• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Madhumeha kc007 gdg
 

Madhumeha kc007 gdg

on

  • 3,167 views

EVALUATION OF THE EFFICACY OF BHUMYAMALAKYADI CHURNA IN MADHUMEHA ,SHASHIDHAR. T. HOMBAL , Post Graduate Studies & Research Center, D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG

EVALUATION OF THE EFFICACY OF BHUMYAMALAKYADI CHURNA IN MADHUMEHA ,SHASHIDHAR. T. HOMBAL , Post Graduate Studies & Research Center, D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG

Statistics

Views

Total Views
3,167
Views on SlideShare
3,167
Embed Views
0

Actions

Likes
1
Downloads
19
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Adobe PDF

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Madhumeha kc007 gdg Madhumeha kc007 gdg Document Transcript

    • EVALUATION OF THE EFFICACY OF BHUMYAMALAKYADI CHURNA IN MADHUMEHA (WITH SPECIAL REFERENCE TO ITS HYPOGLYCEMIC 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 SHASHIDHAR. T. HOMBAL. 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 GADAG.
    • LIST OF ILLUSTRATIONSSl. No. Figure Name Page No.1. Photograph of Haritaki 562. Photograph of Bibhitaki 583. Photograph of Amalaki 604. Photograph of Pippali 625. Photograph of Guggulu 646. Photograph of Madhu 667. Photograph of Gomutra 68
    • List of Master ChartsSl No Master Charts Page No 1. Demographic data 79 2. Data related to Personal history 80 3. Data related to Complaints 81 4. Data related to Associated Complaints 82 5. Data related to Upadravas 83 6 A. Data related to Objective Parameters 84 6 B. Data related to Objective Parameters 85 7 A. Data related to Lab Investigations 86 7 B. Data related to Lab Investigations 87
    • List of FiguresSl No Figures Page No 1. Showing Age and Sex ratio 89 2. Showing the Religion incidence 90 3. Showing the Occupation incidence 91 4. Showing the Economical status incidence 92 5. Showing the Diet incidence 93 6. Showing the Family history incidence 94 7. Showing the Chronicity 95 8 Showing the body weight of Group A 103 9. Showing the body weight of Group B 10310. Circumference of Udara of Group A 10411. Circumference of Udara of Group B 10412. Circumference of Spik of Group A 10513. Circumference of Spik of Group B 10514. Circumference of Sthana of Group A 10615. Circumference of Sthana of Group B 10616. Serum Cholesterol of Group A 10717. Serum Cholesterol of Group B 10718. Serum Triglyceride of Group A 108
    • 19. Serum Triglyceride of Group B 10820. Serum HDL Cholesterol of Group A 10921. Serum HDL Cholesterol of Group B 10922. Serum LDL Cholesterol of Group A 11023. Serum HDL Cholesterol of Group B 11024. Serum VLDL Cholesterol of Group A 11125. Serum VLDL Cholesterol of Group B 11126. Random Blood Sugar of Group A 11227. Random Blood Sugar of Group B 11228. Showing the Result 114
    • CONTENTS Page No.1) INTRODUCTION 12) SHAREERA 93) NIDANA Hetu 19 Samprapti 25 Poorvarupa 30 Rupa 31 Bedha 40 Sadhyasadhyata 43 Upadrava 444) CHIKITSA 475) DRUG REVIEW 546) MATERIAL AND METHODS 717) OBSERVATION, ANALYSIS AND INTERPRETATION 798) CONCLUSION 1159) SUMMERY 118 BIBLIOGRAPHY APPENDIX
    • ACKNOWLEDGEMENT I am highly indebted to my guide, Dr Ch. Ranga Rao, H.O.D.Department of Post Graduate and Research centre, sri D.G.M.AyurvedicMedical College, Gadag for his valuable suggestions and guidance incompleting this work successfully. I am heartily thankful to Dr V.V.S.Shastri. Under whose guidancemy work was started and he was the teacher who inspired me to take thecombination of the drug mentioned in this thesis. I am ever grateful to my Co-guide Dr. Siva Ram Prasad Ketamakkawho was a helping hand throughout the work and supported me incompleting the work in stipulated time. I am thankful to our Principal Dr G.B.Patil for his support incompleting this work successfully. I am very much thankful to Mr. Nandakumar for his valuable help instatistical calculations. I am thankful to Dr A.K.Panda and all other staff of DGM college fortheir help. Acknowledgement
    • I acknowledge to our collage librarian Mr V.M.Mundanamani andhis assistant Mr Sureban for supporting me by providing lot of books forthe study. I am thankful to Mr Giriachar Officer National Information Centre(NIC) Gadag, for giving me information about the work going on indifferent parts of the world regarding this subject. My personal thanks to Mr.N.N.Bhat and Mr C.S.Bhat who helpedme in understanding the Sanskrit versions. I am thankful to Dr.(Mrs) M.D.Gojanur for supporting me byreferring the cases for trial. I am thankful to my colleagues and friends who supported me inclinical trials and made the trial successful. I am thankful to all the patients who agreed to undergo thetreatment with the trial drug. I am highly indebted to my beloved parents, who framed a properpath for my carrier. Acknowledgement
    • I express my heartfelt gratitude to all my family members for theirconstant help, love and care rendered during my study. I am thankful to all my teachers, from primary education to postgraduate education for helping me in building up my carrier. This list is incomplete without remembering my small sunny Kiran(18 months) whose smile inspired and kept me cheerful throughout mywork. I wish to thank all the persons who have helped me directly andindirectly with apologies for my inability to identify them individually. Acknowledgement
    • ACKNOWLEDGEMENT I am highly indebted to my guide, Dr Ch. Ranga Rao, H.O.D.Department of Post Graduate and Research centre, sri D.G.M.AyurvedicMedical College, Gadag for his valuable suggestions and guidance incompleting this work successfully. I am heartily thankful to Dr V.V.S.Shastri. Under whose guidancemy work was started and he was the teacher who inspired me to take thecombination of the drug mentioned in this thesis. I am ever grateful to my Co-guide Dr. Siva Ram Prasad Ketamakkawho was a helping hand throughout the work and supported me incompleting the work in stipulated time. I am thankful to our Principal Dr G.B.Patil for his support incompleting this work successfully. I am very much thankful to Mr. Nandakumar for his valuable help instatistical calculations. I am thankful to Dr A.K.Panda and all other staff of DGM college fortheir help. Acknowledgement
    • I acknowledge to our collage librarian Mr V.M.Mundanamani andhis assistant Mr Sureban for supporting me by providing lot of books forthe study. I am thankful to Mr Giriachar Officer National Information Centre(NIC) Gadag, for giving me information about the work going on indifferent parts of the world regarding this subject. My personal thanks to Mr.N.N.Bhat and Mr C.S.Bhat who helpedme in understanding the Sanskrit versions. I am thankful to Dr.(Mrs) M.D.Gojanur for supporting me byreferring the cases for trial. I am thankful to my colleagues and friends who supported me inclinical trials and made the trial successful. I am thankful to all the patients who agreed to undergo thetreatment with the trial drug. I am highly indebted to my beloved parents, who framed a properpath for my carrier. Acknowledgement
    • I express my heartfelt gratitude to all my family members for theirconstant help, love and care rendered during my study. I am thankful to all my teachers, from primary education to postgraduate education for helping me in building up my carrier. This list is incomplete without remembering my small sunny Kiran(18 months) whose smile inspired and kept me cheerful throughout mywork. I wish to thank all the persons who have helped me directly andindirectly with apologies for my inability to identify them individually. Acknowledgement
    • Madhumeha is emerging as the chronic non-communicable diseaseof concern in developing countries. With changing environment,urbanisation and altered life-style giving more comforts and sedentary lifeto human, simultaneously offering metabolic diseases like Madhumeha. Madhumeha is a disease in which certain pathological changes arenoticed in urine, the most important being the presence of sugar. Sincethis disease is connected with the urinary system with the presence ofsugar in the urine, the comparison of Madhumeha with Diabetes Mellitusis justifiable. Madhumeha is also one of the identified major cause of morbidityand mortality in India 1. In further, Indians have high ethnic susceptibilityfor developing Madhumeha at a younger age group. The disease usuallyoccurs after 30 years of age, seen more in male than in female. Being a slow onset and often relatively asymptomatic disease,remains undiagnosed at onset, or even if diagnosed is often ignored bypersons afflicted with it. In addition lack of awareness amongst healthprofessionals and inadequate health care facilities compound the problemof Madhumeha related complications in our country 2. 1 Introduction
    • The alarming rise in non – communicable diseases like Madhumehawarrants immediate attention of the experts to develop and propose,formulate, establish, not only effective treatment schedules, but also toplan preventive measures against Madhumeha and control the morbidityrate due to this disease. Ayurveda proposes a comfortable remedy aspalliative therapy.ITHIHASA There is precious information given by our Acharyas about all theaspects of the disease, which reveal the pathological aspects of diseaseand make them easy to understand. They had a thorough knowledge ofthe entire disease that can be observed in their literature. We canobserve the classical references which indicate the disease as one of thedreadful and chronic. Our ancestors have tried to know about thedisease from various angles, which made them to think in many aspectsof the disease. By observation alone they have classified the diseaseelaborately. Thus to understand the disease we have to know the subjectalready existing since the days of Vedas which give valuable informationabout the disease.VEDIC PERIOD Vedas are the oldest literature of civilization. Ayurveda is theUpanga of Atharvan Veda. In Vedas we find two words “Asrava” and 2 Introduction
    • “Prameha”. In Atharvana Veda Asrava vyadhis are mentioned in whichNasasrava, Atimootra and Atisara are included 3. The term Asrava ifformed from “A – srava” means to flow. In Atharvana Veda 6 / 44 / 3 “Visanaka” drug is indicated in vatavyadhi. Kesava commenting on this, explained “Vatikruta nasani” as “Vatikruta asravasya nasani”, means it is indicated in Asrava vyadhis. Inthe Manthra 2-3-1-3 of Atharvana Veda, the drugs emerged from valmikaare indicated in Atisara, Atimootra and Nadivranam 4. This clearly indicates the prevalence of this disease with itsremedy in the Vedic period.SAMHITA PERIOD After Vedic period facts about Madhumeha were further explored byAtreya which are recorded in “ Charaka Samhita” a complete treatise ofmedical sciences of its era. He explains various factors pertaining toetiology, pathogenesis, complications and methods of treatment in detailin his treatise. It is a point of historical importance that the bookmentions the loss of sweet substance from urine 5. Charaka also mentioned in sutra sthana that the Madhumehaoccurs due to avrita of Vayu 6, and explains the mythological origin of 3 Introduction
    • Madhumeha in Nidana sthana 7. During the destruction of Daksha’s assacrifice, Gulma first manifested in human being who fled in all directionsdue to the agitations in their body. Because of fleeing, swimming,running, flying, jumping etc. Pramehas and Kustas manifested themselvesin addition to the intake of Ghee. Bhela samhita which is contemporary to Charaka samhita describesthe two types of Madhumeha i.e. prakruta prabhava (congenital) andSwakruta (acquired)Prabhava 8. The most notable contribution of Sushruta was to devote aseparate chapter for the management of Madhumeha and he has triedsome specific preparations of minerals and vegitations. Further he hasalso described in a separate chapter for the management of Carbuncleswhich are the Upadravas of Madhumeha 9. After Sushruta, Vagbhata made great contribution to Indianmedicine. He simplified the existing knowledge and gave some newpreparations and ideas in the text. He classified two types of Madhumehaon the basis of pathogenesis are Dhatukshayaja and Avaranaja 10. Artha shastra of koutilya (321 – 296 BC) mentions a method toinduce Prameha in Human dealing with the sense to injure the enemy. 4 Introduction
    • The spot obtained from burning chanclion (krukalaka) and house lizard(Gruha goulika) together with the intestines of mottled frog (chitra bheka)and honey, if administered causes Prameha. This evidently points theexistence of Diabetogenic technique in the ancient times 11.MEDIEVAL PERIOD This period of history of Indian medicine is known as a period ofcommentators. Hence most of the books of this period are of collectionsand thoughts of previous authors, commentaries of previous books. Madhavakara (9 t h century A.D.) in his book Madhava nidanacompiled the thoughts of his earlier authors without adding any thing newto the knowledge on Madhumeha. Gayadasa (11 t h Century A.D.) commentator of Sushruta Samhitaelucidated that avilata of urine in Prameha was due to the presence ofsome components of dooshyas i.e. meda, mamsa etc 12 . Chakrapani, the commentator of Charaka samhita and the author ofChakradatta, in the same period contributed nothing significant withreference to etiology of Prameha but recommended medicines andregimen prescribed by Charaka and Sushruta and some of his own. 5 Introduction
    • Dalhana, another commentator of Sushruta samhita (12 t h century)contributed a myth that females do not suffer from Madhumeha 13. Sharangadara ( 13 t h century AD) prescribed some new recipes forthe management of Prameha but did not contribute any thing in the fieldof etiopathogenesis. Bhavamishra (16 t h century AD) contributed to the history ofPrameha by adding some new herbal and metallic preparations for themanagement of Prameha 14. After Bhavamisra the development of Ayurveda is not so optimisticand had been stagnated. The concepts of ancient India regardingMadhumeha are quite alike with modern concepts. Descriptions ofCharaka, Sushruta show that even in that ancient time, Indian scholarswere familiar with etiology, pathogenesis, symptomology andcomplications of Prameha, out standing being the knowledge of geneticrole in the etiopathogenesis. The regimen prescribed by them are usefuleven in present era also, and these texts and their concepts do notremain mearly as the historical mile stones but have become the hopeof the Madhumeha cure at present sinerio. 6 Introduction
    • HISTORICAL MILESTONES. 15- Atharvana Veda is the oldest literature, which explains Madhumeha.- In 2500 BC Eabers Papyrus ( Egypt ) wrote the first clinical description as “the disease without pain and melts the body” was documented.- In 600 BC Charaka (India) clinically described Madhumeha and noted role of heredity and Sweetness in urine.- In 400 BC Sushruta (India) described same as that of Charaka.- In 30 BC – 38 AD Celsus (Greece) gave some clinical description.- In 1 s t AD Aretaus (Greece) introduced the name as diabetes meaning “to run through a pipe” .- In 2 n d AD Claudius Galenus proved that by consuming the drinks which weakens the kidney will allow the liquids without change.- In the same century Tchang Tchong king proved this as the disease of thrust. 7 Introduction
    • - In 600 AD Aetius (Amida) treated this disease by using sedatives.- In 980 – 1037 AD Avicenna ( Arab ) explained about Diabetic Gangrene and put forward the question as “ is there any relation between pancreas”- In 1727 Brunner.J.C. ( Swiss ) removed the pancreas from the dogs and found that they developed thirst and polyurea.- In 1770 Thomas willis ( England ) proved the difference between Diabetes Mallets and Diabetes Insipidus.- In 1775 Matheu Dobson Evaporated the specimen of urine of a Diabetic patient and discovered a residue which was almost glucose.- In 1782 Thomas Cawley recorded the disease.- In 1788 Cawley (English) described pathology of pancreas.- In 1815 M. Chevreul found out the presence of glucose in the urine. 8 Introduction
    • - In 1839 Bernard Naunyn studied the relation between the metabolic disturbance and pancreas.- In 1841 Trommer found the test for urine glucose.- In 1848 Claude Bernard proposed that the production of sugar in the liver is the reason for the rise in the blood glucose Laval. He injured the base of the fourth ventricle and proved the increase of blood sugar level, he also proved when the blood sugar level is raised the sugar starts flowing out through urine. Even after the lowering of the blood glucose level the urine contains glucose was the major discovery by Claude Bernard.- In 1845 Boucardet established the relation between the Diabetes and Pancreas.- In 1850 Fehling found the test for testing the urine sugar.- In 1867 Paul Langerhans (Germany) found islets of langerhans.- In 1874 kusmal found the symptoms caused by increase in acitone in the body. 9 Introduction
    • - In 1874 Oacar Minkowski found the acidosis.- In 1886 Joshaf wan maring and Oscar Minkowski proved the induction of diabetes by removing the Pancreas.- In 1870 Clande Bernard ( France ) Noted sugar storage in liver as glucogon and elevated blood sugar in diabetes.- In 1901 E.L.O.Pie proved the increase and decrease in the blood glucose level is due to langerhans.- In 1907 M.L Lane differentiated and named the langerhans as two types “alpha and beta“.- In 1921 J.J.R.Macleod, Frederick . G . Banting and Charles.H. Best (Toronto )discovered Insulin- In 1926 H.C.Hagedorn mixed protimine to insulin and made it to defuse slowly so that it can act for longer time.- In 1944 Von Noorden ( Vienna ) Believed that liver play a role in diabetes. 10 Introduction
    • - In 1952 Sanger found the structure of the insulin.- In 1954 A. Shef found Carbutamide was working as a hypoglycemic agent. This was the first oral hypoglycemic agent, but as it had many side effects it was drown back from the market and a new drug similar in the function of Carbutamide was introduced as Tobutamide which has less side effects.- In 1970 On words Merwin Gliedman and other transplanted pancreas culture of Islets of cells of pancreas transplant of beta cells. Even in 1999 also the research is going on throughout the world.Still we are failing to put full point to these milestones and newer aspectsof the disease are emerging out day by day. Some of the latest research going throughout the country and abroad is givenbelow16,17.- Toxicological Evaluation of Fenugreek seeds in Diabetic patients. By Sharma R.D. at PG Dept, SN Medical college, Agra. –1996- Constitutional study of patients of Diabetes Mellitus vis-Avis Madhumeha by R H Singh at Dept of Kayachikitsa, B.H.U. 1996 11 Introduction
    • - Prognosis of Prameha on the Basis of Insulin level. By Upadhyay at Dept of KC, I.M.S, B.H.U, Varnasi. 1996- Diabetic foot ulcers treated the Ayurvedic way By Ojha J K. at Dept of DG, B.H.U, Varnasi. – 1997- Scope and use of Indigenous Herbal drugs in Madhumeha an Indian Scenario. By Mukherjee.S K at C.D.R.I, Lucknow.- 1997- Potential antidiabetic agents form plant sources. By R K Goyal at Dept of Pharmacology, L M College of Pharmacy, Ahmedabad.- 1997-- Evaluation of hypoglycemic activity of Traditional Herbal preparation By Negam S A at Department of Pharmacology, NRC, Egypt. 1997.- Anti diabetic property of neem seed By Kannan J at Pharmacy Dept, Faculty of tech and Engg, MS University of Boroda. Baroda 1997- Hypoglycemic effect of Trigonella foenum Leaf in Diabetic By A. Barry at Dept of pathology and forensic Medicine, University of Basrah 1997. 12 Introduction
    • References1 API Text book of Medicine pp 2052 Diagnoses of Diabetes pp 23 Ayurveda Ithisa pp 264 Ayurveda Ithisa pp 295 Charaka Nidana 4 / 376 Charaka Sutra 17 / 78.7 Charaka Nidana 8 / 118 Bhela Samhita Nidana sthana 6 / 1 – 4.9 Sushruta Chikitsa 12 / 1610 Astanga .Hridaya.Nidana 10 / 811 Ardha Sastra of Koutilya 16 / 179 / 1.12 Su NI Naya Chandrika Commentory.6 / 6.13 Nibandha sangraha on Su Ni 6 / 3314 Bhava prakasha Madyama kanda 38 / 4515 Sihimootra roga by A. Narayanappa.pp 416 Allied Ayurvedic Medical Research Abstracts (AAMRA)17 Researches in Ayurveda 1997 13 Introduction
    • Charaka explained that the persons who take excess and heavyfood or food with sour and salty taste, new rice, fresh wine and enjoylong sleep will increase, the kapha, pitta, meda and mamsa and obstructsthe Vata together with the ojus come down to the vasti and causesMadhumeha 1. By this it can be seen that the vasti is involved in theproduction of Madhumeha. In Madhumeha, Prabhoota mootrata is themain lakshana. It is a symptom of mootravaha srotodusti also 2. Hence inMadhumeha mootravaha srotodusti is present. Charaka mentioned that Prameha occur whenever the Medas(srotas) is vitiated 3. vrikka and vapa are the moolas of MedovahaSrotas 4. So the involvement of vrikkas is present in Madhumeha.Thrishna is an important lakshana. The cause for trishna is UdakavahaSrotodusti 5. Talu and kloma are the moolas for Udakavaha srotas 6.Hence the involvement of Talu and Kloma are present in the production ofMadhumeha. Liver plays an important role in dhatuparinama. InMadhumeha dhatuparinama alters because of the involvement of most ofthe dhatus present in the pathogenesis. Hence the liver is responsible inthe production of Madhumeha. Thus it can be said that the organs responsible for the productionof Madhumeha are - 13 Shareera
    • 1. Taalu 2. Kloma 3. Vrikka 4. Vasti 5. Yakrit But in ayurveda the knowledge of rachana and kriya of Madhumehaare still in controversy, but with the help of modern science theKriyatmaka vivechana can be discussed.TALU The classical texts in Ayurveda have given the brief descriptionabout Talu. It is located above the kanta and becomes the base of thesiras as it is evident from the deliberations in Bhela samhita. It is themoola for the Udakavaha srotas 7. Charaka mentioned Talushosha andpipasa will exist if Udakavaha Srotas is vitiated 8. Sushruta mentionednine Talugatha vyadhis 9 . Charaka and Kashyapa stated that the union oftwo bones forms Talu 10.KLOMA Ayurveda acharyas stated that Kloma is the moola for UdakavahaSrotas 11. All acharyas mentioned this as one among the Kostangas 12. 14 Shareera
    • Though there are many schools of thoughts regarding the anatomicalidentification, In Sushruta samhita it is said that kloma is explained withYakrit which is located in the right side of the body 13. Dalhana whilecommenting on this said that it is in the right side of body which is layingdown below the Yakrit and it is also called as Tilakam. Vagbhata saysthat Kloma is located along with Yakrit in the right side of the body. Itscombination according to Sharangadhara samhita in Pitta which isagniroopa 14. He has mentioned Agnashaya as its synonym. Adhamallawhile commenting on this says that its formation is with the sonitha kitta.It is in the right side and in contact with the liver. He has also givenTilam as a synonym to Kloma 15. Charaka says that Talumoola and Kloma are the seats ofUdakavaha srotas. If these srotases are vitiated the pathologicalchanges i.e. shosha of above organs and thirst develops 16. Chakrapaniwhile commenting on Kloma said that it is a Pipasa sthana (thirst centre).Sushruta also said as above and on injury to these srotases theimmediate death occurs besides polydipsia. Based on the above descriptions it is clear that Kloma in oneamong the Kostangas and located adjacent to the Yakrit. The nearestorgans to the liver are Gallbladder and Pancreas. It is also clear that 15 Shareera
    • only Pancreactomy causes the polydipsia and death so it can beconsidered as Kloma.VRIKKAS Vrikkas are two in number and are situated in Kosta. All acharyasincluded vrikkas in kostangas. In Dalhana commentary on Sushruta thevrikkas are described as two fleshy bodies, each situated on either sideof spine and their shape as being like rounded bodies 17. These are saidto be composed of the essence of the Rakta and Medas 18. Sharangadarawhile describing their function says that vrikkas are said to be thenourishers of the abdominal fat 19. Adamalla while commenting on theabove states that vrikkas are two rounded bodies in the abdomen whichare derived form the essence of the blood and fat and they originate formfat. They are stated to be concerned with the nutrition of the abdominalfat. Ayruvedacharyas Charak, Dalhana, Chakrapani says vrikkas are twoin number and they are situated below the chest 20.VASTI Embryologically, Vasti is stated to be maternal contribution. It isstated to be derived form the essence of Rakta and kapha supported byPitta in to which Vayu also enters 21. Vasti has been included underkostangas and Ashayas by all acharyas. It is stated to be one in 16 Shareera
    • number 22. The term Vasti, Mutravasti, Vastipudaka, Mutrashaya andMutradhara seem to have been used as synonyms in Ayurvedic texts 23. Charaka while describing the location of Vasti has stated that vastiis situated in between the Sthoolaguda, Sevani, Sukravaha naadies andMotravaha naadies 24. According to Sushruta, Vasti is near to Nabhi, Kati,Guda, Vankshana and Shepha. He further stated that vasti, Pourusha,Vrushana and Guda are all interrelated and situated in the pelvic cavity 25.According to Bhavamishra and Sharangadara, Vasti is located below thePakwashaya. Vagbhata says that it is located inside the kati 26. Sushrutastates that it is situated near the Garbhashaya in females 27. Regarding the shape and structure of the Vasti, Sushruta hasstated that its shape looks like that of “Alabu” and full of Siras andSanyus all around. It is stated to be Tanu twak i.e. a thin volved organ orits coverings are thin and membranous. It has one exit and lies with itsmouth downwards 28. Vagbhata has described its shape as Dhanur Vakrai.e. bent like bow having one opening downwards and composed of littlemuscles and blood. Adamalla described its shape as “CharmakaLatwakara” that is like bag of leather. The Acharyas described it to bethe storehouse of Mootra and seat of “Prana” being one of the importantmarmas. Charaka says that it is reservoir of mootra where all theAmbhuvaha Srotases ends. He also explained vasti as the moola of 17 Shareera
    • Mootravaha srotas. Sushruta stated that Mootraghata, Prameha, Sukradoshas, Ashmari develops from Vasti only 29.YAKRIT Since the Vedic period, the traces of gross anatomical knowledgeof Yakrit are available. Sayana the commentator of Vedas whilecommenting on the word Yakan coined in atharvana veda described thatYakan is situated near the heart. The ward Yakan in his view meansYakrit. Yakrit is described as one of the Matruja angas due to itssoftness 30 and it is included in Kostangas. Yakrit in its embryonic stageis formed by the shonitha. Yakrit is situated on the right side, below theHridaya 31 and it is the moola for the Raktavaha srotas 32. Sushrutamentioned Raktadharakala is present in Yakrit 33. SHAREERA KRIYA Agni plays an important role in manifestation of Madhumeha henceconcept of Agni carries importance in the study of Madhumeha. Agni orJataragni is the main cause for every parinamas, or changes in the body.Dahana (burning) and Paka (Chemical action) are the chief actions ofagni. It splits the Vijateeya dravyas into sajateeya dravyas for easyabsorption. The ingested food after reaching Amashaya enters thedigestion by Antaragni. (Pachaka pitta) in the presence of samana vayu 18 Shareera
    • and Kledaka kapha which effects the digestion. The Ahara parinamakarabhavas are Ushma, Vayu, Kleda, Sneha, and kala which are essential fornormal ahara pachana. The digestion and other metabolism in the bodycan be done only in presence of Agni. The synonyms of Agni are kayagni, antaragni, kostagni,audaryagni. There is no Agni other than Pitta, as its actions perform inthe living body is Paka or pachana. Acharyas mentioned 13 types ofagnis in the body. They are one Jataragni, five bhootagnis and sevendhathwagnis. Samana vayu, which is located nearer to Jataragni movesall over the kosta, collects the ingested food. Then separates prasadaand kitta bhagas of Ahara into Ahara rasa and mootra, pureesharespectively. According to the Ayurvedic physiology Bhutagnipaka followsJataragnipaka and it completes the process of internal digestion, it isonly after the completion of Bhootagnipaka the formation of ahara rasa i spossible. Dhatwagnipaka does not start till the Bhootagnis completes itsprocess of digestion and supply the Sajaatiya nutrients to theDhatwagnis. But it can be said that the site of action of Bhootagnis startsfrom the intestines till the cell membrane, the liver being in between theBhutagnipaka that will be predominant in it. In the event of the failure ofthe function of Bhootagnis, the Dhatwagni will not be in a position to build 19 Shareera
    • the respective dhatus. That is how the deficient function of Bhootagnis isto be understood. Agni assumes names of Vishamagni, Teekshnagni, Mandagni, andSamagni according to doshic influence on it. Charaka says mandagni by its qualities causes ajeerna and malasanchaya, thereby it leads to several diseases. Mandagni vitiates kapha,kapha in turn vitiates the other dhatus particularly medo dhatu, and thisleads to Prameha. Hence the role of agni is to be considerable in thestudy of Madhumeha. Ayurveda has mentioned about the formation of Mootra and itsexcretion. Mootra has been described as the Drava Bhaga of the Kittaand it is produced in Amapakvashaya, The liquid portion is said toseparated form the solid fraction in the pakvashaya by the pureeshadharakala under the influence of Samana vayu, brought in to vasti and fromthere it is excreted by the Apanavata. Mootra is said to be an out comeof the digestion of ingested food, and the seat of its production ispakvashaya. Mootra is stated to be a mala derived form the foodingested in four-fold manner. The liquid portion of kitta bhaga afterabsorption circulates in the body and it is finally carried to vrikkas by twomutravaha dhamanis which divide in to innumerable branches forming themutravaha srotamsi through which it oozes and there it is named Mutra. 20 Shareera
    • From vrikkas, two Gavinis carry it to vasti. Even though Vrikkas havebeen mentioned in Ayurveda their relation with the formation of mootrahas not been clearly described. A deep study of Ayurveda classicsenlightens to certain extent about mootropatti. If Vrikka, Gavini andMedhra are considered as one system of srotas for the purpose of theproduction and excretion of urine, It remains stored in vasti till isexcreted during mutra pravrutti. If so, there can be no difference betweenthe views of Ayurveda and modern medicine. MODERN ASPECT Diabetes mellitus is a chronic disease. It results due to disturbancein carbohydrate metabolism and deficiency of Insulin 34 secreted by theBeta cells of Islets of langerhans of pancreas, but hormones of pituitaryand adrenal glands are also intimately related to the development ofDiabetes State. Liver plays an important role in the metabolism forcarbohydrate. It stores glucose in the form of glycogen under theinfluence of Insulin. Any alteration in this function leads to diabetes 35.So the involvement of organs in diabetes mellitus are - pituitary gland - Pancreas. - Adrenal gland - Liver. 21 Shareera
    • PITUTARY GLAND 36 This is a exceedingly important endocrine gland with a wide rangeof functions including the control of the other endocrine glands and ofbody growth. This gland measures 1.5 cm in the coronal plane, 1 cm in thesagital plane and 0.75 cm in vertical form. It lies within the sella Tarsicaof the sphenoid bone and posterio superior to the sphenoid air sinusesbelow the optic chiasma. It is flattened ovoid lying in the hypophysealfossa (sella Tarasica) and connected to the inferior surface of thehypothalamic part of the brain by the infundibulum. Structurally the glandcan be divided into two main partsa) Anterior lobe which is composed of Adeno hypophyseas tissue.b) Posterior lobe which is Neurohypophuyseas. Posterior lobe of the hypophysis is the expanded inferior end of theinfundibulum and is developed from the brain. The anterior lobe is muchlarger than the posterior lobe and consists of three parts, which partlysurround that lobe and the infundibulum. The distal part forms most ofthe anterior lobe. It is separated form the posterior lobe by the thin sheetof glandular tissues (intermediate part) applied to the posterior lobe. Theinfudibular part is a narrow upward projection of the distal part. The 22 Shareera
    • anterior lobe develops from the ectoderm and has only vascularconnection with the brain. Anterior lobe is the master gland of endocrine system, because itproduces proteotrophic hormones which effects the other ductless glands.In these secretions two hormones are having direct action oncarbohydrate metabolism. If any disturbance occurs it leads toHyperglycemia or Hypoglycemia. The hormones secreted are Growth hormone or somatotrophichormone (GH of STH ) and Adreno Cortico Trophic Hormone (ACTH).The pituitary effect of STH on carbohydrate metabolism is to stimulate itsstorage. Administration of growth hormone in animal or in man produceshyperglycemia and glycosuria. So the growth hormone is diabetogeniceffect especially in man. The hormone is however increases theglycogen content of cardiac muscle. Administration of ACTH producessimilar effects as induced by growth hormone. Both STH and ACTHincrease gluconeogenesis and diminish the rate of oxidation of glucose.Thus the anterior pituitary has a diabetogenic role. GH (growth hormone) is also known as somatotropin, its principalfunction is to act on the skeleton and skeletal muscles, in particular to 23 Shareera
    • increase their rate of growth and maintain their size once growth isattained. GH causes cells to grow and multiply by directly increasing therate at which amino acids enter cells and are built up into proteins. GH isconsidered to be a hormone of protein anabolism since it increases therate of protein synthesis. GH also promotes fat catabolism that is itcauses cells to switch from burning carbohydrates to burning fats forenergy released. At the same time GH accelerates the rate at whichglycogen stored in the liver is converted into glucose and released in theblood. Since the cells loosing fats for energy however they do notconsume as much glucose, the result is the increase in the blood sugarlevel. A condition called hyperglycemia. This process is calleddiabetogenic effect because it masks the elevated blood glucose level ofdiabetes mellitus. GH seems to produce many of its effects by convertingother factors in to growth promoting substance called soerto medians andinsulin like growth factors (IGF). Other hormones can indirectly affect insulin production however forinstance GH raises blood glucose level and the rise in glucose leveltriggers insulin secretion. ACTH by stimulating the secretion ofglucocorticoids brings about hyperglycemia and also directly stimulatesthe release of insulin GHIF (romatostatin) inhibits the secretion of insulin.One stimulus that inhibits GH secretion is hyperglycemia high bloodsugar level. An abnormally high blood sugar level stimulates the 24 Shareera
    • hypothalamus to secrete the regulating factor GHIF (somatisation) GHIFinhibits the release of GHAF and thus the secretion of GH. As a resultblood sugar level decreases.PANCREAS 37 The pancreas is a compound alveolar gland. It has got bothendocrine and exocrine functions. It lies against the posterior abdominalwall behind peritoneum. The adult pancreas consists of a Head, Neck,Body and Tail. The whole organ is about 15 cm long with the right marginof the head in contact with the descending part of the duodenum and thetail is in contact with the spleen. The disease diabetes mellitus isconsidered only to its endocrine secretion that is Insulin, so it is moreimportant to go through its endocrine part.ISLETS OF LANGERHANS The islets of Langerhans are composed of various components thatare organized to form micro-organs. The mass of islets within a pancreasis dynamic and changes both with growth and development and withfunctional challenges. As we learn more about the regulation ofdifferentiation of islet cell types, we also may learn how to enhance thegrowth of islet cells, particularly the beta cells. 25 Shareera
    • Islets function both singly and in concert. Recent work hasrevealed grater diversity in islets than that previously recognized. Thereis functional heterogeneity between islets and beta cells within the sameislet. Numerous peptides other than the four main islet hormones(insulin, glucagon, somatostatin, and pancreatic polypeptide) have beenimmuno-localized in islets. The islets of Langerhans are clusters of endocrine tissue scatteredthroughout the exocrine pancreas. In the adult mammal, the islets are 1to 2% of the pancreatic mass and thus comprise around 1gm of tissue inthe adult human. Islets are a complex mixture of cells and function bothseparately as micro-organs and in concert as the endocrine pancreas.Although the direct secretion of insulin and glucagon form islets into theportal vein has obvious advantages with respect to influence on hepaticfunction. The islet mass is dynamic, adjusting to meet the changingneeds of the individual, whose size and level of activity vary at differentstages of life. When the islet mass cannot adjust to meet the demand,diabetes results. The pancreas of the adult human contains about 200 units, or 8mg,of insulin. The size of an islet can range from only a few cells and lessthan 40 micrometer in diameter to about 5000 cells and 400 micrometerin diameter. 26 Shareera
    • GROWTH OF ISLET The growth capacity of the beta cell depends on the stimulus andthe ability of the cell to recognize the stimulus as well as on the numberof beta cells that can enter the cell cycle and undergo mitosis. There isan increased incidence of polyploid beta cells in the diabetic human.Although there may be numerous stimuli for beta-cell growth, three majorstimuli are known. Glucose has been shown to stimulate modest growthof either neonatal or adult pancreatic beta-cells in culture. Pregnancyhas been shown to cause both increased replication and mass of beta-cells. As a parallel finding, in vitro studies have shown that prolactin,placental lactogen and growth hormone can stimulate replication of beta-cells. Diabetes results only if increased cell loss or functional demandscannot be met.COMPONENTS OF THE ISLETS OF LANGERHANS There are three major endocrine cell types in islets : the insulinproducing beta-cell, the glucagon producing alpha-cell, the somatostatinproducing delta-cell.Alpha-cell The alpha cells are usually smaller and more columnar than thebeta cells and well granulated with granules 200 to 250 nm in diameter.The granules are electron dense with narrow halo of less-dense material 27 Shareera
    • and a tightly fitting granule-limiting membrane. There is little species ofvariation.Beta-cell The beta cells are polyhedral, being trancated pyramids, and areusually well granulated with secretary granules 250 to 350 nm indiameter.Delta-cell The delta-cells are usually smaller than either alpha or beta cells,are well granulated, and are often dendritic in shape. Within a delta cellthe electron density of granules varies greatly. Each granule, 200 to 250nm in diameter, contains material of homogenous moderate density thatfills the granule-limiting membrane. Table showing cells and their relative hormones Cell type Size of secretary granule (nm) % of cells Hormone Beta 250 – 350 60 – 80 Insulin Alfa 200 – 250 15 – 20 Glucagon delta 200 - 250 5 – 10 somatostatinMIC ROVASCULA TUR E The islets are highly vascularized and has a direct arteriolar bloodsupply. The fenestrae render these capillaries highly permeable. The 28 Shareera
    • blood flow to the islets has been found to be disproportionately large (10to 20% of the pancreatic blood flow) for the 1 – 2% of pancreatic volume. Factors regulating islet blood flow may effect islet hormone secretion.High concentrations of glucose have been shown to enhance pancreaticblood flow and to preferentially increase islet blood flow.NERVES The pancreas is innervated by sympathetic fibers from the celiacganglion and by parasympathetic fibers form the vagus nerve. Theseparasympathetic fibers synapse in small ganglia dispersed in thepancreas. They may act as pacemakers for the oscillations in hormonelevels that occur without extrinsic nervous connections, as in the isolatedperfused canine pancreas. Within the pancreas, nerve fibers terminate inperivascular, periacinar, and perinsular areas. Within the islets thenerves follow the blood vessels and terminate within the pericapillaryspace, within the capillary basement membrane, or closely apposed tothe endocrine cells 38Functions of these hormones :INSULIN: The insulin is hypoglycemic, anti diabetic factor and the proteinbound hormone that regulates the blood glucose. It also increases the 29 Shareera
    • oxidation of glucose to CO2 in the tissues and depressesgluconeogenesis i.e. formation of glucose from the sources other thancarbohydrates. Insulin increases combustion of sugar in the tissue and also helpsin the treatment of glucose in the cells. It increases synthesis ofglycogen from sugar and lactate both in the liver and muscle. This iscalled the directive effect of insulin. Insulin promotes the uptake ofglucose inside the cells and the intercellular phosphorylation of glucoseto glucose–6–phosphate. Glucose–6–phosphate itself also appears to bea specific activator of glycogen synthesis.Insulin effect on protein metabolism: It prevents gluconeogenesis Glucose is normally formed fromproteins and lipids in the liver. In diabetes this process is enhanced.High blood sugar level in diabetes is due to over production of glucose.In the starving diabetes dextrose nitrogen ratio is fairly constant. Thisshows that both sugar and nitrogen are coming form the same source i.e.proteins. When insulin is given both sugar and nitrogen excretion fails,showing that formation of new glucose from proteins has been interfered. 30 Shareera
    • Insulin effect on fat metabolism: It prevents formation of ketone bodies (anti ketogenic). In advancediabetes, excess ketone bodies are formed in liver, due to incompletecombustion of fatty acids. After the administration of Insulin more sugarsburn and liver glycogen increases displacing the lipids. Hence lipidcombustion is discouraged and ketosis disappears. Insulin decreases the cholesteremia and lipademia. It also preventsaccumulation of excess lipid in the liver and breakdown of lipid inAdipose tissue.GLUCOGON :- The Alpha cells of the islets of Langerhans secrete Glucogon. It isa polypeptide hormone with 29 aminoacids having molecular weight of3,485. This polypeptide has been completely synthesized. Glucogoncauses glycogenolysis in the liver and antagonist to liver by depriving theaction of Insulin. The blood sugar level chiefly controls the secretary activity ofAlpha and Beta cells. Hyperglycemia stimulates the release of Insulinwhere as, hypoglycemia will release the glycogen. There is no goodevidence that a tropic hormone secreted by the pituitary, directlyinfluences the secretary activity of the pancreatic islets, throughsecretions derived form other endocrine glands for example, the adrenal 31 Shareera
    • gland have some effects. If the islets are completely removed orextensively damaged, the lack of or reduced Insulin formation results inhyperglycemia and the condition of diabetes mellitus (Madhumeha).Relatively normal carbohydrates metabolism can then be restored bysupplementation of insulin. It is necessary to point out however that though a deficiency ofinsulin production and release may result in Diabetes, not all cases ofDiabetes are due to a deficiency in Insulin production. Even pituitary,Liver and Adrenals are also involved in this process. Clinical syndromesinvolving abnormal carbohydrate metabolism and abnormal blood sugarlevels may result from either deficiency or excess production of Insulinand Glycogen. The latter when injected result in an increase in bloodsugar. Excess production of insulin as in cases of Islet tumors results inhypoglycemic and attains neurological changes, excess production ofGastrin, acidity and peptic ulceration.ADRENAL (SUPRA RENAL) GLANDS The adrenal glands are situated on the upper poles of the kidneys.Each gland weighs about 4 gm.Microscopic structure - A distinct connective tissue capsule surroundsthe parenchyma of the gland. Beneath the capsule the cortex is arrangedin 3 layers. They are - 32 Shareera
    • Zona Glomerulosa. Zona Fasculata Zona ReticularisZona Glomerulosa :- The outer layer which varies in thickness formalmost total absence to clusters of a dozen or more small cells is knownas Zona Glomerulosa. Zona Glomerulosa secretes mainly aldosteronethat is concerned with the salt and water balance and acts on the distalconvoluted tubule and collecting ducts of the kidney. It also secrets asmall amount of glucocorticoids and sex hormones.Zona Fasculata : - inside the first layer the cells are larger and formmore or less parallel radial columns. They commonly contain fat dropletswhich give them a spongy appearance. This region is known as a ZonaFasculata. This layer secretes predominantly Glucocorticoide.Zona Reticularis.: - Centre of the gland the regular arrangement of cellsof the Zona fasciculata is replaced by one of anastomosing cell cordsforming the Zona Reticularis, which secretes sex hormones and a smallamount of Glucocorticoids but no Aldosterone. The adrenal Medulla is chiefly composed of chromaffin cells(phaeochromocytes) which either secrete Adrenaline or Nor- adrenaline. 33 Shareera
    • LIVER :- The liver is the largest gland in the body. The greater part of theLiver lies under the covering of the ribs and coastal cartilage. The liveris a dark brown, highly vascular and soft organ that is commonly rupturedor torn in abdominal injuries. It is approximately one fifteenth of the bodyweight in adult. The liver is determined by the surrounding organs it retains theshape of a blunt edge it has two surfaces. Diaphragmatic surfacedivisible into Superior, Anterio, posterior and right parts according to thedirection in which if faces and visceral (posterior) surface facesposteriorly and Inferiorly. Liver is divided into four lobes Right,Quadrate, Caudate and Left lobes.Functions of liver in carbohydrate metabolism are:-1. Storage of Glycogen.2. Conversion of Galactose and fructose into glucose.3. Gluconeogenesis4. Formation of many important chemical compounds from the intermediate products of Carbohydrate Metabolism. 34 Shareera
    • Liver is especially important for maintaining a normal blood glucoseconcentration. For instance storage of glycogen allows the liver toremove excess glucose from blood, store it and then return it in to theblood when the blood glucose concentration begins to fall too low. Thisis called the glucose buffer function of the liver. As an example,immediately after a meal containing large amounts of carbohydrates theblood glucose concentration raises about three times as much in theperson with a non functional liver as in a person with a normal liver. Gluconeogenesis in the liver is also concerned with maintaining anormal blood glucose concentration for glucose neogenesis occurs to asignificant extent only when the glucose concentration begins to fallbelow normal. In such case large amounts of amino acids are convertedinto glucose, there by helping to maintain a relatively normal bloodglucose concentration. 35 Shareera
    • SHAREERA References1 Charaka Nidana 4/42 Charaka Vimana 5/73 Ibid 5/74 Ibid 5/75 Ibid 5/76 Ibid 5/77 Sushruta Shareera 9 / 158 Charaka Vimana 5/79 Sushruta Nidana 16 / 4210 Ibid 16 /4511 Charaka Vimana 5/812 Charaka Shareera 7 /1513 Sushruta Shareera 4 / 2314 Sharangadara Poorva khanda 5 / 6315 Adamalla on Sharngadhara 5 / 8316 Charaka Vimana 5/817 Sushruta Nidana 7 / 1818 Sushruta Shareera 4 / 3019 Sharangadhara poorva khanda 5 / 4020 Charaka Shareera 7/7 36 Shareera
    • 21 Sushruta Shreera 4 / 2622 Ibid 4 / 4723 Charaka Shareera 9/424 Ibid 9/425 Sushruta Nidana 3 / 17,2926 Astanga Hridaya Shareera 4 / 1027 Sushruta Chikitsa 7 / 3328 Sushruta Nidana 3 / 1829 Ibid 3 /1530 Sushruta Nidana 3 / 1531 Dalhana on Su Sh 4 /2332 Charaka Vimana 5/733 Sushruta Shareera 4 / 1034 API Text of Medicine by Sanani pp 20535 Ibid pp 20436 Principles of Anatomy and Physiology by Gregfard Tortara37 Joslin’s diabetes Mellitus. pp1538 Ibid pp 216 37 Shareera
    • HETU It is believed that Prameha is a hereditary disease and manyfactors play an important in the production of the disease as a clinicalentity. They are age, sex, diet, body weight, Infection, pregnancy, etc.Emotional stress and trauma have also been considered as etiologicalfactors of Prameha. Charaka considers Madhumeha as one out of the fourverities of vataja Pramehas 1. He has also stated that all factors thatincrease Kapha are the causative factors of the Pramehas 2. The generaletiological factors of Prameha as stated by Charaka are 3 – “Addiction tothe pleasures of lounging and sleeping, excessive use of curds, meatjuice of domestic, aquatic and wet land animals, milk or diary products,newly harvested grains and drinks and products of jaggery". The etiological factors as stated by Sushruta are similar to Charakaand capable of vitiating mainly the Kapha dosha. Sushruta states that allvarieties of Prameha, if not properly treated and attended to at the onset,may ultimately develop into Madhumeha 4. Based on the etiology,Sushruta has classified Prameha into two varieties as sahaja andapathya nimittaja. Apathya nimittaja is subdivided into two as Aharanimittaja and vihara nimittaja. 36 Nidana
    • 1. Sahaja or Genetic origin. Charaka 4 and Susrata 5 have evaluated that beeja dosha is also acause for Prameha. Further Sushruta has included Madhumeha in theAdibala pravrittaja category of disease. The term beeja has been considered as a sukra and shonitha 5,which correlates with the sperm and ovum of modern concepts. Beejasare vitiated with dosha (Vata especially responsible for division of cellsmakes certain abnormalities in chromosomal galaxy of sperm or ovum)are responsible for genesis of Prameha, In gross the organs which areresponsible for producing Prameha are ambuvaha srotas, mamsa, kleda,kloma, mootravaha srotas. They are deformed since birth and susceptibleto get Prameha, aggravated by nimitta karana. This may be because ofthe selective discriminative of these organs to develop Prameha. As aresult of defective beeja when Prameha is developed, then the person iscalled as a Jatha Pramehi patient. Jata Pramehi 6 has been considered asa Kulaja vikara 7. Few diseases included under this category are Kusta,Arsha, Meha, Kshaya etc. Kulaja vikaras means the diseases, which arecarried from the former generation to the successive generation, and theyare of the defects in the genetic code. 37 Nidana
    • 2. Apatya nimittaja Apathya is the main cause for the disease. Apathya includes bothahara and vihara. All acharyas have stressed the indulgence ofunwholesome food and vihara in the production of Prameha. Ahara andvihara that increases kapha, medas and mootra lead to the genesis ofPrameha. Charaka explains the Nidana 8 as Amla, Lavana, Madhura Rasa andGuru, Snigdha guna dravyas, Curd, Milk, Mamsa rasa of aquatic animals,Fresh cereals. Guda and Guda vikara.aharas and Sitting idle, Excessivesleep, Dislike for walking, activities and to take bath are the viharas forMadhumeha. Sushruta explains the Nidana 9 as Madhura Rasa, Medhya, Snigdha,Sheeta guna dravyas. Nava anna, Wine, Meat of animals living in marshylands and Guda as aaharaj hetus. Laziness, Day sleep, inactiveness asviharaja hetus of Madhumeha. Vagbhata explains the Nidana 10 as Madhura, Amla, Lavana Rasa,Guru, Snigdha, Sheeta, Picchila Guna dravyas, Nava anna, Madhya,Anupa Mamsa, Ikshu rasa, Guda and Guda vikara, Dadhi, Paya as ahara 38 Nidana
    • and Sitting for long time, Sexual intercourse, Sleeping excessively asviharaja Nidana for Madhumeha. Charaka has explained the vishista nidanas, of Prameha accordingto their doshas, they are as follow.Kaphaja prameha nidana 11.Aharaja. The frequent and excessive use of newly harvested rice (Hayanaka), Yavaka, Chanaka, Uddalaka, Naisadha, Itkata, Mukundaka, Mahavrihi, Promodaka and Sugandhaka grains. The use of new blackgram and other pulses The flesh of domestic, land and aquatic animals. Sugarcane juice, or the abundant use of milk, curds, ghee or sweet and unripe articles.Viharaja: Avoidance of cleanliness and exercise, excess indulgence in sleeping, lying or sedentary habits, and all factors which are likely to increase kapha, Medas and mootra The special morbid factor of the humor is excessive fluidity of kapha. 39 Nidana
    • Pittaja prameha nidana 12.Aharaja: The habitual use of ushna, amla, lavana, kshara and katu articles. Adhyashana, Vishama ahara.Viharaja: Teekshna santapa sevana, Sharma , Krodha, Anxiety.Vataja prameha nidana 13.Aharaja The habitual use of rooksha, kashaya, katu, tikta, laghu and sheeta articles.Viharaja: Adhika Vyavaya and Vyayama, Excessive use of panchakarmas. Vegadharana, Exessive indulgence in fasting, Atapa, Udvega, Shoka, Abighata. 40 Nidana
    • Aetiology according to Modern concept The cause of hyperglycemia can be divided into Heredity andAcquired 14, 15.Heredity Positive family history may be obtained in around 40 % of patientswith NIDDM (Non Insulin Dependent Diabetes Mellitus). Genesresponsible for this heretic carriage of the disease are one for insulin(Chromosome 11) insulin receptor (Chromosome 19) and glucosetransporter (Chromosome 1). But a definite association of any of thesegenes with clinical NIDDM is yet to be established.Acquired and environmental factors. Analysis of epidemiological data leads to identification of aging,obesity, composition of diet, physical inactivity, stress and urbanisationas environmental predisposing factors for NIDDM. 41 Nidana
    • SAMPRAPTI The suppression or the incidence of the disease is dependentupon the result of the variations in the etiological factors (nidana).Intensity of the morbid factors (doshas) and susceptibility of the body–elements (dushyas). If these three factors, mainly the etiologicalfactors etc., do not mutually associate or support, or if do so after along lapse of time, or in a very mild form, either there occurs nomanifestation of the disease at all or the disease takes a long period toevolve, or appears ambulatory form. Under the contrary conditions, itgives contrary results. Thus the different causes of the modes ofi n c i d e n c e l a i d d o w n a r e s u p p r e s s e d i n a l l d i s e a s e s 16. The samprapti of a disease explains the method or process bywhich the vitiated doshas reach with the dushyas and produce theanatomical and physiological changes in the target organs leading tothe expression as a disease. In terms of Kriyakalas, the sampraptideals with the chaya, prakopa, prasara and Sthana samsraya of thedisease-causing doshas, which leads to the dosha-dushyasammurchana i.e., the interaction between disturbed functional factorswith the basic structural entities of the body. 42 Nidana
    • Charaka had clearly explained the samprapti of the KaphajaPrameha in the Prameha Nidana. Even though the disease Prameha isstated to be due to the vitiation of the tri-doshas, the specific morbificfactors of the humor is excessive fluidity of Kapha. The specialfeatures of the susceptible body elements(dushyas) are excessivenessand deminished viscousness of Medas, Mamsa, Body fluid (sareerak l e d a ) , S u k r a , R a k t a , V a s a , M a j j a , L a s i k a , R a s a a n d O j u s 17. When there is the simultaneous congress of these threepathological conditions, the kapha is suddenly provoked since it isalready in chaya stage. The vitiated kapha quickly spreads throughoutthe body which is already in degenerated condition. In the path of itscirculation the kapha first encounters and mixes with the medas, owingto the pathological changes in the medas, viz., excessiveness anddiminished viscousness and also owing to the great similarity of thequalities between the kapha and medas. Due to this combination ofvitiated kapha and medas, the latter is vitiated. The vitiated kaphacoupled with the vitiated medas now comes in contact with the sareerakleda and mamsa which are in excessive increase in the body. Thevitiated body fluid is changed into urine. The orifices or pores of themootravahasrotas, represented by the kidneys and bladder are in astate of dilatation due to the actions of vitiated medas and sareera 43 Nidana
    • kleda. The vitiated kapha, upon reaching the mootravahasrotasas,g e t s l o c a l i s e d t h e r e a n d t h u s d e v e l o p s t h e d i s e a s e c a l l e d P r a m e h a 18. The sareera- kleda combined with the kapha and the medas whilebeing converted into urine on its entrance into the mootrasaya,acquires the following ten pathological characteristics of Kapha. Theyare unctuousness, heaviness, sweetness, denseness and slowness.Then it acquires a special name accompanied with the qualities of oneo r m o r e o f t h e o t h e r c o n d i t i o n s b y w h i c h i t h a s b e e n m a i n l y m o d i f i e d 19. The vitiated pitta produces Prameha by the same process asdescribed above 20. Vitiated Vata brings about the manifestation of Vataja Pramehaby the same process as described above. If Vata by its rooksha qualitychanges the ojus which is naturally of sweet taste, into one ofastringent taste and carries it to the mootrasaya, then it causes thec o n d i t i o n c a l l e d M a d h u m e h a 21. Charaka in Prameha Chikitsa has explained the samprapti inb r i e f 22. “the Kapha, having vitiated the medas and mamsa dhatus andthe body fluid, becomes localised in the genito-urinary system andcauses Pramehas7. The pitta, too, which is provoked by ushna dravyasvitiating those very tissues, causes in the same manner other varieties 44 Nidana
    • of Prameha. On the diminution of the other two humors, the morbidVata draws into the genito – urinary system the essential dhatus, andgive rise to the third group of Pramehas. In every case the morbidhumor, having reached the genito-urinary system, vitiates the urine andgenerates Pramehas corresponding to its specific nature”. Sushruta has given more details about pathogenesis ofP r a m e h a 23. “ In a person who indulges in the mithya ahara vihara thethree doshas which are vitiated and in an immature state join themedas and travel to the mootrava srotas, gets localised at the entranceof the vasti, when they are emitted through the urethra the disease isknown as Prameha. “The deranged kapha, in conjunction with the (morbid) pitta, vayuand medas, gives rise to all kaphaja types of Prameha. The derangedpitta, in conjunction with the deranged vayu, kapha, rakta and medasproduced the pittaja ones; while the deranged vayu, in union with thederanged kapha, pitta, medas, majja and vasa, engenders the types ofV a t a j a P r a m e h a ” 24. From the references cited above, the following facts can beelicited:1. The main dosha vitiated in Prameha is kapha. 45 Nidana
    • 2. But the other two doshas are also affected and depending upon the predominance of the signs and symptoms of one particular dosha, the disease is named accordingly.3. The affected dushyas are rasa, rakta, mamsa, medas, majja and shukra. It should be noticed that the asthi dhatu is not mentioned in the dushyas of this disease.4. In addition shareera kleda, ojus, vasa and laseka are also affected.5. Therefore it is clearly understood that the dhatu parinama in general is disturbed.6. The vitiated doshas get localised in mootravaha srotas and disturb its normal functions, by dilating its orfices.7. The main signs and symptoms viz. Polyuria and turbidity expresses itself the pathological changes in the urine.viz Mootravaha srotas and vasti.8. The body-fluid or shareera kleda is transformed into a liquid mala which is excreted as urine. Since all the nutrient elements and malas circulate along with the rasarakta complex, it is clear that there is a change in the composition of the rasarakta complex.9. Because of this change in the composition of the rasarakta complex, the disturbance in the dhatu parinama can be easily understood. 46 Nidana
    • Charaka and vagbhata have described the pathogenesis ofMadhumeha as separate from Prameha. Vagbhata states that thep a t h o g e n e s i s o f M a d h u m e h a i s o f t w o v a r i e t i e s 25. 1. The depletion of the dhatu leading to the vitiation of Vata 2. Obstruction to the normal circulation of Vata by the other doshas leading to the vitiation of the former. This particular information leads us to include that Madhumeha ismainly due to the vitiation of Vata. Even according to Charaka,Madhumeha is enumerated as one of the Vataja Pramehas. Vagbhatahas also stated that any Prameha, if not treated and attended to at theoutset, will ultimately develop into Madhumeha. He has also clearlystated that there is an increase in the sweetness or sweet substancesin the body, which is expressed through the physical qualities of urine,b e i n g t h e c o l o u r a n d t a s t e r e s e m b l e s h o n e y 26. All organs and parts of the body are made of their ultimate unitso r j e e v a p a r a m a n u s 27. These innumerable jeevaparamanus or cells ofdifferent shareera avayavas are held together cemented to formdifferent structures and organs of the body. The substance that unitesand cements a cell with another for the formation of various structuresand organs is the inter-cellular substance. By virtue of its viscosity,smoothness, sliminess and lubricabilituy, the inter – cellular substance 47 Nidana
    • is considered slaishmic in nature. Through this inter-cellularsubstance pass the nutrient material from capillaries to cells and themetabolites pass in the reverse direction. Interference with its functionleads ultimately to the degeneration and decay of the cell andconsequently of the structures or dhatus of the body. The physical and chemical characteristics of cell protoplasm ingeneral are parallel to those of the Kapha and the functionsascribed to both are likewise. Therefore it can be seen that thebody structure including all the dhatus are completely made up ofkapha. Therefore kapha is that factor of the dosha-triad which notonly imparts strength to all dhatus but also prevents their decay anddegeneration 28. If there is a disturbance in the nourishment of the cells, adisturbance in the general dhatuparinama is surmised. Accordingly, therecan be a deficiency in the functions of kapha and also the sleshmika ojusthat is responsible for general immunity of the body. The term kapha has been defined as “kapha the product of jala” 29and therefore there is no surprise to notice that the body’s majorcomponent is water. Since there is the vitiation of kapha in Prameha, itcan be easily understood the functions of shareera kleda or body-fluid. 48 Nidana
    • In the process of Ahara pachana the waste materials are separatedin two forms, one is liquid and the another is solid. The liquid part isabsorbed from the kostha through the purishadharakala to be transformedinto urine and excreted through the mootrashaya 30. The sara bhaga ofthe food is utilised by the respective dhatwagnis and the nutrients areutilised in the construction of the dhatus. This dhatwagni paka ofdhatuparinama also produces different kittas 31. The kittas of thedhatwagni paka which are ejected by cells will naturally enter into thecirculating rasa dhatu to be transported to their respective outlets. Sinceit has been stated that the shareera kleda, which is affected due to thevitiation of kapha, is changed into mootra 32, it is to be understood thatthere is increased production of kitta bhaga in dhatwagni paka. If thereis an increased production of kitta bhaga, it can be easily summarisedthat there is a decreased production of the prasadabhaga which is meantfor the construction of the dhatus or the organs of the body, leading to adeficient repair and so degeneration of the body. The same thing hasbeen explained by the ancient scholars that in a Prameha patient, asshareera saithilyata. The major portion of the kitta bhaga, which is in a liquid state, isexcreted by the mootravaha srotas. The normal function of mootravahasrotas is to allow the kitta bhaga to pass through its pores and to preventthe nutrient material from escaping out of the body. The vitiated kaphaupon reaching the mootravaha srotas gets localised there and along with 49 Nidana
    • the vitiated medas produces dilatation of the pores of the mootravahasrotas. Therefore, not only the substances that are to be excreted butalso some of the nutrient materials are also allowed to pass throughthese dilated pores. According to Vagbhata, there is an increase in the sweetness orsweet substances in the body of a Madhumeha patient 33. This particularfact is noticed by the sweetness of the urine that can be observed andrecognised by attraction and assemblage of ants near the urine 34. Theurine of a normal or healthy person is not sweet in taste. This sweetnessof the urine of a Madhumeha patient is due to the madhuradravya, whichis filtered by the mootravaha srotas from the rasarakta complex but couldnot be reabsorbed completely during the paka or maturation of urine. The madhuradravya is a natural component of the rasaraktacomplex. Even though the ayurveda laid down that a person shouldpartake a food containing the six tastes, the major component of theregular food is madhuradravya. Charaka considered cereals(shukadhanya varga) as main source of food and the others like pulses,legumes, meat, fishes, fruits, spices etc,. As supporting diet articles 35.The main constituent of all cereals is carbohydrate, which aremadhuradravyas. Therefore the main product of the alimentary digestionof these cereals to be absorbed into the blood is also a madhuradravya. 50 Nidana
    • Charaka also states that the madhurarasa confers bala or strengthon the Dhatus and ojus and that madhurarasa is compatible to the body 36.The madhurarasa therefore produces an increase in the body bulk i.e. itis the best in brimhanadravyas 37. A substance which is having thephysiochemical qualities / properties of Pridvhi and Ap is stated to beBrimhana dravya 38. It should also be noted that substance ofmadhurarasa is also having the qualities of Pridhvi and Ap 39. The ShariraBala is of two varieties : 1) Vyayamashakti – the strength required to perform vigorous physical work and 2) Vyadhikshamatwa shakti – the power to resist and overcome forces or factors which bring about disease. Vyayamashakti is dependent of wellformed and it confers theKarmasadhana shakti on body. Vyadhikshamatwa is bestowed in thenormal functioning of Ojus, which is the essence of healthy Dhatus. Ojusis also a madhuradravya. From the above the importance of themadhuradravya for the nourishment and also strength of the body can beclearly understood. 51 Nidana
    • Since it is stated that the madhuradravya is excreted in the urine,there can be only two causes for this excretion: 1) Excess of madhuradravya in the circulating rasarakta complex, more than the amount required for the nourishment and strength of the Dhatus and consequent overflowing through mootravaha srotases. 2) The increased release by the orifices of the mootravaha srotases. It has already been stated earlier that these orifices of the mootravaha srotases have been dilated due to the vitiated Tridoshas. The dhatus of a Madhumeha patient are in a state of Saidhilya 40.These indicate that the Dhatus are not being nourished in a propermanner. But the madhuradravya, which is the main source ofnourishment and strength, is stated to be in excess in the Rasaraktacomplex. It is also a fact that all the organs and parts of the body aremade up of their ultimate units or Jeevaparamanus or cells. Thenourishment of these cells, which constitute the Dhatus of the body, isdependent upon the nutrients derived from the food freely entering intothem for their utilisation. If there is an obstruction to the path orentrance of these madhuradravyas into the cells, the Dhatus do not getsufficient nutrition and they’re by degenerate and decay. Because of thisobstruction entrance of the madhuradravyas into the cell of the body 52 Nidana
    • interfered. There is an excess of such substances in the Rasaraktacomplex developed in the body. The nourishment of the cells of thedhatus is maintained by the utilisation of the respective nutrients by theDhatwagni. This dhatwagnipaka is possible only after the nutrients-madhuradravya in this respect-enter the dhatus. Since there is anobstruction to the entrance of the madhuradravya, the product of thealimentary digestion, into the Dhatus, we have to presume that there is adeficiency in the function of the Bhutagnis. Since the Dhatus are deficiently nourished due to the obstruction tothe entrance of the madhuradravya into the Dhatus, there will be deficientformation and defective functioning of the Ojus, the essence of Dhatus.Sushruta has already stated that Ojokshaya develops due to excessivehunger 41 – the hunger of the Dhatus for the madhuradravya inMadhumeha patient. As stated earlier, the vyadhikshamatwa of a personis dependent on the normal functioning of the Ojus. Therefore in aMadhumeha patient whose ojus is deficiently formed, or vyadhikshamatwashakti is substandard. Therefore his body / dhatus are not capable ofresisting the virulence of diseases especially of the Vaikarika krimi origin.The Vaikarika krimi also thrive to grow powerful in the presence of theexcessive madhuradravya. Not only the disease Madhumeha but also thediseases due to vaikarika krimis cause a hastening of the degenerationand decay of the body. 53 Nidana
    • The important and ultimate aim of a human being is to maintain thelife as long as possible. Therefore when the madhuradravyas essentialfor the maintenance of the life are not allowed to enter the Dhatus, thebody tries to deplete the store-houses of the madhuradravyas to beutilised by the body. In a healthy person, if madhuradravyas areconsumed in excess of the requirement of the body, they are convertedinto medas 42, 43.and stored for future use. Therefore, once the store-house of the madhuradravyas are completely depleted, the medas andother important dhatus (which contain protein mainly) are slowlydisintegrated for maintenance of life. During this disintegration of theDhatus which are mainly effected by the pachakamshas, theproducts/metabolites, which are not capable of nourishing the body, sometimes prove to be noxious producing several complications like moorcha,hridgraha etc. One of the important condition due to this disintegration ofmedas is the dhatuja medovyapat with consequent development ofdhamanipratichaya 44. Thus the knowledge of samprapti is important tohandle the Madhumeha patients. 54 Nidana
    • POORVARUPA The prodormal symptomology of a disease has been described aspoorvaroopa. The knowledge of poorvaroopa has importance in earlymanagement of patient and also in differential diagnosis of disease sothat the disease is controlled easily. The state of prodroma or poorvarupais expressed as when vitiated doshas become localised due tosrotovaigunya leading to the dosha-dushya-sammurchana. Kaphapredominant tridoshas and dhatus along with ojus are chiefly effected inPrameha. Thus poorvaroopa are very much varied in nature.The following are the prodroma of Prameha.1. Burning sensation of the palms of hands and the soles of the feet 45, 46, 47.2. Dryness in the mouth, palate and throat and thirst 48.3. Heaviness of the body 49.4. Coldness or sliminess of the skin and limbs, thermalgia and numbness in the body 50.5. Smell like raw-meet in the body 51.6. Somnolence and continuous torpor and lassitude 52.7. Sweet taste in the mouth 53, 54.8. Slimy mucous deposit on the tongue, palate, pharynx and teeth 55.9. Increased excrement in the body, increased discharge from the orifices in the body 56, 57. 55 Nidana
    • 10. Sweetness and whiteness of urine 58.11. Attraction of insects and ants to the body and urine 59.12. Matting of the hair and inordinate growth of the finger and toe nails 60, 61.13. A bad smelling breath and shortness of breath 62.Vagbhata has mentioned some more additional prodroma for Prameha. 1. Excessive perspiration 63. 2. Laziness 64. 3. Liking of cold comforts 65.From the above prodroma it can be clearly seen that there is anincreased production of kitta bhaga in dhatu parinama as explainedearlier. 56 Nidana
    • ROOPA In the Roopa or actual manifestation of the disease, dosha dushyasammurchana completes, and the onset of the disease will becommenced. The roopas may change from time to time and certainsymptoms may newly appear or some may disappear. Roopa is theprominent diagnostic key, hence the knowledge of the various lakshanasdisease is essential for the benefit of prognosis. Clinical features of the present disease Madhumeha are dividedinto two groups1. General features of Prameha2. Special features of the Madhumeha. Charaka has not described the general features of Prameha whereas Sushruta 66 and Vagbhata 67 have described the general features asa. Avila mootratab. Prabhoota mootrata. 57 Nidana
    • Specific Lakshanas of Madhumeha. It is one of the four Vataja Pramehas. The person with Madhumehapasses urine which is astringent and sweet in taste, yellowish or whitishin colour. The urine contains similar properties of Honey 68, 69, 70. Apart from the above lakshanas, Sushruta described typical lakshanasfor Madhumeha rogi 71, that he desires – 1. To stay while walking. 2. To sit while staying 3. To take rest on bed while sitting 4. To go to sleep while taking rest. 58 Nidana
    • BHEDHA Though Prameha is stated to be developed due to the vitiation ofall three doshas, the disease is mainly divided into three groups. 1. kaphaja Pramehas - which are again subdivided into 10 types 72. 2. Pittaja Pramehas - which are again subdivided into 6 types 73. 3. Vataja Pramehas - which are again subdivided into 4 types 74. Even though the three Ayurveda authorities Charaka, Sushruta andVagbhata agree the same number of Prameha in each group, there seemsto be difference in the nomenclature used by them. Increased quantity ofurine and increased turbidity in the urine are the main symptom in allPramehas. The name of each variety of Prameha is decided according to thecombination of dosha and dushya, and the physical characterresemblance to the urine. 59 Nidana
    • kaphaja Pramehas according to Brihatrayees are Charaka 75 Sushruta 76 Vagbhata 77 Udaka Meha 78 Udaka Meha 79 Udaka Meha 80 Ikshu Meha 81 Ikshu Meha 82 Ikshu Meha 83 Sikata Meha 84 Sikata Meha 85 Sikata Meha 86 Sanair Meha 87 Sanair Meha 88 Sanair Meha 89 Sandra Meha 90 Sandra Meha 91 Sandra Meha 92 93 Sukra Meha Sukra Meha 94 Sukra Meha 95 Sandra prasad meha 96 --- --- Shukla Meha 97 Pishta Meha 98 Pishta Meha 99 Sheeta Meha 100 --- Sheeta Meha 101 Alala Meha 102 --- Alala Meha 103 --- Sura Meha 104 Sura Meha 105 --- Lavana Meha 106 Lavana Meha 107 --- Phena Meha 108 --- It is noticed that there is a resemblance in the symptoms ofsandra prasada meha of Charaka and Sura meha of Vagbhata. 60 Nidana
    • Pittaja Pramehas according to Brihetraye Charaka 109 Sushruta 110 Vagbhata 111 Kshara Meha Kshara Meha Kshara Meha Kala Meha --- Kala Meha Neela Meha Neela Meha Neela Meha Lohita Meha Shonita Meha Rakta Meha Manjishta Meha Manjishta Meha Manjista Meha Haridra Meha Haridra Meha Haridra Meha --- Amla Meha --- There is resemblance in the symptoms of Lohita meha of charaka andShonitha meha and Rakta meha of Sushruta and Vagbhata respectively. Vataja Pramehas according to Brihatraye Charaka 112 Sushruta 113 Vagbhata 114 Vasa Meha Vasa Meha Vasa Meha Majja Meha --- Majja Meha Hasti Meha Hasti Meha Hasti Meha Madhu Meha Kshoudra Meha Madhu Meha --- Sarpir Meha --- There is a resemblance in the symptoms of Majja meha of Charakaand the Sarpir meha of Sushruta. 61 Nidana
    • It is evident form the above table that Vagbhata closely followsCharaka while Sushruta had a slight differences.MADHUMEHA: Madhumeha can be sub classified mainly into two types. Type one a) Kulaja or Sahaja (Hereditary) b) Doshaja or Apathya nimittaja ( acquired) Type two a) Dhatu kshaya janya Madhumeha 115 b) Doshavruta janya Madhumeha Charaka has divided the Madhumeha patients into two verities basingon the line of treatment aspect 116.1. Sthoola (stout or strong)2. Krisha (emaciated or week) Sushruta accepts Sahaja rogi as krisha and the Apathya nimitaaja rogias sthoola rogi in his classification. . 62 Nidana
    • SADHYASADHYATA As discussed earlier, Prameha is classified in to three verieties i.e. 1. Kaphaja Pramehas - 10 2. Pittaja Pramehas - 6 3. Vataja Pramehas - 4The ten kaphaja Pramehas are said to be sadhya (curable) 117, 118. Because a. The medas having homogenous properties is effected b. The kapha is dominant c. Both these factors are amendable to the same type of treatment. The six pittaja Pramehas are only Yapya (palliable ) 119, 120 owing to theproximity of the seat of the vitiated doshas and that of the Medas andowing to the antagonism involved in their treatment. The four varieties of Vataja Prameha due to the vitiation of Vataare known to be incurable 121, 122 because of their seriousness and alsobecause of the contradiction involved in their treatment. Vagbhata adds to the above : a. The kaphaja and Pittaja groups of Prameha if they are developed after full expression of prodroma to are incurable 123. 63 Nidana
    • b. Kaphaja Pramehas gradually develops into pittaja Pramehas and they both transforms into Vataja Pramehas that are incurable. c. If kaphaja Pramehas gradually turns into pittaja Pramehas these are yapya. d. Even the pittaja Pramehas are curable if there is no severe vitiation of medas 124, even this is applicable for Vataja mehas. Charaka has stated that this disease is relapsing in nature.Though certain varieties are stated to be curable they appear to beso only for certain period and relapse is definite. Madhumeha, which is a verity of Vataja Prameha, is also to beconsidered, as incurable but with specific line of treatment these can bepalliable. Jata pramehi or Beeja doshaja are incurable due to leenata of doshaand as they themselves makes influence of prakriti of patient. Sushruta stated that if Prameha patient suffering with pidikas andcomplications like Hridgraha, then he should be considered asincurable 125. Interestingly Basavrajeeyum 16 t h century Ayurvedic text from Andrapradesh, has mentioned a test for urine to know the prognosis of eachdosha group. The urine of a Prameha patient has to be collected in awide mouthed vessel and boiled on a mild flame till evaporation. Theincurability of the disease depends upon the amount of residue. A Vataja 64 Nidana
    • Prameha is considered incurable if the residue is 1/5 t h of the volume ofurine taken for the test. Pittaja Prameha is incurable if the residue is1/7 t h and kaphaja Prameha is incurable if the residue is 1/9 t h of thevolume of urine in the test 126. 65 Nidana
    • VYAVACHEDAKA NIDANA It was stated that cordinal signs of Madhumeha areBahumootrata and Avilamootrata 127. The bahumootrata is noticed asa symptom in many diseases. But the combination of bahumootrataand Avilamootrata is noticed in Prameha only. Urine is stated to be Madhura in the following varieties ofPramehas.Ikshumeha 128 – Due to kapha the patients pass the urine which is sweet, cold, sticky and like a sugarcane juice.Sheetha meha 129 - Due to kapha the patient passes the urine which is cold, sweet and frequency of the urination is increased.Madhumeha 130 - Due to Vata prokopa urine of the patient will be kashya, madhura, pandu and ruksha. The chief physical qualities of the urine of Madhumeha patient arethe colour and the taste resembling honey. Sushruta stated that a patientwho is suffering from pidikas, hridgraha, and other complications inaddition to the other characteristics of urine should be considered asMadhumeha patient. 66 Nidana
    • Vagbhata stated that mootra madhuryata is not diagnostic lakshanaof Madhumeha, but if the patient is having shareera madhuryata, then itis considered as Madhumeha 131. It is observed that the urine and body areattracted by the ants. No specific test for the Madhumeha patient has notbeen ascribed in any Ayurvedic classics. Here the attraction of ants tothe body is an indication of the presence of the madhuryata in the bodyi.e. Rasa and Rakta. Since these two dhatus exist in the superficial partsof the body in abundance as such the ants are naturally attracted towardstwak. The madhuryata corresponds to the raised blood sugar levels inMadhumeha (diabetes mellitus). 67 Nidana
    • UPADRAVA Upadrava is a disease produced after the manifestation of theoriginal disease and depends on this disease irrespective of whetherupadrava is major or minor 132. After the occurrence of the originaldisease the dosha or doshas are further vitiated owing to abnormalahara, vihar etc., thus leading to a secondary disease or complicationwhich is known as an upadrava. If all the Pramehas are not treated properly and attended, theymay ultimately develop into Madhumeha. Madhumeha is consideredto be one of the 20 Pramehas by Charaka. Apart form this Charakahas described the upadravas of Prameha in general. Where asSushruta and Vagbhata have mentioned upadravas separately foreach doshic group. The general upadravas of Pramehas according to Charaka areas follows 133. Trishna, Atisara, Jwara, Daha, Dourabalya,Arochaka, Avipaka, Puti mamsa, Pidika , Alaji, Vidradhi. Charaka mentioned the upadrav as (complications) ofMadhumeha as 134 Trishna, Shwasa, Mamsa kotha, Moha, Hikka,Mada, Jwara, Visarpa among them many of upadravas are seen inpatients, they have been explained under the heading ofobservation. 68 Nidana
    • References1 Charaka Nidana 4 / 442 Ibid 4 / 53 Ibid 4 / 54 Sushruta Nidana 6 / 305 Chakrapani on Ch su 3 / 176 Charaka Chikitsa 6 / 577 Ibid 6 / 578 Charaka Nidana 4 / 59 Sushruta Nidana 6 / 310 Astanga Sangraha Nidana 10 / 311 Charaka Nidana 4 / 512 Ibid 4 / 2313 Ibid 4 / 3614 API Text Book of Medicine. pp 20515 Joslin’s Diabetes Mellitus pp 24016 Charaka Nidana 4 / 417 Ibid 4 / 718 Ibid 4 / 819 Ibid 4 / 920 Ibid 4 / 521 Ibid 4 / 37 69 Nidana
    • 22 Charaka Chikitsa 6 / 5,623 Sushruta Nidana 6 / 424 Ibid 6 / 425 Astanga hridhya Nidana 10 / 826 Ibid 10 / 827 Chharaka Shareera 7 / 1728 Diabetes and treatment by VVS Sastri pp1829 Sabdastoma Mahanidhi30 Astanga hridhya sutra 3 / 6131 Chakrapani on Ch Chi 15 / 1532 Charaka Nidana 4 / 833 Astanga hridhya Nidana 10 / 20,2134 Charaka Nidana 4 / 4735 Charaka sutra 27 / 2836 Ibid 26 / 4337 Asthanga hridhaya sutra 10 / 7,838 Hemadri on Ah su 14 / 339 Astanga Hridhaya sutra 10 / 140 Charaka Nidana 4 / 841 Sushruta Sutra 15 / 2342 Charaka sutra 26 / 43 70 Nidana
    • 43 Astanga Hridhya sutra 10 / 944 Dhamanipratichaya by VVS Sastri.pp 6945 Sushruta Nidana 6 / 546 Charaka Nidana 4 / 4747 Astanga Sangraha Nidana 10 / 748 Sushruta Nidana 6 / 549 Ibid 6 / 550 Charaka Nidana 4 / 4751 Ibid 4 / 4752 Ibid 4 / 4753 Ibid 4 / 4754 Astanga Sangraha Nidana 10 / 755 Sushruta Nidana 6 / 556 Charaka Nidana 4 / 4757 Astanga Sangraha Nidana 10 / 758 Sushruta Nidana 6 / 559 Charaka Nidana 4 / 4760 Sushruta Nidana 6 / 561 Charaka Nidana 4 / 4762 Sushruta Nidana 6 / 563 Astanga Sangraha Nidana 10 / 764 Ibid 10 / 765 Ibid 10 / 7 71 Nidana
    • 66 Sushruta Nidana 6/667 Astanga Hridhya Nidana 10 / 768 Astanga Sangraha Nidana 10 / 869 Charaka Nidana 4 / 4470 Sushruta Nidana 6 / 1471 Sushruta Nidana 6 / 2872 Charaka Nidana 4 / 1173 Ibid 4 / 2474 Ibid 4 / 3875 Ibid 4/476 Sushruta Nidana 6/577 Astanga Sangraha Nidana 10 / 878 Charaka Nidana 4 / 1379 Sushruta Nidana 6 / 1280 Astanga Sangraha Nidana 10 / 881 Charaka Nidana 4 / 1482 Sushruta Nidana 6 / 1283 Astanga Sangraha Nidana 10 / 884 Charaka Nidana 4 / 2085 Sushruta Nidana 6 / 1286 Astanga Sangraha Nidana 10 / 887 Charaka Nidana 4 / 2188 Sushruta Nidana 6 / 12 72 Nidana
    • 89 Astanga Sangraha Nidana 10 / 890 Charaka Nidana 4 / 1591 Sushruta Nidana 6 / 1292 Astanga Sangraha Nidana 10 / 893 Charaka Nidana 4 / 1894 Sushruta Nidana 6 / 1295 Astanga Sangraha Nidana 10 / 896 Charaka Nidana 4 / 1697 Ibid 4 / 1798 Sushruta Nidana 6 / 1299 Astanga Sangraha Nidana 10 / 8100 Charaka Nidana 4 / 19101 Astanga Sangraha Nidana 10 / 8102 Charaka Nidana 4 / 22103 Astanga Sangraha Nidana 10 / 8104 Sushruta Nidana 6 / 12105 Astanga Sangraha Nidana 10 / 8106 Sushruta Nidana 6 / 12107 Astanga Sangraha Nidana 10 / 8108 Sushruta Nidana 6 / 12109 Charaka Nidana 4 / 18110 Sushruta Nidana 6 / 13111 Astanga Sangraha Nidana 10 / 8 73 Nidana
    • 112 Charaka Nidana 4 / 28113 Sushruta Nidana 6 / 41114 Astanga Sangraha 10 / 8115 Astanga hridhya Nidana 10 / 18116 Charaka Chikitsa 6 / 15117 Ibid 6/7118 Sangraha Nidana 10 / 5119 Astanga Sangraha Nidana 10 / 5120 Charaka Nidana 4 / 27121 Astanga Sangraha Nidana 10 / 5122 Charaka Nidana 4 / 38123 Astanga Sangraha Nidana 10 / 41124 Astanga Sangraha Nidana 10 / 17125 Sushruta Nidana 6 / 27126 Basavarajeeyam 9 / 30127 Astanga hridhya Nidana 10 / 7128 Charaka Nidana 4 / 14129 Ibid 4 / 19130 Ibid 4 / 44131 Astanga hridhya Nidana 10 / 21132 Charaka Chikitsa 21 / 40133 Charaka Nidana 4 / 42134 Charaka sutra 17 / 109 74 Nidana
    • The treatment of Madhumeha with herbal drugs is well knownsince the time of Charaka and Sushruta. Even today the herbal drugscarry equal importance because of their effective and safe action. Thefollowing drugs are selected for the trial after keenly observing thepathophysiology of the disease according to Modern and Ayurvedicscience. Properties and actions of Madhunashini, Bringaraj,Bhumyamalaki and Eranda when combined, are found very muchsuitable for treating Madhumeha. All these drugs are abundantlyavailable and very effective. As Madhumeha is asadhya it can be madeyapya with proper and continues treatment, patients have to consumethe drug for long periods, thus an economical and effective remedycan be offered for the patients suffering from Madhumeha. Individual drug used in Bhumyamalakyadi churna is explainedbelow. 72 Drug Review
    • MADHUNASANI 1, 2, 3 Sanskrit - Madhunasani Hindi - Gudamar Kannada - kadachigana balli English - Small Indian Ipecacuanha Latin - Gymnema sylvestre Family - Asclepiadaceae Synonyms 4 - Anyada, Chakrashreni, Meshashrangi, Meshavalli, Sarpadanshtrika.Distribution 5 - A climbing plant common in Central and Southern India, on theWestern Ghats and in the Goa territory.Parts used - Dried panchanga of the plant is used.Brief description 6 - A large woody much-branched climber running over the tops ofhigh trees. Leaves 3.2–5 by 1.3–3.2 cm., ovate, elliptic. Baserounded, petioles 6–13 mm. Long, pubescent. Flowers in pedunculate,densely pubescent, shorter than the petioles, pedicels 3 – 13 mm long,corolla yellow, 4 –5 mm.. follicles 6.3 – 7.5 by 0.8 cm., trerete, rigid.Seeds 1.3cm long, narrowly ovoid, flat with a thin broad marginal wing,brown, glabrous. 73 Drug Review
    • Pharmacological properties 7 –Guna – Laghu, Ruksha.Rasa – Kashaya, tikta.Vipaka – Katu.Veerya – Ushna.Doshaghnata – Kapha vata hara.Chemical composition – Gymnemic acid, Quercitol, calcium oxalate, carbonic acid,Phosphoric acid, Ferric oxide, Manganese, some tartaric acid etc. The sweetness - suppressing polypeptide gurmarin isolatedform the leaves consists of 35 amino acid residues including threeintramolecular disulfide bonds. Herein, the total chemical synthesis ofgrumarin was done and gurmarin being 1.9% based on the startingamino acid resin 8. The sweetness - suppressing polypeptide gurmarin has beenisolated form the leaves of Gymnema sylvestre and consists of 35amino acid residues including three intramolecular disulfide bonds.The primary structure has already been determined. The positions ofthe disulfide bonds were located, by a combination of massspectrometric analysis and swquencing of cystine-containing peptidesobtained bythermolysin – catalyzed hydrolysis of grumarin to be cys3-cys18, cys10-cts23, and cys17- csy33 9. 74 Drug Review
    • Actions concerned to disease – The powdered leaves were found to have an oxidise action onglucose solution and glycolysis occurred which reduced the strength ofthe glucose solution from 2.3 to 0.66 % in 29 hours 10. Drug actsindirectly through stimulation in insulin secretion of the pancreas, as ithas no direct action on the carbohydrate metabolism 11. Destroys glycosuria and other urinary disorders 12. The leaves cause hypoglycemia which sets in soon after theadministration of the drug whether by mouth or by injection, lasts for avariable time, is not necessarily proportionate to the dose and in neverexcessive. They do not contain any water soluble or alcohol solublesubstance which destroys glucose in vitro; nor do they yield anychemical body resembling insulin. The drug has no direct action incarbohydrate metabolism, and acts indirectly through stimulation ofinsulin secretion of the pancreas. Kapha medo hara, Meha hara, sarva Meha hara 13, Extracts of gymnemic acids, which wre taken form gymnemasylverstre ware tested for their action on blood glucose. Theconclusion of the study was gymnemic acids suppress the elevation ofblood glucose level by inhibiting glucose uptake in the intestine 14. 75 Drug Review
    • Gymnemic acid inhibites smooth muscle from uptaking theglucose, which is the energy source of the muscle 15. Intravenous injection of gurmarin did not cause any significanteffect on taste responses at all. These results suggest that gurmarinacts on the apical side of the taste cell. Possibly by binding to thesweet taste receptor protein 16. 76 Drug Review
    • BHRINGARAJ 17, 18 19 , Sanskrit - BRINGARAJ Hindi - Bringra Kannada - kadiggaraga Latin - Eclipta alba Hassk. Family - Compositae 20 Synonyms - Angaraka, Bhringa, Ekaraja, Nilapushpa, Shyamala.Distribtuion 21 - Bangal, Burma, Malay peninsula, Central India, Punjab,W.Rajputana, Peninsular India, Ceylon. (IMP 1361)Parts used - Dried panchanga of the plant is used.Brief discription 22 - It is annual, erect or prostrate, branched. Oftern rooting at thenodes; stem and branches strigose with appressed white hairs.Leaves are sessile, 2.5 – 7.5 cm. Long, variable in breadth, usuallyoblong – lanceolate, subentire, acute or sub acute, sparsely strigosewith appressed hairs on both sides, base tapering. Flower Heads are 6– 8 mm. Diam., solitary or two together on unequal axillary peduncles.Ray flowers are ligulate, ligule small, spreading, white. Disk flowersare tubular, corollas often 4 toothed. Achenes cuneate, compressedand with a narrow wing. 77 Drug Review
    • Pharmacological properties 23 –Guna – Laghu, Ruksha.Rasa – katu, tikta.Vipaka – katu.Veerya – ushna.Doshaghnata – kapha vata shamak.Chemical composition 24 – Alkaloid ecliptine, Resin, Ecliptine, Wedelolactone,Actions concerned to disease – Principally used in Liver enlargements, used in jaundice,scalding of urine 25,Used in derangement’s of the liver 26 78 Drug Review
    • BHUMYA MALAKI 27, 28, 29 Sanskrit - BHUMYAMALAKI Hindhi - Bhuie amla Kannada - Guggri kasa Latin - Phyllanthus urinaria Linn. Family - Euphorbiaceae. Synonyms 30 - Hajata, Bahupatra, Bahuphala, Charati Dalasparshini.Distribtuion 31 - Tropics generally, all over India.Parts used - Dried panchanga of the plant is used.Brief discription 32 - Annual, 30 – 60 cm high, glabrous, Stems erect, slightlybranched; leaf bearing branchlets short, flattened or slightly winged.Leaves closely placed, sessile, 6 – 13 by 2.5 – 6 mm, oblong,rounded, apiculate at the apex, pale beneath, glabrous, base rounded,stipules pelate, very acute,. Flowers minute, axillary, solitary,yellowish. Sepals 0.8 – 1 mm. Long, oblong. Rounded, not enlarged infruit. Capsules 3 mm. Diam., globose, scarcely lobed, echinate.Seeds 1.5 mm. Long, 3 – gonous, rounded on the back, transverselyfurrowed. ( imp 2223) 79 Drug Review
    • Pharmacological properties 33 –Guna – Laghu, Ruksha.Rasa – kashaya, tikta, Madhura.Vipaka –. Madhura.Veerya – Sheeta.Doshaghnata – Kapha Pitta shamak. (DGV 640)Chemical composition 34 – Acrid, sour, cooling, bitter, sweetish; alexipharmic componentsare presentActions concerned to disease – Useful in thirst, urinary discharges 35. in jaundice 36,and it is liverstimulant, thrust controller 37, it is best for urinary disorders especiallyPrameha, controls Daha 38 80 Drug Review
    • ERANDA 39, 40, 41 Sanskrit - ERANDA Hindhi - Endi Kannada - Audala Latin - Ricinus communis Linn. Family - Euphorbiaceae. Synonyms 42 - Gandharva hasthah, Panchangulam, Vatari, Eranda.Distribution 43 - This plant is common and quite wild in the jungles in India, It iscultivated throughout India, chiefly in the Tamil nadu, Bengal andMaharastra Presidencies. And also widely cultivated in tropicalcountries.Part used - Leaves.Brief description 44 - Eranda is eka varshika or bahuvarshayu gulma or vrikshakawhich grows up to 17feet. Leaves are green 30 – 60 cm in diameterwith 5 – 10 projections.leaf stem will be 4 – 12 inch long and tublar.Flowers are unisexual, male flowers are above and the females are 81 Drug Review
    • below in the plant. Fruit is thorny and 1 – 3 cms in diameter. Seedsare oval, shiny, multicolored and hard, which yields oil.Pharmacological properties 45 –Guna – Snigdha, Tikshna, Sukshma.Rasa – kashaya, Madhura.Vipaka –. Madhura.Veerya – Ushna.Doshaghnata – Kapha vata shamak.Chemical composition 46 – Fixed oil 45 to 52 %, Ricinine, proteins 20 pc., starch, mucilage,and ash 10pc.,Actions concerned to disease – Leaves are useful in “vata” and “kapha” diseases, used in livertroubles 47, especially enlarged Liver and Mutravishodaka 48, 82 Drug Review
    • REFERENCE1 The Indian Materia medica pp 5962 Indian Medicinal Plants pp 16253 Bhava prakasha Guduchadi verga pp 4434 Indian Medicinal Plants pp 16275 Indian Medicinal Plants pp 16256 Indian Medicinal Plants pp 16257 Bhava prakasha pp 4448 by Tonosaki K at Central Reseach Laboratories, Ajinomoto Co., Inc. Kawasaki, Japan. In 19969 by Ota M at Central Research Laboratories Ajinomoto Co , Inc, Kawasaki, Japan in 199510 The Indian Materia medica pp 59811 The Indian Materia medica pp 59812 The Indian Materia medica pp 59813 Sushruta Sutrasthana 38 / 13, 7414 by Tanaka K at Division of veterinary pharmacology, Nippon veterinary and animal science university, Tokyo. Japan. In 199715 by Nakajyo S at Division of veterinary pharmacology, Nippon veterinary and animal science university, Tokyo. Japan. In 199616 by Imoto T at Department of physiology, Faculty of Medicine, Tottori University, Yonago, Japan. In 199517 The Indian Materica Medica pp 46918 Indian Medicinal Plants pp 136119 Bhava Prakasha, Gudchadi varga – pp 42920 Indian Medicinal Plants pp 136321 Indian Medicinal Plants pp 136122 Indian Medicinal Plants pp 136123 Bhava Prakasha, Gudchadi varga – pp 43024 The Indian Materica Medica pp 46925 Indian Medicinal Plants pp 136126 The Indian Materica Medica pp 46927 Indian Medicinal Plants pp 2223 83 Drug Review
    • 28 The Indian Materica Medica pp 94929 Bhava Prakasha, Gudchadi varga – pp 46030 Indian Medicinal Plants pp 222331 Indian Medicinal Plants pp 222332 Indian Medicinal Plants pp 222333 Bhava Prakasha, Gudchadi varga – pp 46034 Indian Medicinal Plants pp 222335 Indian Medicinal Plants pp 222336 The Indian Materica Medica pp 94937 Bhava Prakasha, Gudchadi varga – pp 46038 Raja Niguntu pp 26339 Bhava Prakasha, Gudchadi varga – pp 29940 The Indian Materica Medica pp106541 Indian Medicinal Plants pp 227542 The Indian Materica Medica pp106543 The Indian Materica Medica pp106544 The Indian Materica Medica pp106545 Bhava Prakasha, Gudchadi varga – pp 29946 The Indian Materica Medica pp106547 Indian Medicinal Plants pp 227548 Bhava Prakasha, Gudchadi varga – pp 299 84 Drug Review
    • The term Chikitsa is derived form the root “KIT ROGAPANAYANE” 1 .According to Amaarkosha Chikitsa is Ruk Pratikriya. Chikitsa is theprocess by which the doshas and dhatus are brought into normalcy.Madhumeha is a chronic relapsing disease and may also develop as ahereditary disease. Madhumeha patients are divided in two varieties.1. Sthula and 2. Krisa Sthula patients are capable of withstanding the shodhana karma andthe krisa patients are incapable of withstanding it. Therefore a sthulapatient has to be treated with the sodhana chikitsa and drisha withpaliative treatment. For every Shodhana chikitsa the patient should undergo poorvakarma. But the Madhumeha patient is prohibited from undergoing sweda 3karma . In sthula patient after completion of sneha karma the doshasshould be eliminated by urdhava and adhosodhana as Vamana andVirechana respectively. After the completion of the Sodhana karma the patient has to besubjected for samsarjana krama. Even though the madhumeha issantarpana janya roga, the patient should not be subjected to Apatarpanakriya, because it may result in to Gulma, Kshaya, Mehana shoola, vasti 69 Chikitsa
    • shoola and Mootra graha. The Brimhana chikitsa should be carried outconsidering the strength of the jataragni of the individual patient 4 . A krisaor emaciated, and Durbala or weak patient who is not capable ofwithstanding the shodhana karma requires Bhrimhana chikitsa 5 . Even though the vataja Pramehas are stated to be incurable the dutyof physician is to treat the patient and prevent the future complications.Therefore vataja Prameha should be treated.SHAMSAMANA CHIKITSA Shamana chikitsa is indicated for a Prameha patient who is noteligible for shodhana chikitsa, and also the patient who has completed theshodana karma. Many varieties of decoctions, choornas and lehyas have beendescribed for the treatment of the twenty varieties of Pramehas by allAyurvedic authorities. Vyayam, udvarthana, snana, jala sechana and thelepas with Twak, Ela, Agar and chandana are useful in Prameha patient 6 . Avoiding the causative factors (Nidana) is also a treatment 7 . In ourtrial we have used only shamana therapy, which has yield a verysignificant result. 70 Chikitsa
    • The patient of prameha who is not fit for evacuation should besubjected to pacificatory management for alleviation of the disease suchas mantha (churned drink), extracts, linctus made of barley powder andlight edibles. He should eat rough food articles such as boiled barley,barley cakes, flour of parched grains and apupa with palatable meat -soup of wild birds particularly gallinaceous and peckers. He should takeold shali rice with soup of mudga etc. and bitter vegetables added with oilof danti and ingudi or linseed and mustard. In cereals, he should useshashtika and wild rice. The diet of the patient of prameha should consistmainly of barley. One suffering form kaphaja prameha should eat variouspreparations of barley added with honey. Barley grain dipped in decoctionof triphala for the whole night make a saturating food taken with honey.The patient may also take them regularly mixed with vinegar for alleviationof Prameha. He should use flour of parched grains, bolus, parched grainsand other various edibles made of barley impregnated with deccoctions ofdurgs prescribed in kaphaja prameha. Various preparations of barleymixed with the meat of ass, horse, bull, swan and spotted deer should beprescribed. The seeds of bamboo and wheat may also be used in formssimilar to those of barley 8 . 71 Chikitsa
    • REFERENCE1 Shabda Sthoma Mahanidhi3 Charaka Sutra 14 / 164 Charaka Chikitsa 6 / 16,175 Ibid 6 / 156 Ibid 6 / 487 Ibid 6 / 518 Ibid 6 / 18 – 24. 72 Chikitsa
    • MATERIAL AND METHODSMaterials -a. Materials for literary search. Literary search is done from classical Ayurvedic texts, Modern texts, Medlar search and updated through journals.b. Materials for clinical study. Bhumyamalakyadi churna, composed of Madhunashini Eranda Bhumyamalaki Bhringaraj is taken for the clinical trial.Collection of Drugs: - All the drugs were personally collected from Kapat hills, and wereconfirmed their identity by the Botanist.Method of Preparation: - Panchangas of above said drugs were cleaned thoroughly byrunning water to take out physical impurities and dried in the shade. Thedried herbs were powdered separately in the pulvaliser to get a finepowder. 83 Materials & Methods
    • Again the wet drugs are collected, to extract swarasa, which isutilised for giving bhavana to the corresponding herb powders to increasetheir potency. These powders are mixed in proportions and filled in500mg capsules for easy palatability for the patient. CLINICAL TRIALMethods :Selection of Sample Patients suffering from Madhumeha are selected from the Post Graduate And Research Centre OPD/IPD of D.G.M. Ayurvedic College Hospital and medical camp organised exclusively for Madhumeha patients at Post Graduate And Research Centre of D.G.M. Ayurvedic college Hospital, Gadag.Inclusive criteria - - Patients between the age of 25 to 65 years - Irrespective of sex - Less than 5 years chronicity.Exclusive criteria - - Patients having known organic lesions. - Insulin dependent 84 Materials & Methods
    • Laboratory Investigations The selected patients were subjected to following laboratoryinvestigations Fasting blood sugar Post partal blood sugar Urine sugar Serum cholesterolDiagnostic Criteria Diagnosis was made on the basis of subjective parametersmentioned in the classics and objective (lab investigations) parameters. Table showing the normal values of objective parameters. Lab investigations Normal values Fasting blood sugar 80 –120 mg% Post partal blood sugar 110 – 140 mg% Serum Cholesterol 120 – 250 mg% Urine sugar Nil 85 Materials & Methods
    • Lab investigation methods1. Blood Glucose Blood glucose is determined by using Gluzyme Glucose reagentset.Procedure – blood is collected in a sterilized container. Serum isseparated form the cells at the earliest possible time (within 30 min), thenthe blood is mixed with the reagent (working solution) and heated at37°C. for 15 min. and then observed in colorimeter under 520 nm.pipetting scheme Blank Standard Test Working enzyme reagent (ml) 3.0 3.0 3.0 Distilled water (ml) 0.025 - - Standard (ml) - 0.025 - Sample (ml) - - 0.025Calculation Absorbance of sampleGlucose in mg/dl = X 100 Absorbance of standardand the result is recorded in the case sheet.2. Urine sugar Urine is collected in a test tube and mixed with 5ml of Benedictssolution and heated till it boils, it is allowed to cool to room temperatureand then the colour change is noted. 86 Materials & Methods
    • 3. Serum Cholesterol Modified Allain’s method Cholesterol kit is used for measuring thecholesterol level. blood is collected in a sterilized container. Serum isseparated form the cells and mixed with the working reagent and byusing the colorimeter (green filter) the cholesterol was estimated.pipetting scheme Blank Standard Test Working enzyme reagent (ml) 1.0 1.0 1.0 Distilled water (ml) 0.01 - - Cholesterol Standard (ml) - 0.01 - Sample (ml) - - 0.01Calculation -Total Cholesterol in mg% = A of (T) x 200 A of (S)Study design - Prospective clinical trail.Sample size - 30 patients are subjected for the study. They are grouped as A) Hyperglycemic and Hypolipidimic B) Hyperglycemic and Hyperlipidimic 87 Materials & Methods
    • In each group 15 patients are included on the bases of lab investigations.Posology - 3gms / 24 hours in divided doseDuration of treatment - Duration of the study was 30 days from the day of initiation of“Bhumyamalakyadi Churna”.Follow up – All the patients were asked to report every Partnight followup.Diet - Patients were asked to take regular blind diet as far as possible. -Criteria for assessment of treatment – Results of the treatment were assessed on the bases of differencesbetween the base line data and assessment data. The lab investigationvariables were subjected for statistical analysis by applying student ‘t’test and paired ‘t’ test. 88 Materials & Methods
    • Thirty patients are selected for the clinical study and grouped into group A and B each of fifteen. The data collected is as follows – Demographic data Master chart - 1Sl OPD Date of Name A S Rl O E Dt F F Gr ResultNo No Initiation Yrs S H O1 4477 06/07/99 TRR 58 M 1 2 2 M P 1 B Relieved2 7510 24/08/99 SRT 43 M 1 1 3 M M 2 A Palliative3 11186 27/10/99 PNY 50 M 1 1 1 V N 2 B Relieved4 11187 27/10/99 GHK 62 M 1 1 2 V N 2 A Palliative5 11188 27/10/99 HBG 40 M 1 1 3 V P 2 B Palliative6 11189 27/10/99 MBL 42 M 1 1 3 V M 2 A Relieved7 11191 27/10/99 IPM 48 M 1 1 2 V P 2 B Not responded8 11192 27/10/99 VMV 59 M 1 2 2 V P 2 A Relieved9 11193 27/10/99 MBK 64 M 1 1 2 V P 2 A Relieved10 11194 27/10/99 MKJ 48 M 1 1 2 V P 1 B Not responded11 11198 27/10/99 NTB 40 F 1 1 4 M N 1 B Relieved12 11199 27/10/99 CNS 62 M 1 1 4 V P 2 A Relieved13 11201 27/10/99 SSB 39 M 1 2 3 M M 1 B Not responded14 11202 27/10/99 CBG 52 M 1 1 4 M N 2 A Palliative15 11330 27/10/99 RPA 56 M 1 3 1 V N 1 A Palliative16 11346 27/10/99 AAB 38 F 2 2 3 M P 1 B Relieved17 11397 28/10/99 CSP 57 M 1 2 4 V P 2 B Palliative18 11456 28/10/99 ASN 49 F 1 1 3 V P 1 B Relieved19 11627 01/11/99 PHW 58 F 1 1 3 M N 2 B Not responded20 11686 02/11/99 BSM 54 M 1 2 4 M P 2 A Palliative21 11689 02/11/99 GTH 60 F 1 1 4 V N 2 B Palliative22 11709 03/11/99 NKB 45 M 1 1 3 M P 1 A Palliative23 11820 04/11/99 SFN 50 M 1 1 4 M P 2 A Relieved24 11891 04/11/99 TVR 47 M 1 1 3 M M 1 B Relieved25 11895 07/11/99 PSB 39 F 1 1 4 V M 2 A Palliative26 11919 08/11/99 MSA 43 F 1 1 3 V P 2 B Relieved27 12044 11/11/99 AKJ 36 M 1 1 4 V P 2 A Not responded28 12335 11/11/99 MNR 48 M 1 1 4 M M 2 A Relieved29 12357 16/11/99 SSM 39 M 1 1 4 V M 2 B Relieved30 12633 21/11/99 MSB 61 M 1 1 4 V P 2 A Relieved AY – Age in Yea rs, S – Sex (M – Male, F – Female), Rl - Religion (1- Hindu, 2 - Muslim, 3 - others), O - Occupation (1 - Sedentary, 2 - Active, 3 - Labor), ES - Economical status (1= 0-1Lack,2=1-2 L,3=2-3 L,4=3 L & above), Dt - Diet (v - vegetarian, M - mixed) FH – Family history (P- Paternal, M – Maternal,N – nil), FO – Fresh / Old (1 - Fresh, 2 – Old ) Gr – Group ( A – Hyperglycemic & Hypolipidimic, B - Hyperglycemic & Hyperlipidimic), 89 Observation, Analysis & Interpretation
    • Master Chart 2 Sl Complaints No 1 2 3 4 5 6 Result B A B A B A B A B A B A 1 + + + - + - + + - - + - Relieved 2 + - + - + - - - + - + - Palliative 3 + - + - + - - - - - + - Relieved 4 + - + - + - + - + + + + Palliative 5 + + + + + - + + + - + + Palliative 6 + + + - + - - - - - + - Relieved 7 + - + - + - - - - - + - Not responded 8 + - + - + - - - + + + - Relieved 9 + - + - - - - - - - + - Relieved 10 + + + + + - - - + - + + Not responded 11 + - + - + - - - + + + - Relieved 12 + - + - + - - - - - + - Relieved 13 + + + - - - - - + + + - Not responded 14 + + + - + - - - + - + + Palliative 15 + + + - + - - - - - + + Palliative 16 + - + - - - - - - - + - Relieved 17 + + + - + - - - + + + + Palliative 18 + - + - - - + + - - + - Relieved 19 + - + - + - + + + - + - Not responded 20 + - + - + - - - - - + - Palliative 21 + + + - + - - - + - + - Palliative 22 + - + - + - + + + + + - Palliative 23 + - + - + - - - - - + - Relieved 24 + - + - + - - - + + + - Relieved 25 + + + - + - + + - - + + Palliative 26 + + + - + - - - + + + - Relieved 27 + + + - + - - - - - + + Not responded 28 + - + - + - - - + - + - Relieved 29 + - + - + - - - - - + - Relieved 30 + - + - + + - - + + + - RelievedComplaints (1=Prabhoota Mootrata,2=Avil Mootrata,3=Ashaktata,4=Shareera bhara hani,5=Jangha mansa graha,6 = Madhura mootrata, B – Before treatment, A – After treatment) 90 Observation, Analysis & Interpretation
    • Master chart - 3Sl Personal history ResultNo 1 2 3 4 5 6 7 8 9 10 11 12 13 141 + + + + + - + + + + + + + -2 + + + + + + + + + + + + + -3 + + - + - - + + + + + + - +4 + + + + + - + + + + - + - -5 + + + + + - + + + + + + + -6 - + + + + + + + + - - + - -7 + + + + - - + + + + + + + -8 + + + + + - + + + + + + + -9 + + + + + - + + + + + + + +10 + + + + + + + + + + + + + -11 + + + + + - + + + + + + + -12 + + + + + + + + + + + + + -13 + + + + + - + + + + + + + +14 + - + + + + + + + + + + + -15 + + - + + - + + + + - + - -16 + + + + + + + + + + + + + +17 + - + + + + + + + + + - - -18 + + + + + - + + + + + + + -19 + + + + + - + + + + + + + -20 + + + + - + - + + + + + + -21 + + + + + - + + + + - + + -22 + + + + + + - + + + + + + +23 + + + + + - + + + + + + + -24 + - + + + + + + + + + + + -25 + + + + + - + + + + + + - +26 + + + + + - + + + + + + - -27 + + + + + - + + + + + + + -28 + + + + + - + + + + + + + +29 + + + + + - + + + + + + - +30 + + + + + - + + + + + + + - 1. Madhura, 2. Sheeta, 3.Snigdha, 4.Guda, 5. Navanna, 6.Mamsa, 7. Dugdha, 8.Dahi, 9.Gudavikriti, 10.Dugdhavikriti, 11.Avyayama, 12.Diwaswapna, 13.Swapnasukham, 14 Manisika chinta. 91 Observation, Analysis & Interpretation
    • Master Chart – 4 POORVAROOPA poorvaroopa B – Before treatment, A – After treatment.1 – Dantadeenam malatavam, 2 – Pada daha, 3 – Panidaha, 4 – Deha chikkanata, 5 – Shareera durgandha, 6 – Mukha madhurata, 7 – Talu klomashosha, 8 – Kesha jatilata, 9 – Nakhavriddhi, 10 – Alasya, 11 – Trishna, 12 – Maldhikyata in bahya chidra, 13 – Swedadhikya, 14 – Shitaiccha, 15 – Swasa, 16 – Mutramadhurata, 17 – Mutrashuklata. Observation, 92 Analysis & Interpretation
    • Master Chart – 5 SROTAS Udakavaha Medovaha Mamsavaha Mootravaha 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A B A 1 + - + - + - + - + - + - - - - - + - - - - - - - - - - - - - + - - - - - 2 + - + - + - + - + - + - - - - - + - - - - - - - - - - - - - + - - - - - 3 + - + - + - + - + - + - + + - - + - - - - - - - - - - - - - + - - - - - 4 + - + - + - + - + - + - - - - - + - - - + + - - - - - - - - + - - - - - 5 + - + - + - + - + - - - + + + + + - - - + + - - - - - - - - + - - - - - 6 + - + - + - + - + - - - + + - - + - + + - - - - - - - - - - + - - - - - 7 + - + - - - + - + - + - + + - - + - - - - - - - + + - - - - + - + - - - 8 + - + - + - + - + - + + + + - - + + - - + + - - - - - - - - + - - - - - 9 + - + - + - + - + - + - + + + + + - - - - - - - - - - - - - + - - - - - 10 + - + - + - + - + - + - + + + + + - - - + + - - - - - - - - + - - - - - 11 + - + - + - + - + - - - - - - - + - - - - - - - - - - - - - + - - - - - 12 + - + - + - + - + - + - - - - - + - - - - - - - - - - - - - + - - - - - 13 + - + - + - + - + - + - - - - - + - - - - - - - - - - - - - + - + - - - 14 + - + - + - + - + - + - + + + + + - - - - - - - - - - - - - + - - - - - 15 + - + - + - + - + - - - - - - - + - - - - - - - - - - - - - + - - - - - 16 + - + - + - + - + - - - + + - - + - - - - - - - - - - - - - + - - - - - 17 + - + - + - + - + - - - + + + + + - - - - - + - - - - - - - + - - - - - 18 + - + - + - + - + - + - + + + + + - - - - - - - - - - - - - + - - - - - 19 + - + - + - + - + - + + - - - - + - - - - - - - - - - - - - + - - - - - 20 + - + - + - - - + - - - - - - - + - - - - - - - + + - - - - + - - - - - 21 + - + - + - + - + - - - - - - - + - - - + + - - - - - - - - + - - - - - 22 + - + - + - + - + - + - - - - - + - - - - - - - - - - - - - + - - - - - 23 + - + - + - + - + - - - - - - - + - - - - - - - - - - - - - + - - - - - 24 + - + - + - + - + - + + + + + + + - - - - - - - - - - - - - + - - - - - 25 + - + - + - + - + - - - - - - - + - - - + + - - - - - - - - + - - - - - 26 + - + - + - + - + - - - - - + + + + - - - - - - - - - - - - + - - - - - 27 + - + - + - + - + - + - - - - - + - - - - - - - - - - - - - + - - - - - 28 + - + - + - + - + - - - - - - - + - - - - - - - - - - - - - + - - - - - 29 + - + - + - + - + - + - - - - - + - - - + + - - - - - - - - + - - - - - 30 + - + - + - + - + - - - - - - - + - - - - - - - - - - - - - + - - - - -B – Before treatment, A – After treatment.1 – Jihwa shosha, 2 – Talu shosha, 3 – Osta shosha, 4 – Kloma shosha, 5 – Prawridha pipasa, 6 – Sweda, 7 – Snigdhanagata, 8 – Sthula shophata, 9 – Pipasa, 10 – Arbuda,11 – Arsha, 12 – Mamsa shosha, 13 – Shira granthi, 14 – Alpalpa mootrata, 15 – Mootra rodha, 16 – Adhika mootra, 17 – Sashoola mootra, 18 – Basti stabhadata. Observation, 93 Analysis & Interpretation
    • Master Chart – 6 Upadravas UpadravasSl N 1 2 3 4 5 6 7 8 9 B A B A B A B A B A B A B A B A B A 1 - - - - - - + - - - - - + - - - - - 2 - - - - - - + - - - + - - - + - - - 3 - - - - - - + - + - - - - - - - - - 4 + - - - - - + - - - + - - - - - - - 5 + - - - - - + - + - - - - - - - + - 6 - - - - - - + - + - - - - - - - - - 7 - - - - - - + - + - - - - - - - - - 8 - - - - - - + - + - + - - - - - - - 9 - - - - - - - - - - - - - - - - - - 10 - - - - - - + - + - - - - - - - - - 11 - - - - + - - - - - - - - - - - + - 12 - - - - - - + - + - + - - - - - - - 13 - - - - - - - - - - - - - - - - - - 14 - - - - - - + - - - + - - - - - - - 15 + - + - - - - - - - - - - - + - + - 16 - - - - - - - - + - - - - - - - - - 17 - - - - + - + - + - - - - - - - - - 18 - - + - - - - - - - - - + - - - - - 19 - - - - - - + - + - - - - - - - - - 20 - - - - - - + - + - - - - - - - - - 21 - - - - - - - - + - - - - - - - - - 22 - - - - - - + - + - + - + - - - - - 23 - - - - - - - - - - - - - - - - - - 24 - - - - - - + - + - - - - - - - - - 25 - - - - - - - - - - - - - - - - - - 26 - - - - - - + - - - - - - - - - - - 27 - - - - - - - - - - - - - - - - - - 28 + - - - - - + - - - - - - - - - - - 29 - - - - - - - - - - - - - - - - - - 30 - - - - - - + - - - - - - - - - + -1 – Prameha pidika, 2 – Atisara, 3 – Jwara, 4 – Daha, 5 – Arochaka, 6 – avipaka7 – Chardi, 8 – Kasa, 9 – Pratishyaya 94 Observation, Analysis & Interpretation
    • Master chart 7 - A Sl Lab Investigation Result N FBS mg/dl PPBS mg/dl US % SC mg% B A Dif B A Dif B A Dif B A Dif 2 238 113 125 293 148 145 1.5 00 1.5 180 178 2 Palliative 4 213 094 119 500 165 340 02 0.5 1.5 150 150 0 Palliative 6 272 116 156 486 134 322 1.5 00 1.5 232 230 2 Relieved 8 200 126 074 366 131 235 1.5 00 1.5 203 194 9 Relieved 9 265 098 167 350 120 230 01 00 01 128 128 0 Relieved 12 216 124 092 289 130 159 01 00 01 140 136 4 Relieved 14 183 090 093 380 184 196 01 0.5 0.5 154 149 5 Palliative 15 127 102 025 227 153 075 01 0.5 0.5 160 154 6 Palliative 20 197 092 105 234 150 084 0.5 00 0.5 160 160 0 Palliative 22 119 082 037 231 146 085 0.5 00 0.5 210 203 7 Palliative 23 178 112 066 230 136 094 0.5 00 0.5 190 187 3 Relieved 25 296 118 188 341 162 179 1.5 0.5 01 188 182 6 Palliative 27 297 143 154 428 180 248 02 0.5 1.5 212 208 4 Not responded 28 140 103 037 210 132 078 01 00 01 183 181 2 Relieved 30 206 102 104 263 142 121 1.5 00 1.5 168 166 2 Relieved Master chart 7 - B Sl Lab Investigation Result N FBS mg/dl PPBS mg/dl US % SC mg% B A Dif B A Dif B A Dif B A Dif 1 264 117 107 326 136 150 1.5 00 1.5 353 350 3 Relieved 3 107 097 010 157 132 025 0.5 00 0.5 346 341 5 Relieved 5 290 110 180 488 196 292 02 0.5 1.5 324 321 3 Palliative 7 310 142 168 427 136 291 02 00 02 296 292 4 Not responded 10 190 146 044 279 215 064 01 01 00 340 337 3 Not responded 11 122 096 026 155 114 041 0.5 00 0.5 311 306 5 Relieved 13 392 130 262 502 152 350 02 00 1.5 322 320 2 Not responded 16 180 090 090 240 130 110 1.5 00 1.5 311 302 9 Relieved 17 293 104 189 380 156 224 1.5 0.5 01 340 335 5 Palliative 18 160 111 049 182 128 054 0.5 00 0.5 378 374 4 Relieved 19 202 134 068 264 204 060 01 00 01 409 403 6 Not responded 21 160 117 043 208 131 077 02 0.5 1.5 281 279 2 Palliative 24 155 106 049 312 148 164 1.5 00 1.5 286 285 1 Relieved 26 271 117 162 324 151 173 1.5 00 01 406 405 1 Relieved 29 192 095 097 280 127 153 1.5 00 1.5 313 310 3 Relieved B – Before Treatment, A – After Treatment,.FBS – Fasting blood sugar, PLBS – Post lunch blood sugar, US – Urine sugar, SC – Serum Cholesterol,1. Distribution of patients by age 95 Observation, Analysis & Interpretation
    • Age No of patients Percentage Responded Percentage 36 – 45 11 37% 10 91% 46 – 55 9 30% 6 67% 56 - 65 10 33% 9 90% Largest incidences are found in the age group of 36 – 45. It shows middle-aged people are more prone to get into this condition.3. Distribution of patients by sex sex No of patients Percentage Responded Percentage Male 23 77% 20 87% Female 7 23% 5 71% This data shows among 30 patients 23 (77%) are male and only 7 (23%) are female. This indicates the incidence of Madhumeha is more in male.Graphic representation of age and sex is shown in figure 1 96 Observation, Analysis & Interpretation
    • Figure 1 Showing Age and Sex ratio 9 8 7 Number of Patients 6 5 4 3 2 1 Sex 0 Male Female 36 - 45 7 4 46 - 55 8 1 56 - 65 7 33. Distribution of patients by religion No of patients Percentage Responded Percentage Religion Hindu 29 97% 24 83% Muslim 1 3% 1 100% Others 0 0% 0 0% 97 Observation, Analysis & Interpretation
    • The data shows among 30 patients 29 (97%) belongs to Hindu, 1 (3%) belongs to Muslim. It dose not mean that Hindus are more prone for this disease. This may be due to the area from where sampling is being done. Figure no 2 Showing the Religion incidence Others 0% Muslim 3% Hindu 97%4. Distribution of patients by Occupation. Occupation No of patients Percentage Responded Percentage Sedentary 23 77% 19 83% Active 6 20% 5 83% Labour 1 3% 1 100% The data shows among 30 patients 23 (77%) belong to sedentaryoccupation group, 6 (20%) belong to active occupation group and 1 (3%) 98 Observation, Analysis & Interpretation
    • incidence witnessed from labour group. This shows sedentary work orless laborious work might have more susceptibility to the disease.5. Distribution of patients by Economical status Income @ No of patients Percentage Responded % under –1 lakh 2 7% 2 100 1 – 2 lakh 5 17% 4 80 2 – 3 lakh 10 33% 9 90 3 lakh and above 13 43% 10 77 This data shows out of 30 patients, 13 (43%) belong to 3 lakh and above category, 10 (33%) belong to 2 – 3 lakh category, 5 (17%) belong to 1 – 2 lakh, 2 (7%) belong to under 1 lakh group. It clearly indicates the incidence of the disease is more in higher economical class of people, because of high caloric diet in take and less utility of it. Diagrammatic representation of occupation and economical status is shown in figure No 3 99 Observation, Analysis & Interpretation
    • Figure No 3 Showing the incidence of Economical status and occupation 12 10 8 Number of patients 6 4 2Income per @ 0 3 Lacks and 0 - 1 Lack 1 - 2 Lacks 2 - 3 Lacks above Sedentary 1 4 8 10 Active 0 2 2 2 Labour 1 0 0 0 100 Observation, Analysis & Interpretation
    • 6. Distribution of patients by Diet Diet Number of patients Percentage Vegetarian 20 67% Mixed 10 33% This data shows 20 (67%) of the patients are vegetarians and 10(33%) are having mixed (both veg and nonveg) food habits. This may bebecause of more number of patients selected from Hindu religion. Figure no 4 Showing the incidence of Diet Mixed 33% Veg 67% 101 Observation, Analysis & Interpretation
    • 7. Distribution of patients by Family history Family History Number of patients Percentage Paternal 15 50% Maternal 6 20% Without F History 9 30% Maximum patients i.e. 21 (70%) had a family history. Among them 15 (50%) had paternal and 6 (20%) had maternal history. Figure no 5 Showing the incidence of Family History Non 30% Paternal 50% Maternal 20% 102 Observation, Analysis & Interpretation
    • Data related to ResultTotal Result No of patients Percentage Relieved 15 50% palliative 10 33% Not responded 5 17%Group A Result No of patients Percentage Relieved 7 46% palliative 7 46% Not responded 1 6%Group B Result No of patients Percentage Relieved 3 20% palliative 8 53% Not responded 4 26% By the above data we can observe the effect of the medicine issignificant, and is working better on group A patients than in Group B.Graphical representation of it is given in fig No 6. 103 Observation, Analysis & Interpretation
    • Figure No 6 Showing the Results 16 14 12 10 Number of patients 8 6 4 2Result 0 Relived Palliative Not responded Total 15 10 5 Group A 7 7 1 Group B 3 8 4 104 Observation, Analysis & Interpretation
    • Data of Personal history To asses the nidanas of the disease, detailed personal history istaken with more concentration drawn towards ahara and vihara of thepatient.Data pertaining toa. Ahara Ahara No of patients Percentage Madhura 29 97% Sheeta 28 94% Snigdha 28 94% Guda 30 100% Navanna 27 90% Mamsa 20 67% Dugdha 28 94% Dahi 30 100% Gudavikriti 30 100% Dugdha vikriti 29 97% Data revels that more than 90% of the patients are habituated forthe food, which are said to be the nidana of the Madhumeha.b. Vihara Vihara No of patients Percentage Avyayama 26 87% Diwaswapna 29 97% swapnasukham 22 73% 87% of the patients have lack of physical exercise, 97% of thepatients have the habit of Diwaswapna and 73% of the patients have 105 Observation, Analysis & Interpretation
    • swapnasukham , these factors intensifies the disease along with aharajakarana.c. Manasika Chinta No of patients Percentage Present 8 27% Absent 22 73% 73% of the patients are leading happy life without much worries,which is one of the causative factor for Madhumeha. 106 Observation, Analysis & Interpretation
    • Data related to the disease.a. Roopas This table shows the number of patients having particular complaintand its relief after the treatment. Complaints No of patients % Relieve % Sig d P r a bho o ta M oo tr a ta 30 100 18 60 S A v i l a Mo o tr a t a 30 100 28 93 HS Ashaktata 26 87 25 96 HS Shareeara Bhara hani 8 27 2 25 NS Jangha mamsa graha 16 53 9 56 S Madhura mootrata 30 100 22 73 S Key Note; Sin–significance, S–significance, HS-Highly significance, NS–Not significance Prabhoota mootrata, Avila Mootrata and Madhura mootrata arefound in all the patients and among them 60% , 93% and 73% of thepatients are Relieved form the symptom respectively. 87% of the patientscomplained of Ashaktata and 96% of them were relieved from thiscomplaint. 53% of the patients had Jangha mamsa graha and 56% ofthem are Relieved. Shareeara bharahani was complained by 27% of thepatients. 107 Observation, Analysis & Interpretation
    • b. Poorvaroopa. The master chart of poorvaroopa is given in Master chart 4 andanalysis is as under. Associated Complaints No of patients % Relieved % Dantadeenam malatavam 17 57% 15 86% Pada daha 25 84% 19 76% Panidaha 24 80% 20 85% Deha chikkanata 23 77% 21 91% Shareera durgandha 23 77% 22 95% Mukha madhurata 19 63% 16 85% Talu klomashosha 29 97% 24 82% Kesha jatilata 15 50% 9 60% Nakha vriddhi 23 77% 13 56% Alasya 28 93% 26 93% Trishna 30 100% 27 90% Maldhikyata 12 40% 9 75% Swedadhikya 27 90% 25 92% Shitaiccha 19 63% 16 84% Swasa 7 23% 5 71% Mutramadhurata 21 70% 20 95% Mutrashuklata 19 63% 17 85% This data justifies the statement “poorvaroopas are seen along withroopas of the disease” more than 70% of the patients are having poorvaroopa as complaint even after the manifestation of the disease which canbe said as difficulty to treat but 82% of them are relieved from thecomplaints after the treatment.c. Srotas 108 Observation, Analysis & Interpretation
    • Four srotases viz Udakavaha Medovaha Mamsavaha Mutravahawhich are in concern are discussed in Master chart 5 Udakavaha Srotas Udakavaha No of patients % Relieved % J ihwa s hosh a 30 100 30 100 T a lu sh osha 30 100 30 100 Os ta shos ha 29 97 29 100 Kloma shosh a 29 97 29 100 Prow ridha p ip asa 30 100 30 100 All the patients suffering from the udakavaha srotodusti wereRelieved to full extent on getting this treatment. Medovaha Srotas Medovaha No of patients % Relieved % S w e da 17 57 14 82 Sn ig dha nga ta 12 40 0 00 Sth ula shop ha ta 8 27 0 00 Pipas a 30 100 28 93 Patients suffering form medovaha srotodusti is analysed abovewhich indicate the grater success in treating the medovaha srotodustialso. 109 Observation, Analysis & Interpretation
    • Mamsavaha Srotas Mamsavaha No of patients % Relieved % A u bud a 1 3 0 00 Arsha 7 23 0 00 M ams a s hosh a 1 3 1 100 S h ira gra n th i 2 7 0 00 Involvement of Mamsavaha srotas is seen in very less patientscompared with other srotases. Mootravaha Srotas Mootravaha No of patients % Relieved % A l pa lp a mot r a t a 00 0 00 00 M oo tr a r o dh a 00 0 00 00 Adhik a mootra 30 100 28 93 Sas hoo la moo tr a 02 7 02 100 B as t i s tab dh a ta 00 0 00 00 The main symptom in this srotodusti observed was Adhika mootratathat was Relieved in 93% of the patients. 110 Observation, Analysis & Interpretation
    • d. Upadravas Detailed Master chart of upadravas is given in master chart 6 Complaints No of patients % Relieved % P r a me ha p id ik a 4 13 3 75 Atis ara 2 7 2 100 Jwara 2 7 2 100 Daha 19 63 16 84 Arochaka 14 47 12 86 Avipaka 6 20 6 100 Chardi 3 10 3 100 Kasa 2 7 1 50 pratishyaya 4 13 4 100 Data reviles 63% of the patients were suffering from Daha, 84% ofthem were Relieved among them. 47% of the patients were complainingof Arochaka, among them 86% of the patients were Relieved from thiscomplication after the treatment of madhumeha.13% of the patients hadprameha pidika which is Relieved in 75% . Other minor complicationswere also reported and Relieved to a grater extent as shown in the table. 111 Observation, Analysis & Interpretation
    • e. Laboratory investigations. The figures of lab investigations are shown below. 112 Observation, Analysis & Interpretation
    • Figure No. 7 Fasting Blood Sugar of Group A 350 300 F.B.S. in mg/dl 250 200 150 100 50Patient Sl No 0 2 4 6 8 9 12 14 15 20 22 23 25 27 28 30 Before 238 213 272 200 265 216 183 127 197 119 178 296 297 140 206 After 113 94 116 126 98 124 90 102 92 82 112 118 143 103 102 Figure No. 8 Fasting Blood Sugar of Group - B 450 400 350 300 F.B.S. in mg/dl 250 200 150 100 50 0 Patient Sl No 1 3 5 7 10 11 13 16 17 18 19 21 24 26 29 Before 264 107 290 310 190 122 392 180 293 160 202 160 155 271 192 After 117 97 110 142 146 96 130 90 104 111 134 117 106 117 95 113 Observation, Analysis & Interpretation
    • Figure No. 9 Post partal Blood Sugar of Group - A 600 500 400 P.P.B.S. in mg/dl 300 200 100 0 Patient Sl No 2 4 6 8 9 12 14 15 20 22 23 25 27 28 30 Before 293 500 486 366 350 289 380 227 234 231 230 341 428 210 263 After 148 165 134 131 120 130 184 153 150 146 136 162 180 132 142 Figure No. 10 Post partal Blood Sugar of Group - B 600 500 400 P.P.B.S. in mg/dl 300 200 100 0Patient Sl No 1 3 5 7 10 11 13 16 17 18 19 21 24 26 29 Before 326 157 488 427 279 155 502 240 380 182 264 208 312 324 280 After 136 132 196 136 215 114 152 130 156 128 204 131 148 151 127 114 Observation, Analysis & Interpretation
    • Figure No. 11 Urine Sugar of Group A 2.5 2 Urine Sugar in % 1.5 1 0.5Patient Sl No 0 2 4 6 8 9 12 14 15 20 22 23 25 27 28 30 Before 1.5 2 1.5 1.5 1 1 1 1 0.5 0.5 0.5 1.5 2 1 1.5 After 0 0.5 0 0 0 0 0.5 0.5 0 0 0 0.5 0.5 0 0 Figure No 12 Urine Sugar of Group - B 2.5 2 Urine Sugar in %l 1.5 1 0.5Patient Sl No0 1 3 5 7 10 11 13 16 17 18 19 21 24 26 29 Before 1.5 0.5 2 2 1 0.5 2 1.5 1.5 0.5 1 2 1.5 1.5 1.5 After 0 0 0.5 0 1 0 0 0 0.5 0 0 0.5 0 0 0 115 Observation, Analysis & Interpretation
    • Figure No. 13 Serum Cholesterol of Group - A 250 200 in mg / dl 150 100 50Patient Sl No0 2 4 6 8 9 12 14 15 20 22 23 25 27 28 30 Before 180 150 232 203 128 140 154 160 160 210 190 188 212 183 168 After 178 150 230 194 128 136 149 154 160 203 187 182 208 181 166 Figure No. 14 Serum Cholestroel of Group - B 450 400 350 300 in mg / dl 250 200 150 100 50 0Patient Sl No 1 3 5 7 10 11 13 16 17 18 19 21 24 26 29 Before 353 346 324 296 340 311 322 311 340 378 409 281 286 406 313 After 350 341 321 292 337 306 320 302 335 374 403 279 285 405 310 116 Observation, Analysis & Interpretation
    • Analysis of the objective parameters (master chart 7 – A and 7 – B, Figure No 7 to 14 ) are given below with the help of statistical calculation and its significance. The calculation is done by using student ‘t’ test and paired ‘t’ test Test of significanceObjectives Group Mean S.D. S.E. P.S.E t -value p-value RemarkFasting Before 209.80 56.549 14.600 Highly A 15.18 6.726 P< 0.001blood sugar After 107.66 16.162 4.1730 significantFasting Before 219.20 80.109 20.684 Highly B 21.16 4.964 P< 0.001blood sugar After 114.13 17.381 4.4879 significantPost partal Before 321.87 95.517 24.662 Highly A 25.12 6.938 P< 0.001blood sugar After 147.53 18.638 4.8125 significantPost partal Before 308.27 103.52 26.730 Highly B 27.87 5.664 P< 0.001blood sugar After 150.40 30.572 7.8938 significantSerum Before 177.53 29.130 7.5200 Not A 10.47 0.3752 P > 0.05Cholesterol After 173.60 28.250 7.2900 significantSerum Before 328.00 39.740 10.260 Not B 14.64 0.3141 P > 0.05Cholesterol After 323.40 40.740 10.450 significantUrine Before 1.2 0.4900 0.1272 Highly A 0.141 7.326 P< 001sugar After 0.16 0.2400 0.0629 significantUrine Before 1.36 0.5400 0.1419 Highly B 0.156 7.419 P< 001sugar After 0.2 0.2500 0.0654 significant The calculation is done by using student ‘t’ test and paired ‘t’test. By observing all the data above and the calculations of theirsignificance we can conclude that the drug is having a very good action onblood glucose levels, as well as on the urine sugar levels. 117 Observation, Analysis & Interpretation
    • f. Result: The over all result of the study included group A and B as shown in the figure no 6 are summersied as below. The total patients taken for the study are 30, 15 in each group. Result No of patients Group A No of patients Group B Relieved 7 3 palliative 7 8 Not responded 1 4 Group B Not responded Group A Relived 13% 23% Group B palliative 28% Group A palliative 23% Group B Relived Group A Not 10% responded 3% 118 Observation, Analysis & Interpretation
    • In the present trial 30 cases were taken for the study. The trialdrug, “Bhumamalakidi churna” had a very good effect on all the patients,not only by regulating their blood glucose levels down but also byrelieving them from the signs and symptoms. Especially all the patientswere satisfied because of reduced frequency of mituration and burningsensation of hands and feet. Even though the combination of trial drug is not mentioned in theclassics of Ayurveda, we have combined it by observing thepathophysiology of the disease and the actions of the individual drugs,viz Madhu nasani as an established hypoglycemic agent, Bhumamalakiand Bhranjraja are good liver correctors as the liver is the main organinvolved in glucose metabolism. Eranda is included in the combinationbecause of its established vata hara effect, as Madhumeha is a vatajaprameha,. After collecting the herbs personally identified by Botanist and,they were processed as the trial drug. One patient (Sl No 1, OPD No 4477 ) approached our PG Hospitalfor chronic (one and half month duration) non healing ulcers, he wasdetected as a diabetic, he was the first patient for our trial, even thoughthe ulcers were big enough (as shown in the photo graph 5 ) we tookbold steps to treat him with our trial drug (without any allopathic drug),When the patient reported at regular intervals of 15 days, the changes inthe ulcers are noted as (photograph 6 ), and after 31 days the ulcer was 118 Conclusion
    • fully disappeared (photograph 7 ). A camp was set up on 25 – 10 – 99 toscreen the patients for the trial. We screened 46 patients and 18patients were selected among them. By the observation of the laboratory reports of the patients we canassume the trial drug “Bhumamalakadi churna” is highly effective onthe NIDDM (Non Insulin Dependent Diabetes Mellitus ) patients. Twopatients other than that of the trial patients who were on insulin therapywere also given the trial drug out of interest to know the effect on theinsulin dependent patients, even these two patients responded well. Thetask for these two patients was difficult and risky so it was done underclose observation and even though the insulin was slowly reduced (2units per day) the blood sugar level were reduced. This trial of these twopatients out of stipulated inclusive criteria has shown significance ofresult. By the assesment of parameters, it is confirmed that the efficacy oftrial drug “Bhumamalakadi churna´is one of the best alternate therapy forthe patients of NIDDM. It has shown remarkable results over the patientswithin 30 days. Prolonged use of the medicine doesn’t have any sideeffects and further at an economical price the palliation is possible. 119 Conclusion
    • This thesis entitled “ EVALUATION OF THE EF FECT OFBHUMYAMALAKYADI CHURN A IN MADHUMEH A (With special reference toits hypoglycemic effect)” is summarised as follows.- Madhumeha is one out of the 20 varieties of Pramehas. It is Vata predominant there by considered under vataja mehas. Madhumeha is a yapya vyadhi.- Its treatment is to be a vatahara, kaphahara, and dusta medohara along with its action over mootravaha srotas.- The present drug selected is having its effect over Vata, kapha and medas. Moreover its pharmacological action is over the liver, in the process of neoglucogenises as a part of glucose metabolism in the body. Secondly it acts over the Vata, specifically pacifying Vata and its involvement in the disease. Hypoglycemic action of “ BHUMYAMALAKYADI CHURNA” is remarkable.- The classical affirmed pathogenesis, as the involvement of medas with its classical signs and symptoms in Madhumeha are stand still even in 21 s t century. The pratyatmaniyata lakshana of Madhumeha are Prabhutamootrata and Avila mootrata along with ashaktata. 120 Summary
    • - The clinical study of the entitled thesis “ EVALUATION OF THE EFFECT OF BHUMYAMALAKYADI CHURN A IN MADHU MEH A (With special reference to its hypoglycemic effect)” have studied over 30 patients in two groups A ) Hyperglycemic and Hypolipidimic B ) Hyperglycemic and Hyperlipidimic.- Observation of the signs and symptoms, sex, age, incidence, and results are explained in tubular and graphic forms.- Results of the treatment were assessed on the bases of differences between the base line data and assessment data . The lab investigation variables were subjected for statistical analysis by applying student ‘t’ test and paired ‘t’ test.- The subjective and objective parameters under statistical viability have shown high significance rate with respect to both groups. In Hyperglycemic and Hypolipidimic group, 46% of the patient are relieved, 46% are in palliative group and only 6% of the patients are not responded. Similarly in Hyperglycemic and Hyperlipidimic group, 20% of the patients are relieved, 53% palliative and 26% are not responded. This data reveals the effect of Bhumyamalakyadi churna highly significant. Not responded dosent mean their blood sugar did not decrease but it was not up to the mark. 121 Summary
    • BIBLIOGRAPHYCharak Samhita PoorvardhaBy Vaidya Satyanaryana Shastri. 1 s t edition 1962Published by Chowkhamba Vidya Bhavan. Varanasi.Charak Samhita UttarardhaBy Vaidya Satyanaryana Shastri. 1 s t edition 1962Published by Chowkhamba Vidya Bhavan. Varanasi.Sushruta Samhita PoorvardhaBy Kaviraja Ambikadutta shastri. 8 t h editionPublished by Chowkhamba Sanskrit Sansthan, Varanasi.Sushruta Samhita UttarardhaBy Kaviraja Ambikadutta shastri. 8 t h editionPublished by Chowkhamba Sanskrit Sansthan, VaranasiAstanga Samgraha of VagbhataBy Prof K.R.Srikantha Murthy. 1 s t edition 1996Published by Chowkhamba Orientalia, Varanasi.Astanga Hridaya with commentaries of Arunadatta and HemadriBy Harisastry paradakar Vaidya, 1939Published by Nirnaya sagar press Bombay.BhavaprakasaBy Sri Brahmasankara Misra. 4 t h edition 1984Published by Chowkhamba Sanskrit Sansthan, Varanasi. Bibliography
    • Madhava Nidana with Madhukosha sanskrit vyakarna. By Acharya Sri Narindranath shastri. 1 s t edition 1989 Published by Motilal Banarasidas, Varnasi. Rajanighantu By Pandit Narahari. 2 n d edition 1998 Published by Krishnadas Academy, Varansai. Bhela Samhita By Girija Dayal Shukla, 1959 Published by Chowkhamba publication, Varnasi. Essentials of Basic Ayurveda Concepts. By Prof Dr. V.V.S.Sastri. 1999 Published by Publication Division, PGARC, DGM Ay Medical College, GadagJoslin’s Diabetes Mellitus.By C. Ronald Kahn. 13 t h edition 1994Published by Lea and Febiger, A Waverly company, London.API Text book of Medicine.By G.S.Sainani 5 t h edition 1992Published by Association of Physicians of India, Bombay.Indian Materia Medicaby K.M.Nadkarni. Vol 1 - 2 2 n d edition 1982Published by Popular Prakashan Bombay Bibliography
    • Indian Medicinal Plants by Kirtikar & Basu Vol 1 - 3 2 n d edition 1975Shareera kriya vijnanam By M. Ramasundar Rao 2 n d edition 1994 Published by M. Madhava, Metro Printers, Vijayawada.Chakradatta By Priyavrat Sharma. 2 n d edition 1998 Published by Chowkhamba Orientalia, Varanasi.Researches in AyurvedaBy Dr. M.S.Baghel. 1 s t edition 1997Published by Mridu Ayruvedic Publication and Sales. Jamnagar.Cunninghama Manual of Pratactical Anatomy Vol 1 to 3Published at Great Britain, Oxford University Press.Dorland’s Pocket Medical Dictionary.By Douglas M. Anderson. 24 t h edition 1989Published by Oxford & IBH publishing Co. Pvt. Ltd. Bombay.Human PhysiologyBy Dr C.C.Chatterjee 11 t h edition 1992Published by Medical Allide Agency. Calcutta.Digestion and Metabolism in Ayurveda,By C.Dwarkanath,Published by Baidyanath Publications, Calcutta. Bibliography
    • Davidsons Principles and Practice of medicine,by John Maclod 1992Published by Pitman press, Great Britain.Gray’s Anatomyby Henry Gray 1973Published by Longman group Ltd.Introduction to Kayachiktsa,by C. Dwarkanath,Published by Chowkamba offest press, Varanasi.Kashyapa Samhita,by Vridha Jeevaka, 1953Published by Chowkhamba Vidya Bhavan. VaranasiPrinciples of Internal Medicineby T.R. Harrison and Co. 1962A Hand book on Endocrine disordersby Natoobhai. J. Shah 2 n d edition 1962published by Unichem Laboratories, Bombay.Review of medical Physiologyby Willam. F. Ganong, 11 t h edition 1983Published by Lange Medical publications, Maruzen.The Ayurveda Encyclopediaby Swami Sada shiva Tirtha. 1 s t edition 1998Published by Indian books centre, Delhi.Your Guide to Health Bibliography
    • By Clifford R. Anderson. 10 t h edition 1999Published by G.S.Robert Clive, Pune.Yogaratnakara with Vaidyaprabha hindi commentaryBy Dr Indradev Tripathi 1st edition 1998Published by krishnadas Academy, Varanasi.Nidana Chikitsa HastamalakaBy Ranajit Roy Desai. 1st edition 1978Published by Baidyanath Ayurveda bhavan, Nagapur.Clinical Methods in AyurvedaBy K.R. Srikantamurthy. 2nd edition 1996Published by Chaukhambha Orientalia, Varanasi.From Fat to FitBy Dr D.R.Gala. 1 s t edition 1998Published by Navneet Publications Ltd, Gujarat.Schafer’s essentials of HistologyBy Schafers 16 t h edition 1954Published by Orient longmans ltd. Bibliography
    • CASE SHEET FOR “MADHUMEHA” POST GRADUATE AND RESEARCH CENTERE,(KAYACHIKITSA) SHRI. D.G.M.AYURVEDIC MEDICAL COLLEGE, GADAG.Guide : Dr.V.V.S.Sastri, Dr Shashidhar.T.Hombal. D.Ay.M.(BHU) M.D. ScholarCo-guide : Dr. Shivarama Prasad Kethamakka. M.A.(Astro),M.D.(Ay)1. Name of the Patient Sl.No.2. Father’s/Husband’s Name OPD No3. Age - Years IPD No4. Sex - M F Bed No5. Religion Hindu Muslim Christian Sikh Date of Schedule initiation Date of Schedule completion6. Occupation - Sedentary Active Labour7. Economical status Poor Middle class Higher middle class Higher class8.Diet - Veg Mixed9. Address Pin10. Selection Included Group A Hyperglycemic & Hypolipidimic Excluded B Hyperglycemic & Hyperlipidimic11. Result Relived Palliative Not responded Discontinued
    • 12. Chief complaints with duration. Duration AfterNo Complaints Treatment < 1 Yr 1Yr 2 Yrs 3 Yrs 4Yrs 5Yrs 1 Prabhoota mootrata 2 Avila mootrata 3 Ashaktata 4 Shareera bhara hani 5 Jangaha mamsa graha 6 Mootra madhuryata13. History of present illness : Disease was detected As accidental In regular check up By suspicion14. Family history Brother Patient. Sister Brother Father Sister Brother Mother Sister Grandfather Grandmother Grandfather Grandmother15. Personal History. a. Ahara Madhura Sheeta Snigdha Guda Dugdha Nava anna Dahi Gramya Guda vikriti Mamsa Audaka Dugdha vikriti Anupa b. Vihara Avyayama Diwaswapna Swapnasukham c. Manishika- Chinta. Yes No16. Samanaya Pareeksha. a. Pulse b. Blood pressure c. Temprature d. Height e. Respitation f. Weight
    • 17. Poorvaroopa. Lakshanas B A Lakshanas B A Dantadeenam Malatvam Trishna Pada daha Maldhikyata in bahya chidra Pani daha Swedadhikya Deha chikkanata Sheeta iccha Shareera durgandha Swasa Mukha madhurta Mutra madhurata Talu kloma shosha Mutra shuklata Kesh jatilata Tandra Nakha vriddhi Nidra Alasya Shitalangata18. Roopa. Lakshanas Before treatment After treatment Prabhoota mootrata Avila mootrata Madhura mootrata19. Sroto Pareeksha A – Udakavaha B - Mootravaha Lakshanas B A Lakshanas B A Jihwa shosha Alpalpa mootrata Talu shosha Mootara rodha Osta shosha Adhika mootra Kloma shosha Sashoola mootra Prawridha pipasa Basti stabdhata C - Mamsavaha D - Medovaha Lakshanas B A Lakshanas B A Arbuda Sweda Arsha Snighanagata Mamsa shosha Sthulashophata Shira granthi Pipasa20. Upashaya / Anupashaya Upashaya Anupashaya Shita iccha Ushna Madhurrahit ahara Madhuara ahara vyayama Diwa swapana
    • 21. Upadravas Lakshanas B A Lakshanas B A Prameha pidika Avipaka Atisara Chardi Jwara Kasa Daha pratishyaya Arochaka Other22. Lab investigations a Urine Test Before After Sugar b. Blood. Test Before After Fasting blood sugar Post partal blood sugar Serum cholesterol Signature of supervisor signature of scholar.
    • WEL COME
    • “Evaluation of the efficacy ofBhumyamalakyadi churna in madhumeha” (with special reference to its hypoglycemic effect)
    • NIRUKTI“ prachuram varamvaram va mehati mootratyagam karotiyasmin roge sa prameha”Madhumeha = Madhu + Meha Madhu = Honey Meha = Urination
    • NIDANAAsya sukham Swapna sukham dadhini gramyodakanuparasa payamsi |Navanna panam gudavaikratam cha prameha hetu kaphakrut survam || Cha Chi 6/4 M.N. 33/1
    • DOSHA DUSHYAKapha sapitta pawanascha doshamedhoassrasukrambhuvasalasika |Majja rasouja pishitum cha dushyapramehinam vimshathireva meha|| Cha Chi 6/8 M.N. 33/41
    • SAMPRAPTIMedascha mamsacha shareerajam cha kledam kaphovastigatam pradushya |Karoti mehan samoodernamusnisthaneva pittam paridushya chapi ||Kshineshu dosheshwavakrushya vasthou dathun pramehananila karoti | Cha Chi 6/5
    • SAMPRAPTI TALIKAFavorable combination of Nidana, Dosha & Dushya. Kapha immediately aggravates.Aggravated kapha spreads all over the body. First mixes with medas.
    • Vitiated kapha with vitiated medas mixes with mamsa and shareera kleda Vitiation of mamsa provides manifestation of putrified carbuncles = pidika.The liquefied dhatus further vitiate and transfer into urine.
    • Prabhoota mutrata & avila mutrata. PRAMEHA
    • PURVA RUPADhanthadinam maladythwam pragrupam panipadhayoho |Daha chikkanatha dehe trut swadyasyam cha jayate || M.N. 33/5
    • LAKSHANASamanyam lakshanam tesham prabootavilamootrata | M.N. 33/6
    • BHEDADoshadushyavisheshapi tatsamyoga visheshatha |Mutravarnadi bhedena bhedo meheshu kalpyate || M.N.33/6
    • KAPHAJA = 10PITTAJA = 06VATAJA = 04TOTAL = 20 Types
    • CHIKITSAMadhunashini (Gymnema sylvestre)Eranda (Ricinus communis Linn.)Bhumyamalaki (Phyllanthus urinaria Linn)Bhringaraj (Eclipta alba)
    • SADYASADHYATASadhya kaphota dasha pittaja shat yapya na sadhya pavanachatuska |Samakriyatwathdwishamakriyathwath mahatyatwacha yathakramam || Chi Chi 6/7.
    • DISSERTATION REPORT Showing the Results 16 14 12 10 ie s u br f a t Nme op t n 8 6 4 2 0Res ult Relived Palliative Not res ponded Total 15 10 5 Group A 7 7 1 Group B 3 8 4
    • Test of significance Objectives Mean S.D. S.E. P.S.E t -value p-value Remark GroupFasting blood A Before 209.80 56.549 14.600 15.18 6.726 P< 0.001 Highlysugar significant After 107.66 16.162 4.1730Fasting blood B Before 219.20 80.109 20.684 21.16 4.964 P< 0.001 Highlysugar significant After 114.13 17.381 4.4879Post partal A Before 321.87 95.517 24.662 25.12 6.938 P< 0.001 Highlyblood sugar significant After 147.53 18.638 4.8125Post partal B Before 308.27 103.52 26.730 27.87 5.664 P< 0.001 Highlyblood sugar significant After 150.40 30.572 7.8938Serum A Before 177.53 29.130 7.5200 10.47 0.3752 P > 0.05 NotCholesterol significant After 173.60 28.250 7.2900Serum B Before 328.00 39.740 10.260 14.64 0.3141 P > 0.05 NotCholesterol significant After 323.40 40.740 10.450Urine A Before 1.2 0.4900 0.1272 0.141 7.326 P< 001 Highlysugar significant After 0.16 0.2400 0.0629Urine B Before 1.36 0.5400 0.1419 0.156 7.419 P< 001 Highlysugar significant After 0.2 0.2500 0.0654
    • RESULTS Group B Not responded Group A RelivedGroup Bpalliative Group A Group B palliative Group A Not Relived responded
    • CONCLUSIONThe trial drug, “Bhumymalakyadi churna” had a very good effect on all the patients, not only by regulating their blood glucose levels but also by relieving them from the signs and symptoms.
    • Thank you