhatuvaha srotas only. Vrikkaand vapavahana are considered as the moolas of Medovaha srotases 5.With regard to the Medodhatu it is necessary to look into the action of ahormone produced by the adrenal gland on the fat metabolism. Cortisol, aglucocorticosteroid produced by the cortex of the adrenal gland causes amoderate degree of fatty acid mobilization from the adipose tissue. Butpersons with excess cortisol secretion frequently develop a peculiar typeof obesity. This obesity result from excess stimulation of food intakemechanism so that fat is generated in some tissues of the body at a rateeven more rapidly than it is mobilised and oxidised. Glucocorticosteroidsstimulate the fat absorption from the intestines, mobilise fat from thedepot and disintegrate them to form ketone bodies in the liver and theexcess of cortisol redistributes the fat in the body. Chakrapani states that vapa is the snigdha varti located in theabdomen 6. Some authorities consider vapavahana as omentum where fatis accumulated. According to Sushruta, kati and vrikka are the moolas ofMedovaha srotases 7. Kati is the waist, where more accumulation of fat isseen in an obese person. 11 Shareera
  14. 14. Ama Derivation of ama is Aa + ma. “Aa” means near, towards and “ma”means poison. Therefore Ama should denote a substance or group ofsubstances which is “near to poison” or acts like a poison. Due tohypofunctioning of ushma, the food, which is not completely/properly,digested, yields immature rasa in Amashaya and due to the retentionundergoes fermentation and putrefaction. This state of rasa is spoken ofas “Ama” 8. Ama is also produced due to deficit functioning of dhatwagni 9therefore ushma may indicate either jataragni or Dhatwagni in respect ofthe genesis of ama, depending on the pathological processes exhibited. MODERN VIEW Obesity is included under “metabolic disorder”. Metabolism means“all the chemical processes in a living being producing energy andgrowth”. The changes that occur in the digested food stuffs from the timeof the ingestion until the elimination in the form of execration, the sum oftotal chemical changes which takes place within the body is to beconsidered as metabolism which yields energy and enriches growth. Asobesity is deposition of excess fat in the body, it is justified to be underthe heading of metabolic disorders. 12 Shareera
  15. 15. Origin of the body fat is from fats, carbohydrates and proteins inthe food. The carbohydrates and proteins consumed in excess areconverted into fats through the citric acid cycle. Hence study ofmetabolism of carbohydrate, fat and proteins are essential in this regard.Metabolism of carbohydrate 10 Metabolism of carbohydrate may be considered under threeheadings – supply, storage and utility. Supply is regulated by the diet,temporary storage in liver and utility by cells of the tissues and muscles.During the process of digestion, the carbohydrates are changed to simplesugars. Absorption of glucose takes place mainly into the capillaries ofthe small intestines. These capillaries pore their contents into portalvessels, which carries the blood rich with glucose to liver. The liver cellstake this glucose from the blood and convert it into glycogen that isstored in the liver cells. the sugar stored in the liver as glycogen isconverted as glucose, whenever needed it is released into the bloodstream, which will be taken up by the muscles and other tissues. Themaximum storage of glycogen in the body is about 400 gm. Theconversion of glycogen into glucose is under the control of variousenzymes contained in the liver cells and by hormones. The amount ofglucose required is proportionate to the utility of it in the body. 13 Shareera
  16. 16. Metabolism of fat After absorption of the nutrients from intestines, the grater portionof the fat passes into the central lymph channel of each villus. Fromthese small lacteal it finds its way through the larger lymphatic in themesentery to the thoracic duct and then through the thoracic duct to theblood. It seams probably some of the fatty acid and glycerol is absorbedby the capillaries in the villi it self, enters the portal vein and passesthrough the liver before reaching the general circulation. Much of the fatabsorbed form the intestine is deposited in fat storage cells, which arewidely distributed throughout the body. From these cells fat is constantlybeing withdrawn and is carried by the blood to all parts of the body. Thetissues slowly take it out, as they need it in their metabolic process.Some are oxidised to provide energy and remaining is used for synthesisof lipid for cellulose.Role of liver in fat metabolismLiver has many functions in relation to fat metabolism1. It synthesis fatty acids from carbohydrate intermediates.2. Rebuilds fatty acids through lengthening and shortening the chains, saturation and destruction to provide the lipids characteristic to the human. Oxidises fatty acids to acetyl coenzyme A, which may be used for synthesis of other substances such as cholesterol. The liver stores lipids chiefly as phospolipids, neutral fat and cholesterol. 14 Shareera
  17. 17. Metabolism of Protein: As a result of digestion, proteins are hydrolyzed in to amino acids,which are absorbed through the blood capillaries of the villi, pass into theportal vessel and are carried via the liver into the blood or the generalcirculation and distributed in to the tissues. The tissues select and storesome of these substances and in each organ they are either synthesizedinto new tissues or used to maintain and repair tissues. Amino acids notused in synthesis are broken down or deminised in the liver. Indemisation, the amino groups are removed from amino acid molecules.The non-nitrogenous portion of the amino acid molecules is oxidised toliberate energy or is synthesized in to glycogen or fat. Therefore thisportion of the amino acid molecule may be regarded as a source ofenergy.Citric Acid Cycle: The cells of the body do not use food directly for their energy, butuse A.T.P. as a source of energy. A.T.P. is stored in each cell and isconstantly being used and re-formed in the citric acid cycle. All metabolicintermediates from carbohydrates, fatty acids and amino acids enter thecitric cycle. After going through the above description of the metabolismof carbohydrate, fats and proteins, it is very clear that the body storesenergy source derived from excess amount of carbohydrate, fats andproteins in the form of fat or adipose tissue. 15 Shareera
  18. 18. Biochemistry of fat: Lipids are of four types1. Cholesterol Cholesterol is derived from the Greek word “chole” which meansBile and sterol means solid. That is solid material of the bile. Itparticipates in the formation of cell membrane and precursor of bile acid,and able to form the steroid hormones like estrogen, progesterone etc.2. Fatty acids Fatty acids are straight chain compounds of varying lengths. Theymay be of saturated or unsaturated. The main saturated fatty acids inplasma are palmitic and stearic acids. Fatty acids may be esterified withglycerol to form glycerides or they may be in free form as free fatty acids(FFA) or non-esterified fatty acids. In the blood FFA are bound toalbumin mainly. FFA is an immediately available energy source andprovides the significant proportion of the energy requirements of thebody.3. Phospolipids Phospolipids are complex lipids consists phosphate andnitrogenous products, which are water-soluble. The major Phospolipidsin plasma are lecithin and sphingomelin. As these are water soluble,plays an important role in lipid transport.4. Triglycerides Triglycerides consist of glycerol, each molecule of which is esterifiedwith three fatty acids. 16 Shareera
  19. 19. LIPOPROTEINS Lipids are relatively insoluble in water but are carried in the bodyfluids as soluble protein complexes known as lipoproteins. Thelipoproteins are macro molecular complexes of lipid and protein with amajor function of transporting lipids through the vascular and extravascular body fluids. These lipoproteins are classified on the basis oftheir densities as demonstrated by their ultra centrifugal separation.1) Chylo micrones (CM) These are comparatively large particles with density of about 0.95 gm per cm. The principle function is transport of exogenous triglyceride.2) Very low density lipoprotein. (VLDL) VLDL have a density of 0.96 – 1.006 gm / cm the principle function is transport of endogenous triglyceride.3) Intermediate density lipoprotein.(IDL) IDL have a density of 1.02 – 1.063 normally present in the blood stream in only small amounts but can accumulate in pathological disturbances of lipoprotein metabolism.4) low density lipoprotein (LDL) LDL have a density of 1.02 – 1.63, the principle function is the cholesterol transport.5) High-density lipoprotein (HDL) HDL is the heaviest and smallest of the lipoproteins with the density of 1.064 – 1.21 the principle function is the reverse cholesterol transport. 17 Shareera
  20. 20. Fat Cell 11 Fat cells when not too crowded they are spherical and denselypacked they seem to be polyhedral. These fat cells vary in diameter, onan average 50 µm. .Each cell consists of a peripheral rim of cytoplasm, inwhich the nucleus is embedded, surrounding the single large centralglobule of fat.Adipose Tissue 12 It is one of the connective tissue, which is specially meant for thestorage of fat. Adipose tissue occurs in great abundance and constitutesthe principal component. These tissue however seem to have a well-defined distribution within the body. They are distributed where itspresence as a store, will be least inconvenience but it also tend to laiddown where its thermal and mechanical insulation will be of greatestadvantage. Thus adipose tissue fills up such of the bone marrow that isnot needed for blood formation. It is also found around such importantorgans as the heart and kidney. As the omentum it protects theintestines. Superficial Nerves liable to injury are often protected by fat. Itoccurs in abundance in subcutaneous tissue and as localised pads insynovial membrane of major joints. In emaciation these deposits tend tobe spared until a late stage. Elsewhere they help to conserve the bodyheat as they are good nonconductors of heat and in some situations havemechanical functions such as in the soles of feet, palms of the hand andin synovial membranes. 18 Shareera
  21. 21. REFERENCES1. Arunadatta on Astanga Hridaya Shareerasthana 3 / 52. Charaka Chikitsasthana 15/43. Astanga Hridaya Sutrasthana 9/1 Sushruta. Sutrasthana 46/5264. Sharira kriya Vignanam by Dr M. Ramasundar Rao pp 2805. Chraka Vimanasthana 5/86. Chakrapani on Chraka Vimanasthana 5/87. Sushruta Shareerasthana 9/128. Astanga Hridaya Sutrasthana 13/289. Dalhana on Sushruta Sutrasthana 15/3210. Human Physiology by Dr.C.C.Chatterjee. pp 53411. Schafer’s essentials of Histology pp 10012. Gray’s Anatomy pp 1168 19 Shareera
  22. 22. For a crystal clear picture of a diseased condition, it is necessaryto be well versed with the cardinal factors causing the medoroga(Obesity), which are five in number. They are Hetu or Etiology, Purva-rupa or Prodromal signs and symptom, Rupa or actual signs andsymptoms of the disease, Dosha samprapti the actual disease process orpathology occurring in the body, and Upashaya, positive response withtreatment adopted for diagnosing a disease. HETU Among them Hetu, which literally means the causative factor has itsown place of significance. It is a fact highlighted by the assertion ofancient seers that Nidana parivarjana, removal of causative factors itselfis treatment 1. A disease treated symptomatically tends to recur, if thecausative factors are allowed to persist. Hence knowledge of nidana is amust. Comparative study of Nidana according to different texts is given.SN Nidanas Ch2 Su3 AS4 BP5 MN6 Y.R7 1 Shlesmala Ahara - a - - a a 2 Guru,Madhura,Sheeta,Snigdha Ahara a - a a - - 3 Adhika matra sevana a - - - - - 4 Adhyashana - a - - - - 5 Avyayama a a - a a a 6 Divashayana a a - a a a 7 Avyavaya a - - - - - 8 Na chinta and shoka a - - - - - 9 Harsha nityatwa a - - - - -10 Bija swabhava a - - - - - 19 Nidana
  23. 23. AHARAJA HETUShleshmala ahara, guru, madhura, and snigdha ahara, adhika matrasevana and adhyashana all these come under aharaja nidana.Panchabhoutika level of their study reveals 8 1. Guru- Prithvi and Jala 2. Snigdh- Jala 3. Sheeta- Jala 4. Madhura-Prithvi and Jala. 5. Meda - Prithvi and Jala 6. Kapha - Prithvi and Jala There by as a rule, similar qualities increases the quantity, theyincrease Kapha and Medas. Ayurveda is not only very particular about quality but also aboutquantity and mode of taking food. Annapana vidhi, Matrashiteeya 9, DravaDravya vijnaneeya 10 etc chapters are specifically meant for this.Quantities of the food and jataragni are interdependent. It means foodtaken in a proper quantity only maintains Agni 11 and this Matra dependson Agni bala 12. So adhika matra bhojana i.e. excess intake of foodcauses immediate aggravation of all the tridoshas 13. This leads to diseasemanifestation in the body. Adhyashana is intake of the food before the 20 Nidana
  24. 24. completion of digestion of previously consumed food. Dalhana has clearlytold, in the presence of deeptagni also adhyashana produces ama andleads to the formation of madhura anna rasa which in turn formsmedovriddhi 14 . The term “obesity” is derived from the Latin word “obsus” whichmeans having eaten 15. Its very name suggests the root cause of obesityis over eating. Body needs 2000k cal/day to meet basal needs, 500 –2500 k cal/day are required to meet the energy demands of dailyactivities 16, if consumed more than this (i.e. Adhika matra sevana) leadsto obesity. Especially fats and carbohydrates having more caloric value9.3 kcal/g and 4.1 kcal/g 17 respectively becomes the main cause forobesity.VIHARAJA HETU Avyayama, Avyavaya, Divashayana are categorised under ViharajNidana. References from the classics revels Vyayama is a must for aperson who take more fatty foods 18, since it reduces fat 19. Importance ofVyayama is exaggerated by saying “ one who does regular exercise neednot think of guruta and lughuta of the foods”. Contrary to this lack ofexercise or Avyayama along with guru aharas definitely lead tomadovriddhi. Vyavaya is also a kind of physical work where in morecalories is spent for one intercourse. If a person is not indulging in 21 Nidana
  25. 25. vyavaya dhatu kshaya will not take place instead it gives dathu pustiwhich leads to medovriddhi. It is strictly advised for an obese person notto sleep in the day and less sleep even in the night. Because waking inthe night causes rukshata and daytime sleep increases snigdhata 20 thatcauses kaphavriddhi and leads to sthoulya.MANASIKA HETU: Achinta and shoka can be included under this heading Ayurvedaconsiders Manasika karana also as an important entity for diseasemanifestation. Here in sthoulya also harsh nityatwa and Achinta andshoka that are Manasika karanas definitely influence the sthoulya.Mental disturbances cause vata vriddhi that indirectly causes dhatukshaya where as prasanna manas always increases kapha hencebecomes hetu of the sthoulya.BEEJA SWABHAVA Charaka samhita is the only text in Ayurveda that explains beejaswabhava as a causative factor. Commenting over the word beejaswabhava Gangadhara and Chakrapani have clearly told “ atisthula matapitra sonitha sukra swabhavat” 21 which means the character of sthoulya isinherited from obese parents. Study also revels there is 50% of chancefor children being obese when one of the parents is obese, thisproportion rising to 75% with both parents obese. Obesity runs in 22 Nidana
  26. 26. families. Further more, identical twins usually maintain weight levelswithin 2 pounds of each other through out life, if they live under similarcondition. Or within 5 pounds of each other if there condition of life differmarkedly, this might result from eating habits engendered duringchildhood but it is generally believed that this close similarity betweentwins is genetically controlled 22.HORMONAL CAUSE Ayurveda is silent about endogenous obesity Dr Jeffreys Flierexplains there is no established endocrine cause for most cases ofobesity. However endocrinologists frequently are consulted because ofconcern that the patient may have cushing syndrome or hypothyroidism.Endocrine syndromes that may be associated with obesity are cushingsyndrome, Hypothyroidism, Insulinoma, Craniopharyngioma, Turnersyndrome, Male hypogonadism.INFLUENCE OF DIETETICS IN PREGNANCY 23 Disorders such as obesity, diabetes, cancer, Heart disease etc arenot only the result of inheritance but also etiological factors. The newscience of fetal programming suggests that as pregnancy progresses,each month in the womb shapes our health for life. Under nutritionduring the fetus’s first trimester makes obesity more likely in adult hood,perhaps the appetite control center in the brain is programmed to over 23 Nidana
  27. 27. eat. One best evidence can be quoted here. In World War II Nazis triedto starve the population of western Holland from September 1944 untilthe following may. Men who were fetuses during all or part of the periodare studied. If their mothers were starving during the first trimester fromMarch to May 1945 but got adequate food later delivered heavier, longerand with larger head babies than in normal periods. As adults they weremore likely to be obese. If their mothers went hungry only in the finaltrimester (born in Nov 1944) they were lean. If the food is scarce during the first trimester, the fetus develops aso-called thrifty phenotype. Its metabolism is set so that every availablecalorie sticks and scarcity of food may affect the appetite centers in thefetal brain, and sets as “eat whatever is around, you never know whenfamine will hit”. 24 Nidana
  28. 28. REFERENCES1. Madhava Nidana 1 / 192. Charaka Sutrasthana 21 / 33. Sushruta Sutrasthana 15 / 324. Astanga Sangraha Sutrasthana 24 / 185. Bhava Prakasha Madhyamakhanda 39 / 16. Madhava Nidana 34 / 17. Yoga Ratnakara Medoroga nidana / 18. Dravya guna vignana by P.V.Sharma. pp 529. Astanga Sangraha Sutrasthana 1110. Astanga Sangraha Sutrasthana 611. Astanga Hridaya Sutrasthana 8 / 212. Charaka Sutrasthana 5 / 313. Charaka Vimanasthana 2 / 714. Dalhana on Sushruta. Sutrasthana 15 / 3215. Text Book of Medicine by R.J.Vakil pp 28716. Review of Medical Physiology by W.F.Ganong pp 24917. Review of Medical Physiology by W.F.Ganong pp 24918. Astanga Sangraha Sutrasthana 9 / 2119. Charaka Sutrasthana 7 / 3220. Astanga Sangraha Sutrasthana 9 / 2521. Gangadara on Charaka Sutrasthana 21 / 322. Text book of physology by Gyton pp 36723. The News week Sept 27 1999 25 Nidana
  29. 29. SAMPRAPTI The samprapti of the disease explains the method or process bywhich the vitiated doshas reach the dooshyas and produce the anatomicaland physiological changes in the target organs leading to expression as adisease. Usually this process follow a regular pattern according tosamanya siddhantas of Ayurveda that is why “ Samyak prapti of vyadhi isknown as samprapti” Exceptionally in diseases like Medoroga it differsfrom regular samprapti. Hence deep study and detailed analysis overpathogenesis of Medoroga carries importance. The samprapti ofMedoroga has been vividly described in almost all the textbooks ofAyurveda. Views of all the authors goes on a similar line, accept AstangaSangrahakara, where he deviates a little. Absence of physical activity, sleeping during day and Kaphakaraaharas induce Madhuryata to annarasa, which in turn increase the Medasby its Snigdhaguna. This obstructs the nutrient channels of theremaining tissues depriving them of nutrition. So only fat accumulates inlarge quantities in the body 24. Because of obstruction, Vayu in Kostabegins to act fast, increases the digestive activity rapidly, makingvoracious hunger and craving for large quantity of food, just as the forestfire destroy the forest, the Vata and Agni destroy the body 25 resulting intohypermetabolic activity. 25 Samprapti
  30. 30. This samprapti of Medoroga is confusing due to the Medoagnimandyata and formation of ama in presence of teekshnagni and where assuccessive dhatus are not nourished even though Medas is overnourished. Hence here “Rasat Raktam tato Mamsam” theory fails. Thusclarification at the level of process of pathogenesis is required. At thisjunction discussion about Agni, dhatuposhan and Ama concerned toMedoroga is essential.Jataragni In Medoroga both the extremes of vitiated Agni can be seen atdifferent levels. Mandagni, in the manifestation of the disease andteekshanagni, in aggravating the condition. In the beginning none of theauthors have specified about teekshagni, instead it is mentioned afterMedodhatu vriddhi. All the nidanas specified for Medoroga like excessive intake of,Guru, Sheeta aharas 26 and not indulging in sufficient physical exercise 27are the supportive factors for the production of Ama, which is formed dueto hypofunction of ushma 28. This ama or Madhura Annarasa 29 by itssnigdha guna increases Medas there by like other diseases here alsoMandagni is the root cause of the disease 30. After the accumulation of fat,teekshnagni play an important role. Vayu obstructed by Medas in kostaincreases Agni under kumbakar pawan nyaya 31, making for voracious 26 Samprapti
  31. 31. hunger and craving for large quantity of food. 32 This Agni will be so strongand harmful if proper food is not supplied to it, it destroys body as firedestroys the forest 33.Dhatwagni In Medoroga a link between Jataragni and Medodhatwagni isbroken and therefore even when the function of Jataragni is good thefunctions of Medogni is not so. This is because whatever the outcome ofthe Ahar i.e either pakwa rasa or ama rasa, it has to be supplied to alldhatus for their nourishment. In Medoroga rasa is rich in snigdha guna 34,and is similar to Medas. There by it is supplied to Medodhatwagni, whichincreases the Medodhatu. Agni and Ahara are interdependent. Ahara isthe fuel for agni 35 and agnibala depends on the material supplied to it fordigestion 36. In Medoroga excess quantity of ahara rasa is supplied toMedodhatwagni, which causes agnimandya and forms ama at Medodhatulevel.Dathu poshana in Medoroga Since ama represents the vitiated or deficiently formed ahararasaor rasadhatu with poor nutritional capacity, there is a disturbance indhatu poshana. In Medoroga, Medas is increased abundantly 37 Hencethere will be disparity between Medas and other dhatus 38 Charakaaccepts Atimedovriddhi 39 but not mentioned any cause for it. Sushruta 27 Samprapti
  32. 32. tried to clarify it and he tells remaining dhatus are not nourished becauseof Margavarodhata 40. Astanga Sangrahakara further gives theexplanation as, the remaining portion of rasa dhatu being very little inquantity is not enough to nourish the raktadi dhatus 41 and also quotes onesamanya siddhanta as “ that which has undergone increase first will onlyundergo increase further” and tells like vayuadi fat also follow it, there byonly Medo vriddhi is seen compared to other dhatus 42. Dalhana dividesdhatus as Poorvadhatu and Uttaradhatu and explains undernourishmentof uttaradhatu is due to Avruta marga and because of vishistaAharavashat, Adrastavashat and Medasavruta margata, overseadingRakta and mamsa directly Medas is increased 43.Hence poorvadhatuundernourishment is justified at present context. The specific nutrients of one dhatu are not channeled to any otherdhatu. The portion of Ahara rasa meant to provide nourishment to aparticular dhatu does not come in contact with other dhatus 44. Accordingto khalekapota nyaya, as their resting-places attract pigeons, the sthayidhatus attract their requisite nutrients from the Ahararasa through theirspecific dhatuvaha srotases and nourish themselves. Hence whenMadhura annarasa rich in snigdhaguna moves through channels, nourishonly Medas and as Ahararasa is having less quantity of requisitenutrients of other dhatus they are not properly nourished. 28 Samprapti
  33. 33. Ama As both jataragni and dhatwagni are impaired in Medoroga,production of jataragni or dhatwagnijanya ama is common. All the authorshave used the word madhura annarasa 45, Vagbhata specially tellskaphamishrita annarasa 46 acts as ama. Madhukosha commentry says- ifannavaha srotas is coated with madhura annarasa, that turns all the foodinto madhura 47. Sushruta tells, at the time of production of Pitta inannavaha srotas (ama vipaka), if food is consumed it turns into vidhahi 48.As Dalhana tells adhyashana sheelata is the cause for production of amain presence of teevragni, there by it can be said during the time ofproduction of kapha in annavaha srotas (madhura vipaka), food is againconsumed because of adhyashanasheela that leads to the production ofmadhura annarasa or kaphamishrita annarasa. This avipakwa rasa isknown as ama 49 Now it is more appropriate to say, because of jataragnijanya amadhatwagni is impaired and dhatwagnijanya ama is formed. Properconversion of poshakadhatu to poshya dhatus dose not takes place dueto medogni mandyata and more dusta Medas 50 is formed. This Medodhatubeing produced due to dhatwagni mandya is known as samadhatu.Thereby Medoroga is included under samamedodhatu janya vikaras 51. 29 Samprapti
  34. 34. REFERENCES24. Madhava Nidana 34 / 1,225. Charaka Sutrasthana 21 / 5, 6.26. Charaka Vimanasthana 2 / 7 Charaka Vimanasthana 15 / 42 Astanga Sangraha Sutrasthana 8 / 3127. Essentials of Basic Ayurveda concepts by V.V.S.Shastri. pp 9228. Astanga Hridaya Sutrasthana 13 / 2529. Madhava Nidana 34 / 130. Madhava Nidana 35 / 1131. Madhu kosha on Madhava Nidana 3432. Madhava Nidana 34 / 5,633. Madhava Nidana 34 / 7 Astanga Sangraha Sutrasthana 24 / 2234. Sushruta Sutrasthana 15 / 3235. Charaka Sutrasthana 5 /336. Astanga Hridaya Sutrasthana 8 / 237. Charaka Sutrasthana 21 / 438. Astanga Sangraha Sutrasthana 24 /24, Chakrapani on Charaka Sutrasthana 21 / 439. Charaka Sutrasthana 21 / 4 30 Samprapti
  35. 35. 40. Sushruta Sutrasthana 15 / 3241. Astanga Sangraha Sutrasthana 24 / 23,2442. Astanga Sangraha Sutrasthana 24 / 2443. Dalhana on Sushruta Sutrasthana 15 / 3244. Chakrapani on Charaka Sutrasthana 28 / 445. Sushruta Sutrasthana 15/32, Madhava Nidana 34/146. Astanga Sangraha Sutrasthana 24/1847. Madhukosha vyakya on Madhava Nidana 34/1-748. Sushruta Sutrasthana 46/49649. Bhava Prakasha Madhyama Khanda 1/1650. Chakrapani on Charaka Sutrasthana 21 / 3,4.51. Charaka Sutrasthana 28 / 25 Sushruta Sutrasthana 24 / 13 31 Samprapti
  36. 36. POORVA ROOPA The poorvaroopa of Medoroga are not specifically mentioned byany of the authors. The roopas mentioned for Medoroga are 52- Increase in Medodhatu- Pendulum movements of buttocks, abdomen and breast- Lack of enthusiasm in physical activities- Disproportion growth of the body. However the general principle about poorvaroopa states that, “roopaof the vyadhi when found in Avyakta or alpa avastha is considered aspoorvaroopa” 53. So, medovriddhi before to the pendulum movement ofSphik, Sthan, Udara can be considered as Poorvarupa. Before themanifestation of the disease, Agni is depraved and once the medas startaccumulating, it turns into teekshnagni. Similarly as kapha vriddhi isobserved, lakshanas told in kriyakalavastas of kapha are seen. 30 Poorva Roopa
  37. 37. REFERANCE52. Charaka Sutrasthana 21 / 8 Astanga Sangraha Sutrasthana 24 / 26 Madhava Nidana 34 / 953. Madhava Nidana 1/5,6 31 Poorva Roopa
  38. 38. ROOPA Roopa is the prominent diagnostic subjective parameter of adisease. At this stage, dosha dooshya sammurchana is completed andthe onset of the disease takes place, which gives the symptomology ofthe disease. These signs and symptoms may change from time to timeaccording to the progress of the disease. Certain symptoms may newlyappear while some may disappear. We can’t find all the symptoms inevery patient at once unless the disease becomes grave.Signs and symptoms mentioned in different texts are tabulated as below. Sl Laxanas Ch54 Su55 AS56 M.N B.P58 Y.R59 57 No 1 Chala Spik Udara & Stana a - a a - a 2 Kshudra Swasa - a - a a a 3 Ayasa - - a - - - 4 Aalpa bala a - a - a - 5 Ati kshudha a a a a a a 6 Ati pipasa a a a a a a 7 Ati Nidra - a a a a a 8 Ati sweda - a a a a a 9 Dourgandhya a a a a a a 10 Moha - - - a a a 11 Krathan - a - - a - 12 Utsahahani a - a a - a 13 Javoparodha a - - - - - 14 Jadya - - a - - - 15 Soukumaryatwa - - - - - - 16 Kricha vyavayata a - - a a a 17 Gadgadatwa - a a - - - 18 Alpa ayu a - a a - a 31 Roopa
  39. 39. It is very interesting to study how these lakshanas are manifested.1. Chala Spik, Udara, Sthana Though the medas is spread throughout the body, its seats of accumulation are Udara, Spik, and sthana. Thus increased medas accumulates more at these places and leads to pendulum movement of them.2. Kshudra Sw asa Excessive fat accumulation in the abdomen interferes with the mechanism of respiration. Respiration act depends on the movement of the diaphragm. Because of accumulated fat, diaphragm fails to move up and down to the expected extent, hence pressure created during contraction phase will not be sufficient to expel out air from the lungs 60. This excess carbondioxide present in the blood stimulate the respiratory centre which leads to kshudra swasa.3. Alpabala, Ayasa and Sukumarata The main function of medas is giving dridata 61 and bala 62 to the body. In sthoulya we find abundant medas but controversy to it we get symptoms like alpabala, ayasa, sukumarata. Chakarapani has commented over the word medodosha as dustamedas 63. Dustamedas can not be expected to do its normal function i.e. dridatwa to the 32 Roopa
  40. 40. body and at the same time poorva dhatus and uttardhatus of meda are undernourished. So all the sapta dhatu dourbhalya takes place which form the above said conditions.4. Atikshuda and Pipasa. The increased fat obstructs the channels of vata. Vata then begins to act within Amashaya, increases the digestive activity, making for voracious hunger and thirst 64, which are appetitive mechanisms.5. Kriccha Vyavaya Sthoulya rogi faces difficulty in intercourse because of two reasons. Foremost is undernourished shukra dhatu and on the other hand is the alpabala or inability to perform any act. Proper quantity of sukra rises the feeling of enjoyment (arousal) contrary in sukrakshaya condition. After prolonged intercourse in sukra kshaya condition, instead of secretion of sukra, sarakta veerya is being secreted 65. This is definitely a difficult intercourse or kriccha vyavaya. Whole of this act needs utsaha, bala or ability, which is absent in medorogi. So it is a common symptom we find in sthoulya rogi which disturb his mental state as well as sexual life. 33 Roopa
  41. 41. 6. Alpa Ayu. Life is very important factor and body is like a driver for chariot 66. Ayurveda is meant for maintenance and fulfilling the desire of long living. So leaving aside all other things body is to be protected. Since body is produced and maintained by food 67 person should take wholesome foods. Those who cultivate the habit of taking whole some food will not gives rise the victims premature death, loss of strength and enthusiasm. Where as Medorogi become a self-victim for his reduced longevity by adopting unwholesome food habits. Excess increase of medas causes the dhatu kshaya of all other dhatus and is associated with an increased incidence of cardiovascular, gall bladder diseases, diabetes, and other conditions, which are fatal important signs of increased mortality rate 68.7. Ati Nidra In obese patients excess sleep is commonly observed. Kapha, because of its increased quantity, which is not undergoing regularity, obstructs the srotas. This srotorodha causes heaviness of the body, from heaviness follows laziness, which in turn causes excess sleep 69 and lethargicness in the body. 34 Roopa
  42. 42. 8 Sw eda and Dourgandha All classics consider atisweda and dourgandha as lakshanas of sthoulya and further give explanation as – 1. By the presence of fat, at the origin of the channels of sweat increase in secretory activity and 2. Association of kapha makes profound increase of sweat 70. Contrary to this Charaka use the word swedabadha 71 and Chakrapani commenting over it as, “production of sweda is the function of meda where as in sthoulya due to shleshma samsarga this produced sweat is obstructed” 72. Gangadara have also clearly commented swedabadha means “sweda is not excreted” 73. So Charaka accepts the excess production of sweat but he is differing from others by saying as it is not excreted out properly. Meda is having amaghanda by nature, in the presence of dusta medas in sthoulya gives rise still more bad odour 74. Excess production of sweat, which is the mala of meda, gives daurgandha in the body.9. Gadgadhatwa Gadgadhatwa means the “Avyakta vachanam” 75 according Dalhana. Which means stammering or unclear pronouncetion of word or even horsness of the voice, which is the more appropriate word to be considered.9 Krathana. – Excess kapha obstructs pranavaha srotas resulting in krathana. 35 Roopa
  43. 43. In ayurveda, even though all the above said Lakshanas areexplained for sthoulya, a diagnostic key for considering a person asobese is given specifically. The person can be said as obese when hehas lack of enthusiasm in physical activities, disproportional to thegrowth of his body, intense increase in mamsa and meda, and hasmovement of the buttocks, abdomen and breasts 76 Parallel to this some more keynotes are available form modernconcepts. A number of different criteria have been suggested to identifythe obese person. Important among them are mentioned here1. Standard height and weight relation The most influential application of this approach has been through theuse of life insurance data that assesses mortality as a function of bodyweight per height, adjusted for frame size, with obesity defined on purelystatistical grounds as a weight that is above the average weight for givenheight 77. The charts are given below : 36 Roopa
  44. 44. Table No 1 Ideal weights for menHeight Small frame Medium frame Large frame (ft) (kg) (kg) (kg) 5.2 50.8 – 54.4 53.8 – 58.5 57.2 – 64.0 5.3 52.2 – 55.8 54.9 – 60.3 58.5 – 65.3 5.4 53.5 – 57.2 53.2 – 61.7 59.9 – 67.1 5.5 54.9 – 58.5 57.6 – 63.0 61.2 – 68.9 5.6 56.2 – 60.3 59.0 – 64.9 62.6 – 70.8 5.7 58.1 – 62.1 60.8 – 66.7 64.4 – 73.0 5.8 59.9 – 64.0 62.6 – 68.9 66.7 – 75.3 5.9 61.7 – 65.8 64.4 – 70.8 68.5 – 77.1 5.10 63.5 – 68.0 66.2 – 72.6 70.3 – 78.9 5.11 65.3 – 69.9 68.0 – 74.8 72.1 – 81.2 6.0 67.1 – 71.7 69.9 – 77.1 74.4 – 83.5 6.1 68.9 – 73.5 71.7 – 79.4 76.2 – 85.7 6.2 70.8 – 75.7 73.5 – 81.6 78.5 – 88.0 6.3 72.6 – 77.6 75.7 – 83.5 80.7 – 90.3 6.4 74.4 – 79.4 78.1 – 86.2 82.7 – 92.5 Table No 2 Ideal weights for womenHeight Small frame Medium frame Large frame (ft) (kg) (kg) (kg) 4.10 41.7 – 44.5 43.5 – 48.5 47.2 – 54.0 4.11 42.6 – 45.8 44.5 – 49.9 48.1 – 55.3 5.0 43.5 – 47.2 45.8 – 51.3 49.4 – 56.7 5.1 44.9 – 48.5 47.2 – 52.6 50.8 – 58.1 5.2 46.3 – 49.9 48.5 – 54.9 52.2 – 59.4 5.3 47.6 – 51.3 49.9 – 55.3 53.5 – 60.8 5.4 49.0 – 52.6 51.3 – 57.2 54.9 – 62.6 5.5 50.3 – 54.0 52.6 - 59.0 56.7 – 64.0 5.6 51.7 – 55.8 54.4 – 61.2 59.5 – 66.2 5.7 53.5 – 57.6 56.2 - 63.0 60.3 – 68.0 5.8 55.3 – 59.4 58.1 – 64.9 62.1 – 69.9 5.9 57.2 – 61.2 59.9 – 66.7 64.0 – 71.7 5.10 59.0 – 63.5 61.7 – 68.5 65.8 – 73.9 5.11 60.8 – 65.3 63.5 – 70.3 67.6 – 76.2 6.0 62.6 – 67.1 65.3 – 72.1 69.4 – 78.5 37 Roopa
  45. 45. 2. Body mass index A second approach for defining the obese state is body mass index(BMI). It can be calculated by using the formula- BMI = Weight in kg Height in meater 2 Table No 3 Optimal BMI values are given below. Height Body weight in Kilogram (cms) 90 85 80 75 70 65 60 55 50 45 135 49.4 46.6 43.9 41.2 38.4 35.7 32.9 30.2 27.4 24.7 140 45.9 43.4 40.8 38.3 35.7 33.2 30.6 28.1 25.5 23.0 145 42.8 40.4 38.0 35.7 33.3 30.9 28.5 26.2 23.6 21.4 150 40.0 37.8 35.6 33.3 31.1 28.9 26.7 24.4 22.2 20.0 155 37.5 35.4 33.3 31.2 29.1 27.1 25.0 22.9 20.2 18.7 160 35.2 33.2 31.3 29.3 27.3 25.4 23.4 21.5 19.5 17.6 165 33.1 31.2 29.4 27.5 25.7 23.9 22.0 20.2 18.4 16.5 170 31.1 29.4 27.7 26.0 24.2 22.5 20.8 19.0 17.3 15.6 175 29.4 27.8 26.1 24.5 22.9 21.2 19.6 18.0 16.3 14.7 180 27.8 26.2 24.7 23.1 21.6 20.1 18.5 17.0 15.4 13.9 185 26.3 24.8 23.4 21.9 20.5 19.0 17.5 16.1 14.6 13.1 With BMI 25 to 30 are defined as over weight and of those in excess of 30 are defined as obesity. 38 Roopa
  46. 46. 3. waist – to – hip ratio Recent evidence suggests that central obesity as judged by the waist to hip ratio is evident as many of the most important complications of obesity, including insulin resistance, diabetes, hypertension and hyperlipidemia are linked to the amount of intra abdominal fat, rather than to lower body fat (i.e. buttocks and leg) or subcutaneous abdominal fat. A waist – to – hip ratio for men is 0.9 while that for women if > 0.85 is ideal. Waist to hip ratio chart is given below. Table No 4Waist measurement in cmsHip 50 55 60 65 70 75 80 85 90 95 100 105 110 115 120 125 130cms50 1.00 1.10 1.20 1.30 1.40 1.50 1.60 1.70 1.80 1.90 2.00 2.10 2.20 2.30 2.40 2.50 2.6055 0.91 1.00 1.09 1.18 1.27 1.36 1.45 1.55 1.64 1.73 1.82 1.91 2.00 2.09 2.18 2.27 2.3660 0.83 0.92 1.00 1.08 1.17 1.25 1.33 1.42 1.50 1.58 1.67 1.75 1.83 1.92 2.00 2.06 2.1765 0.77 0.85 0.92 1.00 1.06 1.15 1.23 1.31 1.38 1.46 1.54 1.62 1.69 1.77 1.85 1.92 2.0070 0.71 0.79 0.86 0.93 1.00 1.04 1.14 1.21 1.29 1.36 1.48 1.50 1.57 1.67 1.78 1.70 1.8675 0.67 0.73 0.80 0.87 0.93 1.00 1.02 1.13 1.20 1.28 1.41 1.40 1.47 1.61 1.60 1.67 1.7380 0.63 0.69 0.75 0.81 0.88 0.94 1.00 1.06 1.13 1.19 1.25 1.31 1.38 1.44 1.50 1.56 1.6385 0.59 0.65 0.71 0.76 0.82 0.88 0.94 1.00 1.06 1.12 1.18 1.24 1.29 1.35 1.41 1.47 1.5390 0.56 0.61 0.68 0.72 0.78 0.83 0.89 0.94 1.00 1.06 1.11 1.18 1.22 1.28 1.33 1.39 1.4495 0.51 0.56 0.63 0.68 0.74 0.79 0.84 0.89 0.95 1.00 1.05 1.11 1.16 1.21 1.26 1.32 1.37100 0.50 0.55 0.60 0.65 0.70 0.75 0.80 0.85 0.90 0.95 1.00 1.05 1.10 1.15 1.20 1.25 1.30105 0.48 0.52 0.57 0.62 0.68 0.71 0.76 0.81 0.86 0.90 0.95 1.00 1.05 1.10 1.14 1.19 1.24110 0.45 0.50 0.55 0.59 0.64 0.68 0.73 0.77 0.82 0.86 0.91 0.95 1.00 1.05 1.09 1.14 1.18115 0.43 0.48 0.52 0.57 0.61 0.65 0.70 0.74 0.78 0.83 0.87 0.91 0.96 1.00 1.04 1.09 1.13120 0.47 0.46 0.50 0.54 0.58 0.63 0.68 0.71 0.76 0.79 0.83 0.88 0.88 0.98 1.00 1.04 1.08125 0.40 0.44 0.48 0.52 0.56 0.60 0.64 0.68 0.72 0.76 0.80 0.84 0.85 0.92 0.96 1.00 1.04130 0.38 0.42 0.46 0.50 0.54 0.58 0.62 0.65 0.69 0.73 0.77 0.81 0.81 0.86 0.92 0.96 1.00135 0.37 0.41 0.44 0.48 0.52 0.56 0.59 0.63 0.67 0.70 0.74 0.78 0.79 0.85 0.88 0.93 0.96140 0.36 0.39 0.43 0.46 0.50 0.54 0.57 0.61 0.64 0.68 0.71 0.75 0.76 0.82 0.86 0.84 0.91145 0.34 0.38 0.41 0.43 0.48 0.52 0.55 0.59 0.62 0.66 0.69 0.73 0.75 0.78 0.81 0.83 0.88150 0.33 0.37 0.40 0.41 0.46 0.50 0.54 0.57 0.60 0.64 0.67 0.70 0.74 0.77 0.80 0.81 0.84 39 Roopa
  47. 47. REFERENCES54. Charaka Sutrasthana 21 / 455. Sushruta Sutrasthana 15 / 3256. Astang Sangraha Sutrasthana 24 / 19, 2057. Madhava Nidana 34 / 3, 958. Bhava Prakasha madhyama khanda 3959. Yoga Ratnakara Medoroga nidana / 1,2 and 860. Nidana chikitsa hastamalaka pp 19761. Astang Sangraha Sutrasthana 19 / 2062. Bhava Prakasha Poorvakhanda 3 / 14963. Chakrapani on Charaka Sutrasthana 21 / 464. Astang Sangraha Sutrasthana 24 / 2165. Astang Sangraha Sutrasthana 9 / 5766. Astang Sangraha Sutrasthana 9 / 11067. Astang Sangraha Sutrasthana 9 / 11168. Joslin’s Diabetes mellitus pp 35569. Astang Sangraha Sutrasthana 9 / 3370. Astang Sangraha Sutrasthana 24 / 2271. Charaka Sutrasthana 21 / 372. Chakrapani on Charaka Sutrasthana 21 / 373. Gangadhara on Charaka Sutrasthana 21 / 374. Charaka Sutrasthana 21 / 475. Dalhana on Su Sutrasthana 15 / 3276. Astang Sangraha Sutrasthana 24/ 24 Madhava Nidana 34/9 Charaka Sutrasthana 21/877. Joslin’s Diabetes Mellitus pp 352 40 Roopa
  48. 48. CLASSIFICATION OF MEDOROGA Supporting references from the classics are not available to discussthe types of Medoroga. Astodareeya Adhyaya of Charaka, RogagananaPrakarana of Sharangadhara specially deal with types of disease. Charakahave not mentioned Medoroga in his Astodareeaya chapter where asSharangadhara clearly said Medoroga is of only one type. Though the description of Medoroga / sthoulya is mentioned in mostof the classical texts like Charaka samhita, Sushruta Samhita, AstangaSangraha, Bhavaprakash, Madhava nidana, Yoga Ratnakara, Chakradattaetc., but none of the author have classified Medoroga. Vitiation of doshasmay take place at the level of samprapti but ultimately meda dhatu is theonly one that has to be increased, to consider the condition as Medoroga.This may be the reason for not making any types in it. Hence it can besaid that according to ayurveda Medoroga is of only one type. But for the convenience of study it can be classified as following.Type Ii) Aharajanya – Consuming Snigdhadi Ahara, Adhyashana, Atimatra sevan etc,ii) Viharajanya – Diwaswapna etc, 40 Bheda
  49. 49. iii) Manasika Janya – harsha nityatwa etc.iv) Beeja swabhava – heredity.Type II i Sahaja - Beejaswabhava ii Janmottaraj – Ahara, vihara and Manasikakarana janya.Type III i Sadhya Medoroga – Navotpanna, Alpalakshanayukta.ii Asadhya Medoroga – Puratana Upadravayukta, Beejaswabhavaja etc. In modern text we find classification of obesity as Type I I) Exogenous - this is more common and due to excessive caloric intake. Here uniform distribution of fat with little execs under chin and abdomen is seen II) Endogenous – here endocrine factors are at fault and obesity occur inspite of small caloric intake. 41 Bheda
  50. 50. Type II Depending on the distribution of fat this classification is made.i) Generalised type – uniform distribution of fat.ii) Central or trunk – at trunk and neckiii) Superior or buffalo – at face, neck, arms and upper part of trunkiv) Inferior – at lower trunk and legsv) Girdle - at hips, buttocks, Breeches or trochentric – only buttocks.vii) Lipomatous - localised deposits of fat over body.Type IIIi) hypertrophic obesity - increase in amount of fat per fat cell.ii) Hyperplastic obesity – increase in number of fat cells. 42 Bheda
  51. 51. SADHYASADHYATA Before starting the treatment of any disease it is essential to knowwhether that particular state of the disease is curable or incurable.Almost all the texts consider sthoulya as kasta sadhya when comparedwith treatment of krishatwa. But Vagbhata goes to an extent of sayingthere is no treatment for sthoulya; neither Brimhana therapy norLanghana therapy are sufficient to control excessive fat accumulation andto decrease agni and Vata 78. Indu commenting over it states, Brimhanatherapy given to a obese person will decrease agni and Vata but not themedas, where as Langhana therapy will decrease medas but increasesagni and Vata. So treatment is very difficult 79. Modern texts say successful treatment of obesity means sustainedattainment of normal body weight and composition without producingunacceptable treatment induced morbidity, is rarely achievable in clinicalpractice 80 Medoroga can be considered as kasta sadhya, if it is novotpanna,having less intensity, and without complications. 43 Sadhyasadhyata
  52. 52. REFERENCES78. Astang Sangraha Sutrasthana 24 / 479. Indu on Astang Sangraha Sutrasthana 24/4580. Joshin’s diabetes mellitus PP 358 44 Sadhyasadhyata
  53. 53. UPADRAVA Complications appearing after the manifestation of the Primedisease and which are difficult to treat are termed as upadravas. Agniand Vata, in their aggravated state cause many of upadravas inMedoroga 81.Upadravas explained in different texts are tabulated below. Sl No Upadravas Ch82 Su A B M Y 83 S84 P85 N86 R87 1 Vata pitta Vikara a - - - a - 2 Prameha Pidika - a a - - - 3 Jwara - a a a - a 4 Bhagandara - a a a - a 5 Vidradhi - a a - - - 6 Vatavikara - a - - - - 7 Udar roga - - a - - - 8 Prameha - - a a - a 9 Urustambha - - a - - - 10 Kushta - - - a - - 11 Visarpa - - - a - a 12 Atisara - - - a - a 13 Arsha - - - a - a 14 Shleepada - - - a - a 15 Apachi - - - a - a 16 Kamala - - - a - a 17 Jantavo Anavaha - - - a - - Key : a = Present - = Absent 44 Upadrava
  54. 54. It is clearly mentioned, increased medas cause profuse sweatingand bad odour of the skin, which creates a media for production andsurvival of germs (anu jantus) 88. There by many of the skin diseases likekusta, visarpa etc are seen as upadravas and atisweda mentioned aspoorvarupa for Kusta 89. Impairment of Medovaha srotas in Medoroga maylead to the disease Prameha and Prameha pidika. Ama condition present in sthoulya may lead to urustamba, atisara,jwara etc. The etiological factors viz Avyavaya , Avyayama, diwaswapna 90are similar to both Medoroga and Arsha 91. These factors are increasedmore because of inactive nature of obese person, which probably leads toarsha. Obstruction of swedavaha and ambuvaha srotas leads to udara 92,as excess medas obstruct the srotases, this condition may arise asupadrava in obese person. Vata get aggravated because of obstructionand give rise many of the vatavyadhis as upadravas.Modern concept 93 Obesity has psychological, behavioral and medical consequences,the nature and severity of which are influenced by the degree of obesity.The common pathological consequences of obesity are discussed here.Non insulin dependent diabetes – Obesity is major risk factors for NIDDM and as many as 80% ofpatients with NIDDM are obese. 45 Upadrava
  55. 55. Cardiovascular Disease – Epidemiological studies reveal that obesity is associated with anincreased mortality and morbidity from cardiovascular disease. Increasedmass of tissue results in increased cardiac work. Blood volume, strokevolume and cardiac out put are all increased. Obesity is also associatedwith an atherogenic lipid profile.Pulmonary disease – The increased metabolic rate in obese subjects increases oxygenconsumption and CO 2 production, and these changes result in increasedminute ventilation. In subjects with marked obesity, compliance of thechest wall is reduced, the breathing is increased, and the respiratoryreserve volume and vital capacity are reduced, a resultant mismatchbetween ventilation and perfusion may result in hypoxemia. Severeobesity may cause hypoventilation, defined by the development of CO 2retention.Gall stones – Obesity is associated with enhanced billiary secretion ofcholesterol. This results in supersaturation of bile and a higher incidenceof gallstones.Endocrine consequences – Many changes in function of Thyroid, Gonadal, Adernal andPituitary functions can be seen in patients with established obesity. 46 Upadrava
  56. 56. REFERENCES81. Yoga Ratnakara Medoroga chikitsa / 782. Charaka sutrasthana 21 / 783. Sushruta sutrasthana 15 / 3284. Astanga sangraha sutrasthana 24 / 2585. Bhavaprakasha madhyamakhanda 39 / 1086. Madhava Nidana 34 / 887. Yoga Ratnakara Medoroga chikitsa / 1088. Bhavaprakasha Madhyama khanda 8 /1089. Charaka Chikitsa Sthana 7/1090. Sushruta sutrasthana 15/3291. Charaka Chikitsa Sthana 14/1092. Charaka Chikitsa Sthana 13/ 1993. Joslin’s Diabetes Mellitus pp355 47 Upadrava
  57. 57. It is important to emphasis that with optimal management andproper education about the disease to the patient only, reduces obesityalong with gaining confidence from the patient.Few facts acting over the disease are - General considerations in development and reduction of obesity. - Individual dietary requirements and meal planning. - The role of exercise. - Effects of medications. - Commonly associated conditions like Diabetes, Hypertension etc. - Importance of regular check-up. It is an established fact that the person who has acquired properunderstanding of the causes responsible for his obesity can lose hisexcess weight more easily and effectively, which is explained as chiefprinciple i.e. Nidana parivarjana.There are three ways of reducing over weight:a) Increase the output of workb) Reduce the food intake, andc) Plan for a suitable medication. In other words Ahara, Vihara and Aushadha are the three lines oftreatment 47 Chikitsa
  58. 58. AHARA Even-though the disease is santarpanajanya; langhan iscontraindicated 1 as it increases the Vata that is the prime cause forMedoroga. There by if the food is not supplied timely aggravates Agniand create many disturbances in the body 2. Keeping this in mind,dietetics has to be planned in such a way that Ahara should be guru foragni but at the same time it should cause apatarpana, kapha and vatashamana 3. Many of the Ahara dravyas are advised on this line, which arementioned in pathyapatha. Many experimental studies have been done onfasting and the inference is that during the period of fasting, the bloodpressure goes down, ketosis and hyperurecaemia occurs. Thus it isadvised to undertake prolonged fasting program under medicalsupervision 4. So instead of advising for Langhana it is better to follow theclassical treatment which explains to enhance Agni, which does notcause santarpana. It almost sounds similar to more quantity but lesscaloric diet. Diet for obese person should be planned that the body get about 50 –60 gm of protein per day, which is necessary for maintaining nitrogenbalance in the body, 100 gm of carbohydrate, 40 – 50 gm of fat. Thisproportion of protein, carbohydrate and fat has to be maintained whichotherwise disturbs the metabolism 5. The total calories allowed to anindividual will depend on the present weight, activity levels of the patient. 48 Chikitsa
  59. 59. Model diet plan supplying about 1,000 calories during the course of a dayis given below 1. Early morning - one glass of hot water with lemon or lime juice. 2. Morning breakfast – any one or two items from the list given below a) ¾ cup of milk without adding sugar or one cup of tea or coffee with a little milk. In tea or coffee saccharin, and not sugar, may be used b) An orange or a mosambi or any other fruit (except banana) of an ordinary size. c) One slice of bread or one small khakhara. Those who are heavily overweight should avoid them. d) One egg e) 2 to 3 small tomatoes or cucumbers 3. Mid–day meal a) take a cup of vegetable soup or any other soup before starting the meal or one glassful of water b) Before other courses are taken, take green–salad containing 4 to 5 tomatoes or 2 to 3 medium size cucumbers. Chew them well. These can be taken in a larger quantity also. c) One small bowl-full of a low-caloric cooked vegetable from the list given below; green leaf bhaji, carrots, cucumber, 49 Chikitsa
  60. 60. unripe tomatoes, brinjals, cabbage, beat, radish, white gourd, French-beans, bhindi, etc. d) One or two small chapaties or bread slices. e) One small cupful of moong soup or any other soup made from a common pulses or cereals. f) Some meat or fish. 4. Afternoon / Early evening – As per the morning breakfast, if patient feel restless 5. Dinner – same as the mid-day meal. But a small cupful rice or khichadi can be taken instead of bread or chapati.Caloric values of the uncooked and cooked food articles mentioned in theappendix ( Table No 5 and 6 ) are according to NIN (National institute ofnutrition), Hyderabad.VIHARA Vyayama, vyavaya, anidra, chinta, shoka, shrama, Gamana 6 are thevihara roopa treatment mentioned in the classics. Lacks of these factorsare mentioned as nidana for sthoulya. Hence, we can say this is one ofthe nidana parimarjana line of treatment. Regular exercise isrecommended as an important component of all obese managementregimens. Exercise help a person to spend energy and reduce his weight;and increases the basal metabolic rate of the body which in turn burns 50 Chikitsa
  61. 61. away the excess fat 7 and benefits in lipid abnormalities. Exercisesimprove the muscle tone and remove wrinkles and flabbiness of skin 8.Simple walking or exercise, when energy worth 3500 calories is spent,the weight is reduced by 1 pound. Table below show energy spent indifferent types of the physical activity. Table No 7 Sl No Type of the physical activity Energy spent per minute 1 Sitting, standing, reading, writing 1.5 2 Driving car, tailoring, 2.0 3 Household chores 2.2 4 Gardening 5.0 5 Walking 5 km / hr speed 3.0 6 Fast walking 9 km / hr speed 9.0 7 Light exercises of yoga 4.0 8 Cycling (depending upon speed) 3.5 – 8.0 9 Table tennis 5.5 10 Games like kho-kho etc. 8.0 11 Lawn tennis 6.0 12 Dancing 5.0 13 Swimming 3 km / hr speed 9.0 14 Skipping 7.0 15 Running (depending upon speed) 10-25 16 Heavy exercise 8.0 51 Chikitsa
  62. 62. AUSHADHI This can be discussed under two headings 1. Shodhana. 2. Shamana1. Shodhana Under the heading of Shodhana we can consider Rooksha Udwarthana, snana 9, Lekhana Basti 10 and Shodhana 11. The general term Shodhana is used by Vagbhata which indicate all the panchakarmas. But when we see the dos and don’ts of panchakarma it reveals – a. Snehana – As a general rule Snehana should not be administered in Medorogi 12 but tila taila prayoga is indicated in Medoroga. It may be because of its gunas like sukshma and vyavayi through which it opens the medovritha srotas and ushna guna of it reduces the kapha 13 b. Swedana – Swedana for obese patient is contra indicated 14 but if essential Mrudu sweda is advised 15. c. Vamana – not indicated in sthoulya 16 where as in conditions like amadoshayukta 17 and kapholbana vamana could be advised with yastimadhu 18. 52 Chikitsa
  63. 63. d. Virechana – not indicated 19 but with special precautions it can be used. e. Basti – Lekhana Basti is indicated f. Nasya and Raktamokshana - clear-cut indication is not available.2. Shamana Eventhough Meda, Vata and Kapha Nashana is said as chikitsa sutra 20, the drug planned should have deepana and pachana property to enhance Agni and digest ama. As obstruction of srotas is main factor in Medoroga, the drugs must have Rookshana and Chedan property 21 to Produce sroto vishodhan. Along with these Ati teekshna, ushna, rookshna guna dravyas are also advised 22 as they are opposite to manda, snigdha and sheeta gunas of kapha and Meda. There by they subside Meda and Kapha. Five types of fat reducing drugs are used in modern science. a. anti appetite b. drugs reducing the level of sugars in the c. Metabolic stimulants d. Laxative drugs e. Diuretics. And surgical treatment is also advised in the treatment of obesity as lipo suction. 53 Chikitsa
  64. 64. REFERENCES1. Astanga Sangraha Sutrasthana 24 / 452. Charaka Sutrasthana 21/53. Charaka Sutrasthana 21/204. Runcie,j and Itilditch, T.E (1974) – B.M.J, ii,2505. From fat to fit pp 616. Bhaishajya Ratnavali 39/17. From fat to fit pp 728. Bloom.w.l. (1968). To fat or to exercise (B M.J.clin. Nutr, 21,1475)9. Astanga Sangraha. Sutrasthana 24/26 Charaka Sutrasthana 21/1010. Sushruta Sutrasthana 15/3211. Astanga Sangraha Sutrasthana 24/2612. Charaka Sutrasthana 15/53 Sushruta Chikitsa 31/4613. Charaka Sutrasthana 13/44,4614. Charaka Sutrasthana 14 / 1715. Astanga Hridaya Sutrasthana 17 / 2416.Charaka Siddhisthana 2/8 Sushruta Chikitsa 33/1417. Astanga Sangraha Sutrasthana 27 / 3018. Sushruta Chikitsa 30 / 919. Charaka Siddhisthana 2/8,11 Sushruta Chikitsa 33/1820. Astanga Hridaya Sutrasthana 14 / 2121. Sushruta Sutrasthana 15 / 3222. Astanga Sangraha Sutrasthana 24 / 26 54 Chikitsa
  65. 65. PATHYA – APATHYA Pathya pathya is the part and parcel of the successful treatment.Especially in Medoroga it is most important. The aharas and viharasexplained by different acharyas, which help in curing a disease, arediscussed below. PathyasAHARACharak samhita prashatika, Priyangu, Shyamaka, Yavaka, Yava, Kodrava, Mudgha, Kulatha, Chakra mudgha, Patola, Amalaki, Modhoodaka, Arista.Sushruta samhita Madhu, Yava, Mudgha, Kodrava, Uddhalak.Astanga hridaya Kulatha, Yavaka, Yava, Shyamaka, Mudgha, Madhoodhaka, Aristaka, Mastu and Takra.Yoga ratnakara Purana shali, Mudgha, Kulatha, Uddhalaka, Kodrava, Yava, Shyamaka, Madhu.Sharagadhara samhita Shyamaka, Priyangu, Yava, Kulatha, Chanaka, Massora, Mudga, Madhu, Laja, Takra, Sura.
  66. 66. VIHARACharak Jagarana, Vyavaya, Vyayama, Chinta.Sushruta Causative factors should be avoided.Vagbhata Jagarana, Vyavaya, Vyayama, Chinta.Yoga ratnakara Jagarana, Vyavaya, Vyayama, Chinta, Margagamana.Sharagadhara Chinta, shrama, jagarana, Vyavaya, Langhana, Atapasevana, Hasti and ashwa Yana, bhramana. Apathyas Ahara - rasayana Dravyas, naveen shali, godhuma, ksheera vikruti, ikshu vikruti, masha, matsya, mamsa. Vihara - sheetala jala snana, diwaswapna, sugandha dravya sevana, drinking water immediately after consuming food.Apart form this, factors mentioned under causative factors are Apathyas.
  67. 67. Pippalyadi Guggulu, is a combination of Pippali, Triphala, Haritaki,Guggulu, Madhu and Gomutra.Criteria for selection Sthoulya or Medoroga is santarpanotha vikara 1, caused by atisnehadravya sevana 2. Accumulation of excess medas is chief sign ofMedoroga. Keeping all these points in view the present combination isselected. While explaining snehavyapat, Vagbhata affirms, excessivesnehana therapy give rise to all the diseases which might be caused byAtisneha sevana 3 it has to be treated with a combination of takrarista,uddala, Yava, Shyamaka, Kodrava, Pippali, Triphala, Honey, Pathya,Gomutra and Guggulu 4. As sthoulya is also santarpana vikara, thiscombination is found suitable for treatment. Among the above said,Pippali, Triphala, Honey, Pathya, Gomutra and Guggulu are onlyAushadhis, explained by Acharyas, thus the present yoga is selected astrial medicine. In addition to the above references except Pippali, all the otherherbs viz Triphala, Honey, Pathya, Gomutra and Guggulu are mentionedas treatment for sthoulya by Sushruta 5, while explaining the treatment forsantarpanotha vyadhi. Charaka offer a combination of Haritaki and Madhuwhile scheduling treatment of santarpanotha vikaras, especially for 54 Drug Review
  68. 68. sthoulya. This gives waitage to have Haritaki as separate part apart fromTriphala in the present combination. Individual drugs are also studied andeach of them are found to have Medohara effect. Pharmacologicalproperties of these drugs are also suitable for treating the selecteddisease. Medicine is prepared in tablet form, as Guggulu is Medohara andquickly absorbed in oral route. It can be taken for a long time withoutany ill effects 6. Herbs selected for formulating the medicine are verysimple, economical and abundantly available in all parts of India. Thereby present trial drug is an economical, suitable, long-term and convenientremedy for sthoulya. 55 Drug Review
  69. 69. DESCRIPTION OF INDIVIDUAL DRUG OF THE COMPOUND MEDICINE 1. HARITAKI Sanskrit - Haritaki Hindi - Harad Kannada - Anale kayi Latin - Terminalia chebula Family - Combretaceae.Synonyms - Pathya, Abhaya, Amruta, Vijaya.Distribution - Forests of Northern India, Common in Madras and Mysore 7Part used - Dried Phala Majja.Short description - Fruits are oval in shape and about 2 inch long and are of dull yellow in colour.Pharmacological properties –Guna – Laghu, Ruksha.Rasa - except lavana all the five.Vipaka – katu.Veerya – ushna.Doshaghnata – . Tridoshagna 56 Drug Review
  70. 70. Chemical composition – This contain astringent principles – Tannin, a brownish yellowcolouring matter, chebulinic acid- which when heated in water splits upinto tannic and gallic acids.Actions concerned to disease – It does Lekhan karma 8 and subsides all the Santarpanotha vyadhis 9Haritaki with Madhu is considered as best treatment for sthoulya 10 57 Drug Review
  71. 71. 2. BIBHITAKISanskrit - BIBHITAKIHindi - BahedaKannada - TarekayiLatin - Terminalia BelliricaFamily - Combtaceae.Synonyms - Karshaphala, Kali Druma.Distribution - Common in Indian forests and plains.Parts used – Dried phala majjaShort description - Fruits are 12 – 25 mm dia ovoid in shape grey incolour, suddenly narrowed into a very short stalk, Obscureles, 5 angled.Pharmacological properties –Guna – Laghu, Ruksha.Rasa - KashayaVipaka – Madhura.Veerya – Ushna.Doshaghnata – Tridoshagna. 58 Drug Review
  72. 72. Chemical composition – Gallotannic acid, colouring matters, resins and greenish yellow oil.Actions concerned to disease – Diseases due to Rasa, Rakta, Mamsa, Meda dushyas are subsided 11by Bibhitaki 59 Drug Review
  73. 73. 3. AMALAKI Sanskrit - AMALAKI Hindi - Avala Kannada - Nellikayi Latin - Emblica officinalis Family -. Euphorbiaceae.Synonyms - Dathri, Amraphala, Vayastha..Distribution - Deccan and sea coast Districts and Kashmir.Parts used - Dried phala majja.Short description - Fruit is 1.3 – 1.6 cm in diameter, fleshy with 6 obsure vertical furrows and pale yellow in colour.Pharmacological properties - Guna – Guru, Ruksha, Sheeta. Rasa - Except Lavan all the five Vipaka – Madhura. Veerya – Sheeta. Doshaghnata – Tridoshagna. 60 Drug Review
  74. 74. Chemical composition – Fruit contains Galic acid, Tannic acid, Sucrose, Albumin, Cellulose,Calcium and very rich with Vitamin C.Actions concerned to disease – It subsides Medas 12; and useful in the liver complaints, thirst, piles,etc. it is very good rasayana 13. 61 Drug Review