Madhumeha kc007 gdg


Published on


1 Like
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Madhumeha kc007 gdg

  1. 1. 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.
  2. 2. 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
  3. 3. 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
  4. 4. 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
  5. 5. 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
  7. 7. 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
  8. 8. 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
  9. 9. 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
  10. 10. 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
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. 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
  15. 15. “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
  16. 16. 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
  17. 17. 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
  18. 18. 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
  19. 19. 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
  20. 20. - 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
  21. 21. - 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
  22. 22. - 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
  23. 23. - 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
  24. 24. - 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
  25. 25. 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
  26. 26. 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
  27. 27. 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
  28. 28. 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
  29. 29. 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
  30. 30. 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
  31. 31. 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
  32. 32. 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
  33. 33. 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
  34. 34. 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
  35. 35. 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
  36. 36. 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
  37. 37. 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
  38. 38. 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
  39. 39. 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
  40. 40. 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
  41. 41. 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
  42. 42. 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
  43. 43. 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
  44. 44. 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
  45. 45. 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
  46. 46. 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
  47. 47. 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
  48. 48. 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
  49. 49. 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
  50. 50. 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
  51. 51. 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
  52. 52. 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
  53. 53. 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
  54. 54. 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
  55. 55. 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
  56. 56. 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
  57. 57. 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
  58. 58. 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
  59. 59. 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
  60. 60. 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
  61. 61. 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
  62. 62. 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
  63. 63. 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
  64. 64. 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
  65. 65. 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
  66. 66. 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
  67. 67. 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
  68. 68. 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
  69. 69. 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
  70. 70. 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
  71. 71. 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
  72. 72. 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
  73. 73. 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
  74. 74. 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
  75. 75. 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
  76. 76. 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
  77. 77. 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
  78. 78. 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