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A CLINICAL STUDY ON THE EFFECT OF ASANADI KWATHA IN MADHUMEHA ANIL KUMAR G. 2006, S.D.M. COLLEGE OF AYURVEDA, KUTHPADY, UDUPI

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Madhumeha kc010 udp

  1. 1. A CLINICAL STUDY ON THE EFFECT OF ASANADI KWATHA IN MADHUMEHA By ANIL KUMAR G. B. A. M. S. Dissertation submitted to theRajiv Gandhi University of Health Sciences, Karnataka, Bangalore In partial fulfillment Of the requirements for the degree of DOCTOR OF MEDICINE (Ayu) In KAYA CHIKITSA Under the guidance of DR.U.N.PRASAD, M.D. (AYU ) Professor Department of Kaya Chikitsa Co-Guide DR. V. K. SRIDHAR HOLLA M. D. (Ayu) Assistant professor Department of Kaya Chikitsa S.D.M. COLLEGE OF AYURVEDA, KUTHPADY, UDUPI 2006 I
  2. 2. Rajiv Gandhi University of Health Sciences DECLARATION BY THE CANDIDATEI hereby declare that this dissertation / thesis entitled “A clinical study on theeffect of Asnadi kwatha in Madhumeha”is a bonafide and genuine researchwork carried out by me under the guidance of Dr. U.N.Prasad. M.D. (Ayu),Professor, Department of Kaya Chikitsa and co-guidance of Dr. V.K. SridharHolla M.D.(Ayu), Assistant Professor, Department of Kaya Chikitsa.Date: Signature of the candidateUdupi Anil kumar.G II
  3. 3. Rajiv Gandhi University of Health Sciences CERTIFICATE BY THE GUIDEThis is to certify that the dissertation entitled “A clinical study on the effect ofAsnadi kwatha in Madhumeha” is a bonafide research work done by Anilkumar. in partial fulfillment of the requirement for the degree of DOCTOR OFMEDICINE (Ayu)Signature of the co-guide Signature of the GuideDr.V.K.Sridhar Holla, M.D.(Ayu) Dr.U.N.Prasad, M.D(Ayu)Asst.Professor, Dept.Of Kaya Chikitsa Professor, Dept.Of Kaya ChikitsaPlace - UdupiDate: III
  4. 4. Rajiv Gandhi University of Health Sciences ENDORSEMENT BY THE HOD, PRINCIPAL / HEAD OF THE INSTITUTIONThis is to certify that the dissertation entitled “A clinical study on the effect ofAsnadi kwatha in Madhumeha” is a bonafide research work done by Anilkumar.G under the Guidance of Dr.U.N.Prasad. M.D. (Ayu), Professor,Department of Kaya Chikitsa and co-guidance of Dr. V.K. Sridhar Holla.M.D. (Ayu), Assistant Professor, Department of Kaya Chikitsa.Signature of the H.O.D Signature of the PrincipalDr.U.N.Prasad Dr.Bala.Krishna.BhatDate: Date:Udupi Udupi IV
  5. 5. COPYRIGHT Declaration by the candidateI hereby declare that the Rajiv Gandhi University of Health Sciences, Karnatakashall have the rights to preserve, use and disseminate this dissertation / thesis in printor electronic format for academic / research purpose.Date: Signature of the CandidateUdupi: Anil kumar.G © Rajiv Gandhi University of Health Sciences, Karnataka V
  6. 6. DEDICATION I Would Like to Place This Dissertation on the Lotus Feet of My ParentsDate: Signature of the CandidatePlace: Anil kumar.G VI
  7. 7. ACKNOWLEDGEMENTSI am Ever Indebted To Lord Almighty, My Venerated Parents, Respected Teachers And Affectionate Friends VII
  8. 8. ABSTRACTBackground and Objectives: Besides the miraculous achievement of modern medicalscience, humanity is passing through a horror of disease and drug phobia, particularly indeveloping countries like India, where poverty and illiteracy account for the man’signorance towards the principles of healthcare. Symptomatology of Madhumeha isequivalent to the features of Diabetes mellitus in modern medical science. Among theseveral health problems, Diabetes mellitus is a giant disease considered as one of the archenemy of the mankind. Diabetes and its complications pose a major threat to futurepublic health resources throughout the world. Thus it becomes a challenge for ayurvedists to search for an effective treatment.The present study is focused on the literary review & clinical study of the Madhumehaand to evaluate the effect of Asanadi Qwatha in patients of Madhumeha with outalteration in their routine dietary and physical activities.Methods: It is a single blind clinical study with pre and post test design where in 20patients diagnosed as Madhumeha between the age group of 30 – 75 yrs and FBSbetween 120 mg/dl to 180 mg/dl; PPBS level between 160 mg/dl to 300 mg/dl. AndNIDDM patients devoid of other systemic complication were selected. All wereadministered with Asanadi Qwatha for a period of 30 days. The relevant investigationswere adopted for diagnosis and to assess the improvement.Results: Good remission in the symptoms of Madhumeha and significant reduction inFBS, PPBS was recorded. Paired t test also proved the statistically highly significantimprovement in prabuta mutrata, avila mutrata, karapada daha, karapada suptata, trushna,FBS, PPBS. No improvement was observed in Sthoulya.Keyword: Madhumeha, Diabetes mellitus, Asanadi qwatha. VIII
  9. 9. IX
  10. 10. TABLE OF CONTENTS1. Introduction Page No. 1- 42. Objectives Page No. 53. Review of Literature Page No. 6 - 1084. Methodology Page No. 109 - 1135. Observation and Results Page No. 114 - 1336. Discussion Page No. 134 - 1437. Conclusion Page No. 144 - 1458. Summary Page No. 146 - 1509. Bibliographic References Page No. 151 - 16510. Annexure-Profoma IX
  11. 11. LIST OF TABLESS.No. Table No. Content Page No. 1 1 Nidana 20 - 22 2 2 Classification Of DM 43 3 3 Poorva Roopa 47 4 4 Samanya Upadrava 62 5 5 Vishishta Upadravas 62 6 6 Prameha Pidakas 63 7 7 Sapeksha Nidana 66 8 8 Differential Diagnosis 67 9 9 Mutra Laxana In Different Diseases 70 -71 10 10 Pathya in Sthoola Madhumehi 93 11 11 Pathya in Krusha Madhumehi 94 12 12 Apathya Ahara, vihara, vichara 95 13 13 Ingredients of Asanadi Kwatha 97 14 14 Asanadi Kwatha - Rasa panchaka 108 15 15 Age Incidence 117 16 16 Sex incidence 117 17 17 Marital Status 118 18 18 Educational status 118 19 19 Religion Incidence 119 20 20 Socio - Economic Status 119 21 21 Occupational Incidence 120 22 22 Incidence of Addictions 120 23 23 Dietary Habits 121 24 24 Deha Prakruti 121 25 25 Sara incidence 122 26 26 Samhanana 122 27 27 Satva incidence 123 X
  12. 12. 28 28 Rasa Satmyata 12329 29 Status of Agni 12430 30 Bala incidence 12431 31 Family History 12532 32 Effect on Prabuta mutrata 12833 33 Effect on Avila mutrata 12834 34 Effect on Kara pada Daha 12935 35 Effect on Kara pada suptata 12936 36 Effect on Bahuashee 13037 37 Effect on Trishna 13038 38 Effect on Ati Sweda 13139 39 Effect on Daurbalya 13140 40 Effect on Sthoulya 13241 41 Effect on FBS 13242 42 Effect on PPBS 13343 43 Effect on Urine Sugar 133 XI
  13. 13. LIST OF FIGURESSl.No. Graph No. Name of the Graph Page No. 1 1 Age Incidence 117 2 2 Sex incidence 117 3 3 Marital Status 118 4 4 Educational status 119 5 5 Religion Incidence 119 6 6 Socio - Economic Status 120 7 7 Occupational Incidence 120 8 8 Incidence of Addictions 121 9 9 Dietary Habits 121 10 10 Deha Prakruti 122 11 11 Sara incidence 122 12 12 Samhanana 123 13 13 Satva incidence 123 14 14 Rasa Satmyata 124 15 15 Status of Agni 124 16 16 Bala incidence 125 17 17 Family History 125 18 18 Effect on Prabuta mutrata 128 19 19 Effect on Avila mutrata 128 20 20 Effect on Kara pada Daha 129 21 21 Effect on Kara pada suptata 129 22 22 Effect on Bahuashee 130 23 23 Effect on Trishna 130 24 24 Effect on Ati Sweda 131 25 25 Effect on Daurbalya 131 26 26 Effect on Sthoulya 132 27 27 Effect on FBS 132 XII
  14. 14. 28 28 Effect on PPBS 13329 29 Effect on Urine Sugar 133 XIII
  15. 15. Prologue PROLOGUE The present era is full of chaos, stress & strain due to life style modifications,change in dietary habits, urbanization and industrialization. This has lead in the upsurgeof many diseases and one of them is Madhumeha. Though Madhumeha is a diseaseknown since ancient times to the mankind, its upsurge is quiet alarming. On the basis ofits symptomatology Madhumeha can be correlated to the features of Diabetes mellitus.. DM is one of the major killers of the modern world. It is a disorder which is sparingneither the developing nor the developed nations. Irregular food habits, lack of exercise,stress and strain are some causative factors that make an individual more prone todevelop diabetes at an early age. India has been projected by the W.H.O. as the countrywith the fastest growing population of Diabetics. It is estimated that By 2025 the Indiandiabetic population will be 79,441,000. W.H.O. has predicted that the new millenniumpopulation may see an epidemic of Diabetes. The reasons of its fast spread in the urban aswell as in the rural areas are ill understood. Diabetes mellitus is all the more dreadedbecause of its complications in almost every part or rather every cell of the body. The modern management of diabetes inspite of many advances still remainsunsatisfactory. Drug intolerance, hypersensitivity and resistance to insulin, the danger ofacute and chronic complications, the fear of hypoglycemic episodes with Sulfonylureasmakes it all the more important to search out safe, effective and cheaper remedies. Suchremedies could be explored from the huge wealth of Ayurveda which still remainsunexplored on the modern technological advances. 1
  16. 16. ProloguePrevious works on Madhumeha1. A Study on Madhumeha by Dr.B.V.Prasanna –1981-GAMC, Mysore.Trivanga bhasma and Jambu phala Beeja majja choorna was selected for clinicalstudy. 10 patients on drug and diet; 5 patients only on diet. Moderate Results wereobserved in drug and diet group.2. A clinical study on the role of Asana and Guduchi Rasayana in the management ofMadhumeha (DM). – 1999 Dr.Ranjana D. Siddhapathaki GAU, JAMNAGAR.Group I - Asana Kashaya in two divided doses per day prepared from 40 gm ofAsana coarse powder - 2months; Group II – 6 gm Guduchi churna and then samequantity of Asana Kashaya in two divided doses per day – 2 months; Group III –Asana vati 4 gm of drugs in three divided doses per day – 2 months; Asana Kashayashowed better relief.3. Effect of Salasaradi gana basti on Stoolamadhumehi Dr.Kiran.M.Goud – 1999 –GAMC – Mysore. Group A - 17 pts. – Pancha kola churna (10gm/tid)Salasaradi basti therapy 16 days; Cap. Nishaamalaki 32 days with diet & exercise.Group B – 17 pts - pancha kola churna (10gm/tid) cap. Nishaamalaki 32 daysPlacebo. Cap for16 days with diet & exercise. Group A showed better results.4. A clinical study on the effect of Nisha amalaki in Madhumeha – a controlled studyDr. Kishore kumar.R –2002 – S.D.M.C.A, UDUPI.Group I –12 pts - Nishaamalakichoorna (4 gm tid ) along with diet & exercise, before food for 60 days Group II –12 pts - Placebo with diet & exercise Group I showed better results. 2
  17. 17. Prologue 5. A comparative study on the role of Basti Therapy and Pramehaghna drugs in the management of Madhumeha (DM) – 2003 by Dr.Pawar Anand M. – G.A.U, Jamnagar. Group I – Pramehaghna vati to15 patients - 2 gm tid; Group II- Pramehaghna Basti to 8 patients. Total of 16 Basti including Niruha and Anuvasana (Kala Basti) Group III - placebo group - 6 patients were given empty capsules with strict diet pattern. Group I showed better results as compared to group II in the management of DM. More than 200 thesis works were conducted all over India on Madhumeha in the form of shodhana and shamana line of treatment. In shamana chikitsa different formulations have been used so for, in the form of kashaya, vati etc. Asanadi Kwatha is anubhuta yoga which is been prescribing in S.D.M. Ayurveda hospital, Udupi, Karnataka. Since 20 yrs. This being Tikta, Katu, Kashaya Rasa, Katu Vipaka, Laghu, Ruksha & Tikshna Guna pradhana Aushadhi may easily help in the dissociation of Pathogenesis of Madhumeha. They also possess mehagna, medhohara, Rasayana, Deepana and Pachana properties and anti diabetic action. Hence Asanadi Kwatha has been selected for the present study.The present dissertation work entitled “A CLINICAL STUDY ON THE EFFECT OFASANADI KWATHA IN MADHUMEHA” consists of following parts. Conceptual study Clinical study Discussion Summary and conclusion 3
  18. 18. Prologue The conceptual study includes three separate chapters. The historical aspect of thedisease Madhumeha is elaborated in the chapter on historical review. Nidana panchaka aswell as treatment of this disease is made clear in the second chapter. Full account of thecomposition of Asanadi Kwatha is given in the chapter on drug review.The details of the present research work that include material and methods, observation,results and statistical analysis all are methodically presented in chapter entitled clinicalstudy. The critical analysis of the results obtained is the subjective matter of the chapterdiscussion. The conclusion drawn from this clinical study is listed in the final chaptersummary and conclusion. 4
  19. 19. A CLINICAL STUDY TO EVALUATE THE EFFECT OF VAMANA AND SHATYADI CURNA IN PATIENTS OF TAMAKA SHWASA. By MADHUSUDHANAN.I.K., B. A. M. S.Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka in partial fulfillment of the regulations for the award of the degree of DOCTOR OF MEDICINE (AYU) IN KAYA CHIKITSA GUIDE: DR.G. SRINIVASA ACHARYA., M.D. (AYU) Asst. Professor, S. D. M. C. A., Udupi CO-GUIDE DR.SHRILATHA KAMATH.T., M.D. (AYU) Lecturer , S. D. M. C. A., Udupi. DEPARTMENT OF POST GRADUATE STUDIES IN KAYACIKITSA S. D. M. COLLEGE OF AYURVEDA, UDUPI – 574 118 2005 - 2006 I
  20. 20. Rajiv Gandhi University of Health Sciences DECLARATION BY THE CANDIDATEI hereby declare that this dissertation entitled “Clinical study to evaluate the effect ofVamana and Shatyadi Curna in patients of Tamaka Shwasa” is an above-boardresearch work carried by me under the guidance of Dr.G.Shrinivasa Acharya., M.D.(Ayu) and co-guidance of Dr.Shrilatha Kamath.T., M.D. (Ayu). MADHUSUDHANAN.I.K. B.A.M.S.Date:Place: Udupi. II
  21. 21. Rajiv Gandhi University of Health Sciences CERTIFICATE BY THE GUIDEThis is to certify that the dissertation entitled “A Clinical study to evaluate the effect ofVamana and Shatyadi Curna in patients of Tamaka Shwasa” is an above-boardresearch work done by Madhusudhanan.I.K in partial fulfillment of the requirement forthe degree of M.D. (Ayu). Signature of the Guide: DR.G. SRINIVASA ACHARYA., M.D. (AYU) Assistant Professor, S. D. M. C. A., Udupi. Signature of the Co-Guide:Date: DR.SHRILATHA KAMATH.T.M.D. (AYU)Place: Udupi. Lecturer, S. D. M. C. A., Udupi. DEPARTMENT OF POST GRADUATE STUDIES IN KAYACIKITSA III
  22. 22. Rajiv Gandhi University of Health Sciences ENDORSEMENT BY THE HOD, PRINCIPAL / HEAD OF THE INSTITUTIONThis is to certify that the dissertation entitled “A Clinical study to evaluate the effect ofVamana and Shatyadi Curna in patients of Tamaka Shwasa” is an above-boardresearch work done by Madhusudhanan.I.K, under the guidance of Dr.G.ShrinivasaAcharya., M.D., (Ayu) and co-guidance of Dr.Shrilatha Kamath.T., M.D. (Ayu). Signature of the H.O.D. Signature of the Principal Dr. U. N. Prasad, M.D. (Ayu) Dr.K.Balakrishna Bhat., B.S.A.M Professor and H.O. D., PRINCIPALDepartment of P.G Studies in Kayachikitsa. S. D. M.C.A, S.D.M.C.A, UDUPI.S. D. M.C.A, S.D.M.C.A, UDUPI.Date:Place: Udupi. IV
  23. 23. COPYRIGHT Declaration by the candidate I here by declare that the Rajiv Gandhi University of Health Sciences, Karnataka shallhave the rights to preserve, use and disseminate this dissertation / thesis in print orelectronic format for academic / research purpose. MADHUSUDHANAN.I.K B.A.M.SDate:Place: Udupi. © Rajiv Gandhi University of Health Sciences, Karnataka V
  24. 24. Review of Literature History HISTORY Study of sequential evolution is prime step in the research field. Study of historyis important to know about the systematic development and progress of the subject todetermine the future plans for further establishment and research designing. History ofMedicine starts from the very moment when the human being came into existence that iswhy the ancient treatise is full with description of diseases and their treatment. Here thepresent review related to Madhumeha is explained. The evolution of Madhumeha can be traced from Vedas but in rudimentary form,when we go through the Atharva Veda there is a reference related to the disease Asravaalong with its management. Sayanacharya opined that Asrava means Mutraatisara theEnglish translator Whitney (1962) interpreted it as flux and Griffith (1962) as morbidflow, while layman has translated the meaning of Asrava as Diabetes Mellitus.Sayanacharya highlighted the vatic nature of this ailment.(A) Samhita Period: Explorative description of disease Madhumeha occurs atSamhita period.(1) Charaka Samhita: In this ancient treatise of medical science, Charaka explainedthe etiology, pathogenesis, symptomatology, complications and treatment Modalities indetail in Nidana 4th and Chikitsa 6th chapter. While in Sutrasthana 17th chapter hedescribed the Avaranajanya pathogenesis of Madhumeha, this is the unique contributionof this treatise.(2) Susruta Samhita: Susruta also explained the Madhumeha in elaborative mannerwith separate chapter on its management. He used Kshaudrameha synonym toMadhumeha in Nidana 6th chapter. He typically mentioned the kashayas according to 6
  25. 25. Review of Literature Historyeach type of Prameha and mentioned the body constitution and symptoms related toSahaja and Apathyanimittaja Prameha.(3) Astanga Hrudaya: Detail description about the disease is given as in Charakaand Sushrutha samhitas with slight moderations. He added some new herbs and herbalcompounds as well as rasa aushadis for the treatment.(4) Harita Samhita: Harita mentioned it as Papajanya and enumerated 13 types ofPrameha with nomenclature different than above treatise like, Puyameha, Ghritameha etc.(5) Bhela Samhita: He described Prameha is of two types i.e. Svakrita andParakritameha.(6) Kashyapa Samhita: He mentioned the symptoms of Pramehi child inVedanadhyaya and noted the disease as Chirakari.(B) Medieval Period: In this period commentaries mainly written, but most of themcontains only the collection of thoughts from previous authors.(1) Madhava Nidana: He collectively repeated the description of Charaka, Susrutaand Vagbhata in 33rd chapter.(2) Gayadasa: Explained the Avilamutrata because of the presence of Doosya in it.(3) Sharangadhara Samhita: Only mentioned the 20 types of Prameha in PrathamaKhanda 7th chapter.(4) Bhavaprakasa: He described Prameha and Madhumeha along with some newherbomineral preparations in Madyama khanda 38th chapter.(5) Yogaratnakara: Explained Prameha and Madhumeha along with treatment. 7
  26. 26. Review of Literature HistorySome of inventive landmarks about the DM:(1) Areatus (Christian era): Firstly he mentioned the disease as diabetes.(2) William Cullen (1709 AD): Added suffix mellitus to the diabetes.(3) Mathew Dobson (1775 AD): He found that sweetness of urine is due to sugar.(4) Thomas Cowley (1781 AD): He suggested that pancreas may be the cause of diabetes.(5) Poul Langarhans (1869 AD): Name itself suggests that he described the group of cells in pancreas.(6) Gusteve Edouard Laguosse (1893 AD): Named after Langerhans as islets of langerhans(7) Opie (1901 AD): He put forth the hypothesis that, diabetes is due to alteration in the islets of langerhans.(8) FG Babting and Charles best (1922 AD): Discovered insulin. 8
  27. 27. Review of Literature Nirukti and Paribhasha NIRUKTI AND PARIBHASHAI. Nirukti: Madhumeha is a compound word made up of Madhu and Meha.Madhu: The word madhu is derived from the root ‘mana’ and the meaning as ‘manaavabhodane’ i.e. which brings gratification to the mind1.Meha: Meha is derived from the root ‘Miha’, which is employed in the sense of Sinchana(to moisten), Ksharana (to flow) Prasrava (to flow excessively).Prameha: is derived from Pra + Miha. A condition characterized by excessive outflowand a condition where there is excess urine flow.II. Paribhasha: Madhumeha is a Mootradosha2, characterized by Bahumootrata, whichresembles Madhu in Rasa or Varna.III. Paryaya: Prameha: Means Prakarshena mehati – excessive urine out flow3Meha: Is referred to as Prameha by Amara4.Mootradosha: A urinary disorder.Bahumootrata: A disease where there is excessive urination.Madhumeha: A condition characterized by excess urination, resembling honey either incolour or taste. This word has been used synonymously with Prameha.Kshoudrameha: Kshoudra is a synonym of Madhu.Ojomeha: Ojas is considered as Tejas or essence of all Dhatus, which is a casualty inMadhumeha hence Ojomeha has been used by Charaka to describe this disease.Paushpameha: Narrated in Anjana Nidana. Paushparasa is again resembles with Madhu.From above synonyms, we can postulate that unanimously all Acharyas mentioned theurine culture concordant with Madhu. 9
  28. 28. Review of Literature Nirukti and Paribhasha Diabetes MellitusDefinition5: The W.H.O. expert committee on Diabetes mellitus (DM) in its secondreport has defined DM as a chronic disease caused by inherited and/or acquireddeficiency in production of insulin by the pancreas, or by the ineffectiveness of theinsulin produced. Such a deficiency results in increased concentrations of glucose in theblood, which in turn damage many of the bodys systems, in particular the blood vesselsand nerves. Sir. William Osler in his book The Principles & Practice of medicinepublished in 1923, defined DM as a disorder primarily of carbohydrate & secondarily offat & protein metabolism due to the failure of the system to burn sugar and dependent onthe deficiency or absence of internal secretion of pancreas resulting from functional ororganic disease of islet cells of Langerhans. This definition is held valid to this day. 10
  29. 29. Review of Literature Nidana NIDANA Knowledge of Etiological factors and their role in the pathology is very muchnecessary to find out the vitiated constituents like dosha, dushya, mala, progression of thedisease and their role in diagnosis and prognosis. Nidana has been classified under various headings with different views. Amongthem, one classification is bahya hetu and abhyantara hetu. Bahya hetu is an extrinsiccause to the shareera to cause a vyadhi and this includes ahara, vihara, achara,vichara,kala etc,. Abhyantara hetu is an intrinsic cause and this mainly comprises thedoshas.Bahya hetus of Madhumeha is the discussion of this chapter and abhyantara hetuwill be discussed in the samprapti chapter. For the convenience of the study, the bahya hetus are being classified intosamanya and vishesha hetu. Specific nidanas are explained for Madhumeha only bycharaka. The samanya nidanas of Prameha and vataja Prameha nidanas are attributed toMadhumeha, as Madhumeha is one of the types of Prameha and vataja Prameha.Samanya Nidana The key word in Samanya nidana of Prameha is the Hetu, which causes Kaphavriddhi (Kapha kriccha sarvam)6. It becomes contextual here to take note of the fact thatKapha is the main dosha involved in Prameha and hence all those Hetu that cause Kaphavriddhi automatically become the Hetu for Prameha7. The samanya nidana can again beclassified into A). Ahara Sambandha, B).Vihara Sambandha.A). Ahara8: Any Ahara which is Madhura and Lavana rasa pradhana, Guru, Manda,Sheeta, Snigdha, Shlakshna, Sandra, Sthira, Picchila guna pradhana, Madhura vipaka andSheeta veerya, including unboiled, unroasted, unfried food articles and Anoopa mamsa, if 11
  30. 30. Review of Literature Nidanataken in excess quantity increases Kapha which attains ‘Aparipakwa Avastha’ and mainlyeffects the Medas and Kleda leading to Madhumeha due to Avarana.B).Vihara9,10: 1. Atinidra: it aggravates kapha and tamasa guna and results in accumulation of medas. 2. Asya atisukha: Excessive Asya sukha and Swapna sukha causes Snigdhata leading to Kapha vriddhi 3. Divaswapna: Causes inertia in the body and the accumulation of Prithvi and Ap mahabhoota, leading to aggravation of Kapha. 4 Vyayama varjana: A man is generally supposed to balance between the nutrient intake and energy spending to maintain equilibrium. When this balance is not maintained, it results in accumulation of Medas and Kapha. Hence adequate amount of Vyayama is necessary to avoid Prameha. 5. Alasya: It is nothing but the state of lethargy of mind where a man is unable to carry out or undertake any enthusiastic task not because he is incapacitated due to ill health but only because he is unwilling to do it. This results in inactivity causing excessive nourishment. This mainly because of kapha and medha. 6. Chinta tyaga: An attribute of the mind that is antagonistic to Kapha and Medas. When a person becomes free from Chinta, he starts accumulating excess Kapha and Medas. 7. Samshodhana varjana: Samshodhana therapy is essential in any individual for cleansing the body. Being a form of Langhana, Samshodhana causes Medas and Kapha kshaya. If this is not resorted, it causes accumulation of Kapha and Medas. 12
  31. 31. Review of Literature Nidana 8. Mruja varjana: Mruja is udvarthana and its varjana leads to Kapha and medha dushti.Vishesha Nidana: Though the Kapha is the Arambhaka dosha in the Samprapti ofMadhumeha, Pitta and Vata play an important role in complicating the disease. For e.g. ifan affected person starts indulging in Pittakara ahara vihara then 6 types of Pittaja mehamanifest. Similarly when Kapha and Pitta are in Ksheenavastha, the Vata causes 4 typesof Vataja Prameha.1. Kaphaja Prameha nidana: Are the same as explained in Samanya nidana becausekapha is dosha vishesha in Prameha but it should be in bahu drava.2. Pittaja Prameha nidana11:Ahara Sambandhi: 1. Ushna guna ahara atisevana 2. Amla rasa ahara atisevana 3.Lavana rasa ahara atisevana 4. Katu rasa ahara atisevana 5. Ahara sevana in spite ofAjeerna. 6. Vishama ahara sevana.Vihara Sambandhi: 1. Ati atapa sevana, 2. Ati santapa, 3. Shrama, 4. Krodha.3. Vataja Prameha Nidana: The causes for aggravation of Vata can be mainly groupedinto two categories 1. Margavarana12 2. Dhatu kshaya13 The Margavarana is a result of accumulation of Kapha or Pitta dosha in the Vatavahasrotas due to the respective Nidana sevana, this leads to Vataja Prameha. In Prameha,Dhatu kshaya is an invariable consequence of Aparipakvata of Dhatu. This leads toaggravation of Vata causing Vataja Prameha. Apart from this pathological classificationof Vataja nidana14, the following factors are also responsible for aggravation of Vata.A. Ahara Sambandhi: 1. Katurasa ahara atisevana, 2. Kashaya rasa atisevana, 3. Tiktarasa ahara atisevana, 4. Laghu and rooksha guna ahara atisevana. 13
  32. 32. Review of Literature Nidana B. Vihara Sambandhi: 1.Vyavaya atiyoga, 2.Vyayama atiyoga, 3.Vamana atiyoga, 4. Virechana atiyoga, 5. Asthapanaatiyoga, 6. Vega sandharana, 7. Anashana, 8. Abhighata, 9. Atapa sevana, 10.Udwega, 11.Shoka, 12.Shonita ati sechana, 13.Ratri jagarana, 14.Vishama shareera nyasa. All these factors are basically designed to provoke the Rajasika guna in the body. Vata that is predominantly Rajasika gets aggravated leading to Vataja pramehas.Sahaja (Hereditary): Sushruta mentioned the Sahaja word showing genetic predisposition in thepathophysiology of the disease Madhumeha. He narrated two causative factors there i.e.patient is eating dry and less food and is always want to wonder (unstable)15. Charaka, while describing the prognosis of Madhumeha Clearly noted that this isKulaja Vikara resulting due to defect in the Beeja. Chakrapani opines that it can cause byFather, Mother or grand parents, it means the disease inherited from generation togeneration16. Charaka narrated that Sahaja type of diseases can occur due to defect inbeeja, beejabhaga or beejabhaga avayava. We can correlate beeja to ovum and sperm,beejabhaga to chromosomes and beejabhagavayava to genetic coding17.Chakrapanicommented that this defect is because of the indulgence of faulty foods at the time ofpregnancy. Caraka narrated that indulgence of Madhura rasa by mother at the time ofpregnancy causes Madhumeha and Sthaulya18. Thus genetical predisposition and the over indulgence of etiological factors at thetime of pregnancy by mother helps to precipitate the disease Madhumeha, but theimportant thing is genetic predisposition. 14
  33. 33. Review of Literature NidanaAETIOLOGY19,20,21Genetics: The mechanism of inheritance of DM either insulin dependent or non-insulindependent is unclear. The genetic predisposition is probably permissive and not casual.Genetic susceptibility in IDDM: This probably involves more than one gene. Candidateloci have been proposed on chromosomes 2, 6, 11, & 15 though primary genetic site inhumans is believed to be located in the major histocompatibility locus on the short arm ofthe 6th chromosome. While definite associations exist between class I alleles & type 1DM, the D locus is considered of primary importance (A, B, C & D are the four loci ofHLA human leucocyte antigen) encoded by the MHC (Major HistocompatibilityComplex) found to be closely associated with IDDM]Genetic Susceptibility in NIDDM: Modes of inheritance of NIDDM in variant calledmaturity onset DM of the young (MODY) have been more or less conclusive than theother forms. It is highly likely that ordinary NIDDM is polygenic. Genetic influence ispowerful. Since the concordance rate for DM in monozygotic twins with type 2 diseasemay be as high as 80%, risk to offspring and siblings of patients with NIDDM are higherthan in type I DM. Nearly 4/10ths of siblings and 1/3rd of offsprings eventually developabnormal glucose tolerance or frank DM.Autoimmunity: The basic pathology of DM spins around one factor i.e. insulin and itssource of production viz. islet β cells. Complete or partial destruction of islet β cells orperipheral resistance of insulin is causal of DM, but an autoimmune process destroyingthe islet β cells is nevertheless Insulin dependent. The autoimmune destruction of the βcells may be best explained by the existence of a β cell specific protein that for unknownreasons acquires auto-antigenic properties and eventually becomes target for autoimmune 15
  34. 34. Review of Literature Nidanareaction. Gradual β cell loss becomes clinically manifest only when β cell mass isreduced to a critical part after which metabolic compensation is not possible.Heredity: The mechanism of inheritance of IDDM is unclear. At various times,transmission has been postulated to be autosomal dominant, autosomal recessive andmixed. While IDDM occurs with increased frequency in some families, familialaggregation is uncommon. So, deduction of mechanism of inheritance is difficult.Analysis of pedigrees shows a low prevalence of direct vertical transmission. The chanceof a child developing type 1 DM when another first-degree relative has the disease is only5-10%. HLA identity in a sibling increases the risk. The presence of NIDDM in a parentincreases the risk for IDDM in the offspring. It is not known whether the intermixing ofIDDM and NIDDM in the same family represents operation of a single genetic trait orwhether two common genetic predispositions coexist in a family by chance. While thelow rate of transmission of IDDM makes it difficult to discern the mechanisms ofinheritance through study of families, they are reassuring to diabetics who wish to havechildren. The risk of type 1 DM is up to five times higher when the father has the diseasethan when the mother is a diabetic.Environmental factors:Viral Infections: As noted earlier, the fact that a significant proportion of monozygotictwins remain discordant for IDDM suggests that non-genetic factors are required for thedevelopment of DM. An environmental factor in many cases is believed to be a viralinfection of a β cell. A viral etiology was originally suggested by seasonal variations inthe onset of the disease and by what appeared to be more than a chance relationshipbetween the appearance of DM, preceding episodes of mumps, hepatitis, infections, 16
  35. 35. Review of Literature Nidanamononucleosis and coxakie virus infections. The isolation of coxakievirus B4 frompancreas of a previously healthy boy who died after an episode of ketoacidosis andinduction of DM in animals inoculated with isolated virus also suggested a viral etiology.Further support for viral theory comes from the observation, that about 1/5th ofindividuals with congenital rubella develop DM. Despite its attractiveness, the viraltheory should be treated with considerable caution. Serological studies seeking evidenceof recent viral infection in patients with new onset IDDM are inconclusive at best.Bovine albumin: It has been suggested that exposure to cow’s milk or milk products earlyin life predisposes to autoimmune DM. In an initial study, diabetic subjects were found tohave attributes to bovine albumin. Exposure to cow’s milk is presumed to induce animmune response to 17-amino acid fragment in some infants and cross reactivity of theantibody. This hypothesis has not received wide support.Obesity: Type 2 DM is almost non-existent in individuals with a body mass index below22 Kg/m2 and increased risk of DM with obesity has a strong familial tendency. Whenone or both parents are diabetic, 100% offspring’s will develop DM, if they becomesufficiently obese. If neither parent has DM, less than 20% of obese offspring developDM.Life Style: Epidemiological studies of type 2 DM provide evidence that over eating,especially when combined with obesity and under activity is associated with developmentof type 2 DM.Malnutrition: It is proposed that malnutrition in utero and in infancy may damage β celldevelopment at a critical period predisposed to type 2 DM at a later stage. Impaired β cell 17
  36. 36. Review of Literature Nidanafunction and peripheral insulin resistance have been major factors involved in NIDDM.Pregnancy also induces NIDDM in genetically susceptible individuals.Causes of secondary DMa) Secondary to Pancreatic disease: Congenital Pancreatic Aplasia, Acute and ChronicPancreatitis, Pancreatic Carcinoma, Cystic fibrosis & Haemochromotosis.b) Secondary to Endocrine Disorders: Hormones with an insulin antagonistic affect suchas, Growth hormone, glucocorticoids, catecholamines, thyromine and glucagon causeimpaired glucose tolerance or even overt DM when produced in excess as a result oftumor or hyperplasia of the respective gland of origin. Endocrine syndromes frequentlyassociated with carbohydrate abnormalities of variable intensity are Acromegaly,Cushing’s syndrome, Phaeochromocytoma, Glucogonoma, Hyperthyroidism, Conssyndrome and Carcinoid syndrome.Chemically induced DM: Two groups of drugs causing permanent or transienthyperglycaemia can be distinguished. 1) Substances with cytotoxic effect on β cells and2) Substances inhibiting insulin secretion without β cell destruction. The first groupincludes Alloxan, Glyoxal Streptozotocin, Oxine dithiazone and recently Asparaginase,Pentamidine Esthionate, N-3-Phyridyl methyl N- p- mitro ethyl urea (PNU). The secondgroup includes Diazoxide, Diphenyldydation Cyproheptadine and Manaoheptolose.Majority of these drugs have been used only experimentally in laboratory animals.Rare causes of DM: Numerous rare genetic syndromes (Lipoatrophic DM,Leperchaunism, Acanthosis Nigricans types A & B, Ataxia Telangiectasia, Stiff mansyndrome, Bardet Biedl syndrome) may be associated with either glucose tolerance orovert DM. Special islet lesions have not been described in any of these syndromes, there 18
  37. 37. Review of Literature Nidanais an absolute or relative insulin deficiency in such diseases. The high coincidence ofcirrhosis and DM is long established (Naunyn’s DM). This may be due to reduced insulindegradation by cirrhotic liver with subsequent hyperinsulinism and insulin resistance.a) Pituitary DM: The growth hormone of the pituitary appears to have diabetogenicpower (Houssay). Administration of hormone leads to atrophic changes in the β cellsassociated with an early reversible phase of DM, followed by an irreversible phase withcomplete destruction of β cells. DM may be associated with Acromegaly.Hypophysectomy will arrest the course of DM in the experimental animal.b) Adrenal DM: There is convincing evidence that Adrenal cortical hormones may affectboth the experimental and human disease. Adrenalectomy will arrest or modify theprogress of experimental DM. Adrenal hyperplasia or tumors may be associated withDM. The administration of hydrocortisone causes DM by inhibiting insulin action.c) Gestational DM: During normal pregnancy, insulin sensitivity is reduced through theaction of placental hormones and this affects glucose tolerance. The term gestational DMrefers to hyperglycaemia occurring for the first time during pregnancy. Repeatedpregnancy increases the risk of developing permanent DM especially in obese women. 19
  38. 38. Review of Literature Nidana Table No. 1: Nidana and Guna KarmaNidana Predominant of Rasa, Guna, Veerya, Vitatiates Vipaka01) Guruguna ahara Prithvi,Ap Madhura rasa Kapha, Medas02) Snigdhaguna ahara Prithvi, Ap Kleda03) Dravaguna ahara Ap Kapha & Kleda04) Picchilaguna ahara Prithvi, ap Kapha & Kleda05) Sheetaguna ahara ap Udaka & vata with dravaguna06) Madhura rasa ahara Snigdha, Guru, Kapha, Rasa, Rakta, Sheeta veerya, Mamsa, Medas, Madhura vipaka Majja, Shukra and Ojas07) Lavana rasa ahara Kleda, Kapha vilayanaMilk & its products08) Goksheera Kapha & Medas09) Mahisha ksheera Atisneha, Atinidra, Kapha & Medas Mandagni10) Avika ksheera Abhishyandi Pitta and Kapha11) Dadhi Kapha & Medas12) Godadhi Kapha & Medas13) Mahisha dadhi Kapha & Medas14) Avika dadhi More abhishyandi Kapha & Medas15) Mandaka Mootrala TridoshaGhrita16) Goghrita Kapha & Medas17) Mahisha ghrita Kapha & Medas18) Piyusha, Morata, Kapha Kilata Sugarcane and its products Kapha19) Ikshu Madhura rasa Kapha Sheeta veerya Snigdha and sara Guna and vidhahi20) Phanita Guruguna Guru in guna Tridosha abhishyandi21) Guda Kshara, Madhura Kapha & Medas in rasa, Snigdha, Sheeta in guna and veerya22) Matsyandika, Snigdha, Guru Kapha & Medas Khanda sharkara guna, Madhura rasa vimalajatha23) Madhusharkara Rooksha guna, Liquifies Kapha dosha (Crystals of honey) Kashaya, Madhura rasa, Chedini in action, - Madhura vipakaVegetables (shaka)01) Trapusha (Cuccumis sativas) Guru guna Kapha, Medas 20
  39. 39. Review of Literature Nidana02) Irvaruka (Cuccumis memordika) Madhura rasa Kapha, Medas Sheeta veerya03) Keluta Vishada in guna Kapha, Medas &04) Kadamba (Adina cardifolia) Sheeta veerya mootra05) Nadi Masha Abhishyandi06) Induka07) Tarata08) Shrungataka (Trapabis spinosa) Guru guna, Kapha & Medas09) Shaluka (Nymphase lotus) Sheeta veerya10) Krounchadana (A water tuber) and Vishtambhi11) Kasheruka (Scripus crossus) in nature12) Ankoladya (Root of sweet lotus)13) Kamuda (Nymphae lotus) Sheeta veerya Kapha & Vayu14) Utpala, nala, phala and pushpa Madhura kashaya in (A blue lotus) rasa15) Pushkara beeja shaka (Nymphase stellata)16) Vidarikanda (Convolvulus paniculatus) Madhura rasa Mootra & Kapha sheeta veerya, balya and mootrala in action17) Upodika (Basella cordifollia) Madhura rasa & Kapha Vipaka, Snigdha in guna, Sheeta veerya18) Chatraka Sheeta veerya, Kapha Madhura rasa, Guru guna19) Phalanki (Spinacia alleracea) Guru, sara, pichilla, Kapha guna, sheeta veerya20) Ardraka Tikta, Madhura in Mootrala rasa, Mootrala in action21) Palandu (Alium cepa) Snigdha guna, Kapha Madhura rasa & vipaka, guru pichilla in action22) Tanduliyaka (prickly Amaranth) Sheeta veerya, Kapha Madhura rasa and vipaka23) Munjataka Snigdha, Sheeta, Kapha & Medas Guru guna, Madhura rasa, Brimhana in action24) Kooshmanda (pumpkin) Madhura rasa and Kapha25) Tumba vipaka,26) Kalinja Vishtambana and27) Karkaru (Cucumis utilismen) Abhishyandi in28) Tindisha (A kind of cucumber) action29) Chanaka (Pancium miliaceum)30) Chirbhata (Cucumis memordica)31) Hayanaka (A red variety of rice) Madhura rasa, Guru, Kapha & Mootra32) Yavaka (Hordeum vulgare) Snigdha guna33) Uddalaka (Phaseolus aconitifolium) Snigdha, Guru guna, Kapha & Medas Madhura rasa, Balya 21
  40. 40. Review of Literature Nidana34) Vreehi Madhura rasa, Guru Mootrala guna35) Tila (Sesamum indicum) Snigdha guna, Kapha Madhura rasaKrutanna Varga1) Vilepi (variety of Prepared with Mamsa and Shaka is Amla Kapha & Medas cooked food) in Vipaka2) Krushara Kapha and Pitta3) Payasa (Food like Guruguna, Vishtambhi, Balya in action Kapha & Medas rice, wheat boiled with milk and sugar)4) Palala (Tila churna Kapha preparation)5) Pishtanna Abhishyandi Kapha abhishyandiMadhya Dravaguna and Agni bhoota DravagunaGramya, Anoopa and Audaka mamsaAnoopa1) Koolachara (living eg. Gaja, Gavaya, Madhura rasa and Mootrala & at river side) Mahisha etc. vipaka, Sheeta, Kapha vardhana veerya, Snigdha guna2) Plava (Birds eg. Hamsa, sarasa Sheeta veerya, Mootrala which swim) Krouncha etc. guna, Madhura rasa and vipaka3) Koshastha (Live eg. Shanka, Shukti Madhura rasa and Shleshma vardhana In burrows) Shambooka etc. vipaka, Sheeta veerya Snigdha guna4) Padina (which eg. Koorma, Balya Mootrala have limbs) Khumbeera, Shishumora etc.5) Matsyaa) Nadeya (Fishes Madhura rasa, Guru Shleshma of river) and Snigdha gunab) Samudra (Fishes eg. Timingala Guru, Snigdha, Ushna Shleshma of sea) Kulisha etc. guna, Madhura rasa and vipakaVihara1) Nidra atisukha Increases Tamoguna Shleshma vardhana2) Asya atisukha Increases Tamoguna Shleshma vardhana3) Diwa swapna Increases Tamoguna Shleshma vardhana4) Tyakta chinta Kapha and Medas5) Mruja varjana Inactiveness, laziness Kapha and Medas6) Tyakta vyayama Increases Agnimandya, Shareera gourava Kapha and Medas7) Alasya prasakta Kapha8) Failure to perform Tridosha Samshodhana therapy 22
  41. 41. Review of Literature Samprapti SAMPRAPTI Samprapti is defined as the description of the evolution of the disease insequential order, commencing with dosha vaishamya till the disease manifest fully22. Itincludes the vaishamya of dosha, dushya, agni, srotas. Knowledge of this is very helpfulto the physician both for correct diagnosis of the disease and also for deciding theappropriate treatment. According to Sushruta, too much indulgence in the etiological factors related toPrameha results into Aparipakva Vata, Pitta, Kapha and Meda, which further proceedthrough the Mutravaha Srotas to get localized in the Basti Mukha and thus leading todisease Prameha23. Sushruta has stated that, all the Prameha if left untreated or treatedimproperly get terminated into Madhumeha24 Vagbhata described two types of pathogenesis of Madhumeha i.e.Dahtukshayatmaka and Dosha Avaranatmaka. Further, Vagbhata25 interpreted that in alltypes of Prameha, the Dosha and Dushya remain same but still the difference in MutraPravritti is due to specific type of Samyoga between specific Dosha and AnukulaDushya26. Charaka has explained the pathogenesis in a detailed manner i.e. SamanyaSamprapti of Madhumeha and vishesha Samprapti of Madhumeha.Samanya Samprapti of Madhumeha27: Charaka has explained Samanya Samprapti of Madhumeha elaborately. It may beexplained on the basis of Shat kriyakala. The Samanya Samprapti process commencesfrom the Nidana Sevana. 23
  42. 42. Review of Literature Samprapti1. Sanchaya: The excessive indulgence in Nidana Sevana of Guru, Snigdhadi Ahara andAvyayamadi Vihara leads to Kapha Dosha Sanchaya. It is important to mention that theKapha Dosha, which gets Sanchita here is having the quality of Bahudravatva, vividlysupported by Charaka28. Due to Nidana Sevana the kapha dosha gets Bahudravatva.2. Prakopa: The three factors i.e. Nidana, Dosha and Dushya get combined together insuch a precise way that they lead to Prakopa of Bahudrava Kapha rapidly andMadhumeha in future.In the first two stages the Anukulatva between Nidana and Dosha ensues. KaphakaraAhara Vihara vitiates Kapha Dosha without any resistance due to similar properties.The Bahudrava Kapha is prone to develop Madhumeha and as it is already present inexcess quantity from the beginning, hence it gets aggravated rapidly when the AnukulaNidana are continued. This type of Anukulatva may be seen in person having KaphajaPrakriti and who are having genetic predisposition for Prameha.3. Prasara: In this stage, the provoked Kapha gets spread all over the body owing toSharira Shaithilya. Sharira Shaithilya being one of the Anukula factors for Nidanatowards the Dosha.4. Sthana Sanshraya: Vikrita Kapha has affinity towards Bahu-Abaddha Meda due totheir similar properties and gets lodged there. Vikrita Kapha after combining with Bahu-Abaddha Meda causes its vitiation; the other important Dushya are Sharira Kleda andMamsa, which are already increased in large quantity, prior to vitiation of Kapha. Theprovoked Kapha with vitiated Meda gets combined with Sharira Kleda or Mamsa or both. 24
  43. 43. Review of Literature SampraptiThis is an important stage because the prodromal symptoms of the disease are manifestedin this stage. It is essential to diagnose the disease at this stage to prevent further progressof the disease for better prognosis.5. Vyakta: In this stage, two types of manifestation will occur:1. Puti Mamsa Pidika due to Mamsa Dhatu vitiation – The vitiated Kapha and Medacombines with Mamsa Dhatu leading to Puti Mamsa pidika.2. Mutravaha Srotodushti due to Sharira Kleda Dushti – If vitiated Kapha and Medacome in contact with Sharira Kleda, then it changes in Mutra, the vitiated Kapha impedesthe openings of Mutravaha Srotas, which are already filled with vitiated Meda and Kleda,thus producing the disease Madhumeha.The above two manifestations of Kleda and Mamsa Dushti will occur simultaneously orin two stages.6. Bheda: In this stage various complications of the disease manifest and the diseaseprogresses towards Asadhyata i.e. the disease becomes incurable. The Madhumehaattains Sthairya (stability) and Asadhya (incurability) status because of its Prakriti andVikriti. Here Chakrapani has explained the term Prakriti and Vikriti that if all the naturalproperties of Kapha become abnormal, the Prameha gets chronic and if Kapha getsprovoked further condition of incurability ensues. Involvements of Raktadi Dhatu whichare not similar in qualities to Kapha are considered as Vikriti. 25
  44. 44. Review of Literature SampraptiVISHESHA SAMPRAPTI:1) Kaphaja Prameha: The etiological factors first cause the provocation of Kaphabecause of its close similarity to the related Hetu. This aggravated Kapha then spreads allover the body rapidly due to Sharira shaithilya. Meda Dhatu being excess in quantity,Abaddha and having similar properties with Kapha, the provocated Kapha whilespreading gets amalgamated with Medha Dhatu causing its vitiation. This annexation ofvitiated Meda and Kapha comes in contact with Sharira-Kleda and Mamsa, which arealready in excess quantity resulting Putimamsapidaka On the other hand the vitiatedKleda gets converted into Mutra. The Kapha along with Meda and Kleda impede theopenings of Mutravaha Srotas resulting into Prameha29 Sushruta narrated Dushya in each Doshik type of Prameha. He narrated vitiationof Kapha along with Vata, Pita and Meda in Kaphaja Prameha302) Pittaja Prameha: Due to its etiological factors provoked Pitta manifests as PittajaPrameha. Here similar pathogenesis occurs as described in Kaphaja Prameha31Depending on different properties of Pitta Dosha the Paittika Prameha develops into sixtypes. Pittaja Prameha is not entirely Paittika but it does have Pitta predominance as it ismentioned Charaka. There is dominance of Pitta Dosha in comparison to Kapha Doshaand Vata Dosha, in Paittika Prameha.(Chakrapani). Sushruta related Shonita along withVata, Kapha and Meda in the pathogenesis of Pittaja Prameha32(3) Vataja Prameha: Here Vata gets provoked due to its own etiological factors anddraws out Vasa-Adi Dhatus from the body towards Basti resulting into four types ofVataja Prameha. When Oja is drawn towards Basti due to vitiation of Vata, the natural 26
  45. 45. Review of Literature SampraptiMadhura Swabhava of Oja due to the Ruksha Guna of Vata gets transformed intoKashaya Rasa leading to the manifestation of Madhumeha33 One more pathogenesis of Vataja Prameha is described in Chikitsa Sthana. Hereprovoked Vata due to depletion of other two Dosha carries vital Dhatus towards Basti,resulting into Vataja Prameha34 As per Sushruta Kapha, Pitta, Meda, Vasa and Majja takepart in pathogenesis of Vataja Prameha35.Madhumeha due to Margavarana: Due to the Nidana sevana, the kapha, Pitta & Medas attain an Atipravruddhavastha. This causes Margavarana of Vata, resulting in Vata dushti. The Dushtavata does the Adana of the Ojas into the Basti producing Madhumeha. The Vata, Pittaand Kapha doshas start manifesting their symptoms intermittently depending on theirextent of Dushti. Subsequently, they attain Kshayavastha due to Kshaya of Dhatus againleading to Vata vriddhi. Here kshaya avasta means pitta and kapha are less severelyvitiated when compared to vata.This process of Margavarana of Vayu due to Kapha & Pitta occurs in two kinds ofpeople, firstly in those who are Sthoola and secondly in those who are not Sthoola buthave indulged in Kaphamedokara ahara and vihara. If the Nidana for Pitta are significantthen it also gets Dushta. Anyway, it should be remembered that the role of Pitta is onlysecondary in nature. In Sthoola people, the Sthoulya is the result of two reasons. First isdue to excess indulgence in Kaphakara ahara vihara and second is due to Beeja dushti. Inthe former case, the vriddi of Medas occurs due to the Nidana sevana. Whereas in thelatter case, the Medo vriddi occurs even in the absence of Kaphamedokara ahara viharaas the Beeja dushti would have occurred in the Medas in such a way. In both the cases, 27
  46. 46. Review of Literature Sampraptithe Kapha, Medas and Pitta if involved cause Margavarana of Vayu leading toMadhumeha. Hence, this variety of Madhumeha has been conspicuously identified bySushruta as Apathya nimittaja Madhumeha36.Madhumeha due to Dhatukshaya: This variety of Madhumeha is triggered by Dushta vata due to Dhatu kshaya. TheDhatukshaya avastha is essentially seen in Sahaja Madhumehi and as a terminalconsequence of other Prameha. The patients with Sahaja Madhumeha are Krusha,Alpashee, Pipasubhrisham and Paribhramanasheela unlike Sthoola Madhumehi who areSthoola, Bahvashee and with Shayyasana swapna sukherati. Madhumeha occurs inSahaja Madhumehi as a direct consequence of Vata because of the inherent nature ofsuch Rogi.But Madhumeha as a result of Dhatukshaya in patients, who were Sthoola in thebeginning but became Krusha due to long standing disease, aggravates further due toDhatukshaya janya vata vriddhi. This stage can also be seen a terminal consequence ofPrameha due to other causes.Samprapti of Sahaja Madhumeha: Madhumeha has been described as a Sahaja vyadhi because it is caused due toUpatapa of Beeja, Beeja bhaga or Beejabhaga avayava, resulting in Madhumehaarambhaka dosha dushti in parents suffering from Madhumeha. Hence, this disease istransmitted from generation to generation making Madhumeha a Kulaja vikara, justifyingSushruta’s inclusion of Madhumeha under Adibala pravrutta vyadhi. 28
  47. 47. Review of Literature Samprapti The Beejabhaga avayava responsible for the genesis of Vapavahana, undergoesUpatapa during the formation of Garbha depending on the existence of the disease inMata, Pita or both of them. The extent of Upatapa depends on the predominance of theDoshas during the formation of Garbha. This results in “Jatah khavaigunya”. Thedevelopment of the disease in such people also depends on the predisposition to thedisease in the factors like Prakruti, Desha, Kala, Bala, Nidana and the resultant Doshadushya sammurchana. Accordingly, the disease manifests early in the Balya avastha or inlater stages of life depending on when one or more of these factors exert their influence. Hence, it can be conveniently inferred that a patient born to parents, both ofwhom are Madhumehis has a higher chance of developing the disease than a patient oneof whose parent is Madhumehi. Moreover, the patient whose Mata is a Madhumehi ismore likely to develop the disease than in the patient whose Pita is Madhumehi, becausethe Dushyas in Madhumeha are mainly Matruja avayavas and Dhatus like Vapavahana,Medas, Mamsa and so on. The Sahaja Madhumehi hence is usually Krusha, Alpashee, Pipasabhrisha andParibhramanasheela leading to Dhatukshayajanya vata dushti. Therefore a preexistingKhavaigunya in Vapavahana is initiated by Dushta vata leading to Madhumeha38.SAMPRAPTI GHATAKA OF MADHUMEHA:Dosha: Shleshma Pradhana Tridosha. Shleshma is the Pradhana dosha responsible forMadhumeha inspite of the fact that Madhumeha is a Tridoshaja vyadhi. Hence it is alsocalled Madhumeharambhaka dosha. It is known that Shleshma is a Rasa mala. TheShareerastha shleshma is continuously nourished by this Rasa mala shleshma duringParinama of the Ahara rasa into Rasa dhatu by the action of Rasadhatvagni. When a 29
  48. 48. Review of Literature Sampraptiperson indulges in Shleshmakara ahara vihara as in Madhumeha, the Agnimandya ofJatharagni leads to Asamyak ahara parinama of ahara especially with relation toShleshma resulting in Aparipakvata of shleshma or in other words, Amaroopi sleshmautpatti. This Amaroopi shleshma attains Aghanata as there is loss of Samhanana in theKaphaswaroopa. This leads to Bahudravata of Shleshma set to cause further Dhatudushti. Therefore evidently, Shleshma is the primary dosha of the diseas, the otherDoshas like Vata & Pitta only trigger off this Samprapti and associate as Anubandha.Dushya: Rasa, Rakta, Mamsa, Meda, Majja, Shukra, Vasa, Oja, Lasika, Kleda andAcording to Vaghbhata Sweda.Srotodushti: The Srotodushti lakshana occur as Sanga of Kapha leading toVimargagamana and Atipravrutti of Kleda through the mootra.Agni: Vaishamya of all Agni (or Dhatvagnimandya)Ama: Medogata Ama produced due to Jatharagnimandya and Dhatvagnimandya.Adhisthana: BastiUdbhavasthana: AmashayaBhedavastha: Occurrence of Upadrava such as Puti Mamsa, Pidika etc.Nature: Chirakari, Anushangi39(A) Dosha: All the three Doshas are responsible for manifestation of Madhumeha.i) Kapha: It plays the dominant role in the Samanya Samprapti of Madhumeha. It is thefirst Dosha to get vitiated. Acharya Charaka while describing the causative factors used 30
  49. 49. Review of Literature Sampraptithe term ‘Kaphakrut Cha Sarvam’ in it. It indicates the significance of this Doshadushti inMadhumeha. Sharirashaithilya is the consequence of Bahudrava Kapha. Other ensuingmanifestations are Alasya, Atinidra, Tandra, etc.(ii)Pitta: Here, in Avaranajanya Madhumeha mainly the symptoms manifest because of 40Vriddhi of Pitta Dosha (Trishna, Daha, Kshudha and Trunshavriddhi) Pitta is inKshaya Avastha as compared to Vata in the Vataja Prameha pathogenesis. So, KshayaLakshana of Kapha Dosha and Pitta Dosha may manifest in Kshayajanya Madhumeha. 41,Pitta Kshayajanya Lakshanas are Mandagni, Prabhahani, Shitata etc while KaphaKshayajanya Lakshanas are Bhrama, Hriddrava, Slathasandhita etc.(iii)Vata: This is the prime Dosha in the pathogenesis of Madhumeha. Here Vata getaggravated either because of its own etiological factors or because of Avarana caused byKapha Pitta and Meda. This provoked Vata carries the vital constituents of the body likeVasa, Majja, and Oja towards Basti and excretes them outside through urine resulting indepletion of the Dhatu. Thus due to severe depletion of Dhatus, the symptom manifestsare Karshya, Daurbalya, Angasuptata and Parisaranshila nature. In Sushruta samhitha it is described that Vyana and Apana are the main culprits inPrameha. Here mainly the function of Vyanavayu gets hampered because of theaccumulation of vitiated Dushya at macro and microcellular level. Thus in all theSamprapti of Prameha Vyana acts as gatherer of Kleda and Apana as excretor.Thefunction of Apana Vayu gets aggravated resulting excretion of vital Dhatus through theurine outside the body42. 31
  50. 50. Review of Literature Samprapti(B) Dushya: Nidana, Dosha and Dushyas are the three factors responsible for themanifestation of every disease. But when they are having Anukulatva disease establishesin its way. So Anukulatva of these factors is important in Madhumeha. The following areDushya involved in Madhumeha:i) Rasa: Rasa is the seat of Kapha Dosha and at the same time it is the Mala of Rasadhatu.So provoked Kapha has affinity towards the Rasadhatu. The symptoms like Alasya,Gaurava, Karshya, Hrillasa, Angamarda, Sada, Pandutva, Klaibya etc. are produced as aresult of Rasa Dushti.ii) Rakta: It mainly gets vitiated in Pittaja Prameha. The Rakta Dusti Lakshana are Daha,skin diseases like Kustha, Visarpa, Pidika, Dadru, Charmadala, Pama, Kotha,Asramandala or the systemic diseases like Kamala as Raktapradoshaja Vyadhi43 areproduced as a result of Rakta Dusti.iii) Mamsa: Mamsa and Kapha are having the same qualities i.e. both give strength to thebody. When Kapha gets vitiated, Mamsa losses its normal consistency and developsShaithilya and provides space in between for the accretion of morbid matter. Thisconsequently results into the Puti Mamsa Pidika. "Mamsaleshu Avakasheshu"44iv) Meda: It is the dominant Dushya in all types of Prameha. It gets vitiated bothquantitatively and qualitatively. Kapha and Meda have close resemblance as they havethe same qualities. Both get vitiated more or less by same etiological factors.In Madhumeha vitiation of Meda results in two ways:- 32
  51. 51. Review of Literature SampraptiQualitative [Abadhdha, (Asamhata)]: Normal function of Meda is to produceunctuousness in the body along with Dridhatva i.e. compactness. So this Abaddhatvacauses derangement in the structure of Meda producing Shaithilya in the body.Quantitative (Bahu): Here in the pathogenesis, Meda is in excess quantity. This MedoDhatu is Aparipakva (Ama). 45Meda Dhatu is the most Anukula Dushya for provoked Kapha Dosha. Guru SnigdhadiAhara and Avyayamadi Vihara leads to. Bahutva of Meda Dhatu, due toDhatvagnimandya. Whatever food obese persons take, it gets converted into Meda andother Dhatus remains under-nourished leading to Dhatukshaya. Along with Bahutva,Dhatvagnimandya also results into Abaddhatva of Meda. Such an Abadhdha Meda gives‘Sharira Shaithilya’ and instead of doing Asthi Poshana; Meda Dhatu gets itself overburdened which is harmful to the body.Meda Dushti may manifest in many ways .The deranged Meda produces following signsand symptoms which are the eight Doshas of Atisthula person. 46Ayushorhrasa, Javoparodha, Kricchravyavayata, Daurbalya, Daurgandhya, SwedabadhaKshudha-Ati Matra, Pipasa-Atiyoga.By observing above description certainly it can be asserted that in Samprapti ofMadhumeha, Meda plays the foremost role.v) Majja: Due to Vata Prakopa Kshaya of Majja Dhatu occurs. Thus vitiated Majjaproduces clinical symptoms like, Netragaurava. Angagaurava in Madhumehi47vi) Shukra: Shukra Dhatu gets affected in the pathogenesis of Prameha, which due to itsvitiation produces symptoms like Daurbalya and Kricchravyavayata. In Sahaja Prameha 33
  52. 52. Review of Literature SampraptiShukra has an important role to play. Prameha is a Kulaja Vikara and occurs as result ofBeeja Dosha. Sushruta has described that Shukra Dosha and Prameha get precipitatedbecause of the vitiation of Vyana and Apana Vayu. Vata causes depletion of ShukraDhatu and also Shukrameha. So one can appreciate the importance of Shukra Dushti inPrameha.vii) Vasa: It is an Upadhatu of Mamsa and is ‘Sleshmika’ in character. The provokedVata draws Vasa towards Basti and excretes it through the urine in the form of Sneha. Incase of Madhumeha, the Dushti is illustrated in the form of Bahutva as well asAbaddhatva (Chakrapani) but still the manifestations are not described concerning VasaDushti.viii) Lasika: The aggravated Vata propels Lasika towards the Basti and then excretes itthrough the urine leading to increased micturation. Lasika is described as a Dushya inHastimeha.ix) Oja: Oja is supreme extract of all the Dhatus and gives strength and immune power tothe body. Oja is the purest quality of Sleshma in its constitution, Guna and Karma. Oja isan important Dushya in the Samprapti of Madhumeha. Here provoked Vata transformsthe Madhuratwa of Oja into Kashayatwa and carries Oja towards Basti and excretesthrough urine leading to Ojakshaya. So the symptoms of Ojakshaya like Murccha,Mamsakshaya, Moha, Daurbalya (excessive weakness), Vyathita Indriya, Rukshata,Gurugatrata, Nidra, Tandra etc. may manifest.x) Kleda: It is also an important Dushya after Meda. The literal meanings of Kleda are –wetness, moisture, dampness etc.). It has been mentioned by Charaka that Kleda gives 34
  53. 53. Review of Literature SampraptiShaithilya to Sharira. Charka has given Ambu as a synonym to Kleda. Normal function ofMutra and Sweda has been described by Vagbhata as follows.48 Under normal physiological conditions Mutra and Sweda maintain balance ofKleda in the body. If this Kleda gets vitiated it directly affects the Mutra and Sweda anddisrupts the physiology of bodily elements causing Shaithilya. Arundatta has mentionedthat absence of Kleda may lead to the dryness of the body. In the Samprapti, KledaDushti is in the form of ‘Vriddhi’ and not the Kshaya. Hence, Bahu Kleda will manifestas Prabhuta Mutrata and Avila Mutrata because extensively increased Kleda is excreatedout of the body as Mutra. The other manifestations of Kleda Dushti may be Shithilangata,Ati Sweda Pravritti, Visra Sharira Gandha (due to excessive sweating), Sharira Mruduta,Snigdhata etc 49xi) Sweda: This Dushya has been mentioned only by Vagbhata. Sweda is mainly relatedwith Meda and Kleda. Due to the vitiation of Meda and Kleda, Swedavaha Srotodushtioccurs leading to the manifestation of Ati Swedapravritti, Daurgandhya, Picchilagatrata,Snigdhagatrata Visra-sharirgandha etc. Sushruta mentioned that in Madhumeha Sweda 50becomes Sweet in nature The whole pathological phenomenon described in Kleda andSweda Dusti can be correlated with water and electrolyte imbalance.C) Srotodushti: In the Samprapti of Madhumeha two types of Srotodushti are found:1. Atipravritti 2.VimargagamanaD) Agni:Madhumeha is a complex metabolic disorder which results from the Dhatwagnimandya.All the metabolic activities are governed by Agni and its derangement leads to so many 35
  54. 54. Review of Literature Sampraptimetabolic disorders and Madhumeha is one of them. Agni functions at the level ofJatharagni, Bhutagni and Dhatwagni. When they function properly, each & every Dhatuis nourished & formed properly. But when there is derangement in these Agni, thenDhatu are not nourished & formed properly. In case of Avaranajanya Madhumeha due toKaphakara Nidana, Dhatvagnimandya & particularly Medodhatvagnimandya developsand due to this, excessive but Sama Medodhatu is formed leading to more vitiation ofspecific Dhatu which obstructs the Gati of Vata leading to its provocation. Due to thisprovocation of Vata, Jatharagni gets stimulated leading to increased appetite. This cyclegoes on. Therefore, in Madhumeha the Dushya Dushti mostly occurs in the form ofVriddhi reflecting Dhatvagnimandya. Due to Medodhatvagnimandya there is lessnourishment to further Dhatus which results into Kshaya Lakshana of Majja and ShukraDhatu.E) Ama: Sushruta has illustrated the role of Ama in the pathogenesis of variousdisorders. He mentions that the Samprapti of Prameha takes its origin from the Ama only.He states51 that is from the very beginning, Agnimandya has been developed due to Guru,Snigdhadi Ahara and Avyayamadi Vihara which leads to production of Ama. Dalhanaadds that not only Dosha but Meda Dhatu is in the Ama form. Hence Ama is a part andparcel of Samprapti. Ama means Aparinamitta. Anything which remains in undigestedform, being harmful to the body is Ama. It is Apakva (undigested), Asyaukta (Shithila),Durgandhi, Picchila in nature and it produces Gatrasada. In the Samprapti ofMadhumeha, we also get the dominance of Ama regarding Kapha Dosha, Meda Dhatu,Mamsa Dhatu, and Kleda. The undigested Kapha and Meda acts as Ama vitiating the 36
  55. 55. Review of Literature SampraptiMutravaha Srotas leading to Madhumeha. This vitiation is in the form of Srotasobstruction.CLASSIFICATION AND PATHOGENESIS OF DIABETES MELLITUS52Primary DM: The basic categories of classification of DM are based on therecommendations by the National diabetes data group. The disease DM is dividedbroadly into Primary DM & Secondary DM. Primary implies that no associated disease ispresent while in the secondary category some identifiable condition causes or allows adiabetic syndrome to develop. Insulin dependence in this classification is not equivalentto insulin therapy rather the term means that the patient is at risk for diabetic ketoacidosis(DKA) in the absence of insulin. Many patients classified as non-insulin dependentrequire insulin for control of hyperglycemia although they do not become ketoacidotic ifinsulin is withdrawn. The term type 1DM is often used as a synonym for insulin dependent diabetesmellitus (IDDM) and type 2 DM is considered equivalent to non insulin dependentdiabetes mellitus (NIDDM). This linkage is not ideal because subsets of patients withapparent non-insulin dependent DM become fully insulin dependent & prone toketoacidosis. Hence a modified classification has been suggested so that the terms,insulin dependent & non-insulin dependent describe physiologic states (Ketoacidosisprone & ketoacidosis resistant respectively) while the terms type 1 and type 2 refer topathogenetic mechanisms (immune mediated & non immune mediated respectively).Using such a classification three major forms of primary DM would be recognized, Type1 IDDM, Type 1 NIDDM and Type 2 NIDDM. 37
  56. 56. Review of Literature SampraptiCategory (2) is an intermediate range of autoimmune destruction in which the capacity toproduce insulin is sufficient to prevent ketoacidosis but not to maintain normal bloodglucose. This variant likely occurs when the autoimmune process begins at an older ageand progresses more slowly than usual. A subset of obese people with apparent non-insulin dependent can become transiently insulin dependent and develop diabeticketoacidosis. Such individuals do not have markers of autoimmunity suggestive of type 1DM and may not require insulin permanently after recovery from DKA. Presumablydiminution of insulin renders such subjects vulnerable to stress induced metabolicdecompensation & causes transient insulin dependence.Secondary DM: There are several secondary forms of DM. Pancreatic diseaseparticularly chronic pancreatitis in alcoholics is a common cause. Hormonal causesinclude pheochromocytoma, Acromegaly, Cushing’s syndrome & administration ofsteroid hormones. “Stress hyperglycemia” associated with severe burns, acute myocardial infarctionand other life threatening illness is due to endogenous release of glucagons &catecholamines. Hormonal hyperglycaemia results from various combinations ofimpairment of insulin release and induction of insulin resistance. A large number of drugscan lead to impaired glucose tolerance or hyperglycaemia and even ketoacidosis can bedue to quantitative or qualitative defects in the insulin receptor or to antibodies directedagainst it. The mechanism is essentially pure insulin resistance. Genetic syndrome associated with impaired glucose tolerance or hyperglycaemiaincludes the lipodystrophies, myotonic dystrophy and ataxia telangiectasia. The finalcategory i.e. others is poorly defined and is meant to include any condition that does not 38
  57. 57. Review of Literature Sampraptifit elsewhere in the aetiologic scheme. The appearance of abnormal carbohydratemetabolism in association with any of these secondary causes does not necessarilyindicate the presence of underlying DM although in some cases mild asymptomaticprimary DM is made overt by secondary illness.Pathogenesis of IDDM: Pathogenesis begins with a genetic susceptibility to the disease,with the destruction of islet β cells of pancreas almost complete due to an autoimmuneprocess. Viral infection is a triggering factor but non-infectious agents may also beinvolved. Autoimmune attack then follows. The islet β cells become infiltrated bymonocytes/macrophages & activated cytotoxic T cells. This infiltration is usually calledInsulitis or sometimes called Isletitis. Multiple antibodies against β cells antigens arepresent in the blood. The patients’ state while the immune attack is underway butunrecognized is termed pre-diabetes. This stage may by brief or prolonged and may beprogressive and uninterrupted or intermittent. What is clear is that the insulin reservesteadily diminishes until it is insufficient to maintain blood glucose within normal limits.At this point the diagnosis is DM. Rarely type 1 DM develops exclusively from anenvironmental result, as from the ingestion of Vacour-a rat poison. It is also possible thatan autoimmune DM can develop in the absence of an environmental trigger i.e. can bepurely genetic. Usually however the pathogenetic sequence is, Genetic predisposition Environmental insult Autoimmune destruction of β cells Diabetes mellitus (IDDM) 39
  58. 58. Review of Literature SampraptiDestruction of β cells and development of IDDM: The loss of insulin reserve occurs overa few to many years. The earliest sign of abnormality is the development of islet cellantibodies when the blood sugar & glucose tolerance are normal and when insulinresponses to glucose load are intact. The second phase ensues after this where there isonly decreased glucose tolerance. Fasting blood sugar remains normal. This is the lastpre-diabetic stage. In the third phase, fasting hyperglycemia develops but ketosis does notoccur even when the DM is poorly controlled and the clinical appearance is that ofNIDDM. Continued destruction of β cells then leads to insulin dependent stage and apropensity for ketoacidosis especially during stress. Once this stage is acquired thepatient ordinarily requires lifelong insulin therapy. The immune directed destruction of βcells probably involves both humoral & cell mediated mechanisms. Cells involved in theattack on β cells include natural killer cells, activated cytotoxic T lymphocytes andmacrophages cell destruction may be at least partially due to release of cytokines such asinterlukin I (IL-I)) and tumour necrosis factor α (TNF α) from activated macrophages.Cytokines may work through induction of nitric oxide or of super oxide. β Cells have alow capacity for free radical destruction and are especially vulnerable to oxygen toxicity.Pathogenesis of NIDDM: NIDDM is more common than IDDM. Its pathogenesis is lesswell understood. The relation between the β cells abnormality and insulin resistance isnot resolved. The major environmental factor is obesity. Both β cell defects and insulinresistances are present in the overt disease, which more commonly exhibits familialaggregation. Patients with type 2 NIDDM have two physiologic defects viz. abnormalinsulin secretion and resistance to insulin action in target tissues, which of theabnormalities is primary is not known. Descriptively, three phases can be recognized in 40
  59. 59. Review of Literature Sampraptithe usual clinical sequence. In the first phase, plasma glucose remains normal despitedemonstrable insulin resistance because insulin levels are elevated. In the second phase,insulin resistance tends to worsen so that postprandial hyperglycaemia develops despiteelevated insulin concentrations. In the third phase, insulin resistance does not change butdeclining insulin secretion causes fasting hyperglycaemia and overt DM. Most authoritiesbelieve that insulin resistance is primary and that hyper insulinaemia is secondary i.e.insulin secretion increases to compensate for the resistance state. However, hypersecretion of insulin may cause insulin resistance i.e. a primary islet cell defect causesinsulin hyper secretion and insulin hyper secretion in turn leads to insulin resistance.Explanatory hypotheses increased fat synthesis in the liver and enhanced fat transport(Via very low-density lipoprotein VLDL) leading to secondary fat storage in the muscle.Increased fat oxidation could impair glucose uptake and glycogen synthesis most patientswith NIDDM are obese and obesity per se causes insulin resistance, but obesity is not thesole cause for insulin resistance. It is also true that a modest reduction in weight oftenresults in major improvement in the blood sugar control in obese patients of NIDDM.The late decline in insulin release could be due to the underlying genetic defect or tometabolic toxicity in β cell. High levels of glucose or increased tissue levels of long chainfatty acids (lipotoxicity) could be the damaging molecules. In summary, it is likely that an insulin secretory defect and insulin resistance areboth required for DM to be expressed since massively obese persons with marked insulinresistance may have normal glucose tolerance. Presumably the β cell lesion is not presentin such persons. This fact suggests that the primary defect resides in the insulin producingcells. β cell mass is intact in type II NIDDM in contrast with the situation in type 1 41
  60. 60. Review of Literature SampraptiIDDM. The α cell population is increased resulting in an elevated ratio of α to β cells andin excess of glucagon relative to insulin that characterizes all hyperglycemic statesincluding NIDDM.Role of Amylin: Although insulin resistance in type II NIDDM is associated withdecreased numbers of insulin receptors most of the resistance is post receptor nature. Ithas long been known that deposits of amyloid are found in the pancreas of patients withtype 2 DM. This material is a 37 amino acid peptide termed Amylin. Amylin is co-packaged with insulin in secretory granules and is released simultaneously with insulin inresponse to insulin secretogogues. In animals, amylin has been reported to induce insulinresistance but in diabetic subjects an amylin derivative has hypoglycemic effectsapparently because it causes delayed adsorption of nutrients from gastrointestinal tract.Amylin deposition in islets may be the consequence of overproduction secondary to theinsulin resistance to which it contributes. Alternatively accumulation of amylin in theislets might contribute to the late failure of insulin production with long standingNIDDM. A definitive role for amylin is not established. 42
  61. 61. Review of Literature Samprapti Table No. 2: Classification of DM:I. Primary 1) Autoimmune (type 1) DM a) Non insulin dependent Diabetes mellitus (type 1 NIDDM) - Transient b) Insulin dependent Diabetes mellitus (type 1 IDDM) 2) Non Auto immune DM a) Insulin dependent Diabetes mellitus (type 2 IDDM) - Transient b) Non insulin dependent Diabetes mellitus (type 2 NIDDM) c) Maturity onset Diabetes mellitus of the young (MODY)II. Secondary a) DM caused by pancreatic disease b) DM caused by hormonal abnormalities c) Drug or chemical induced DM d) DM caused by insulin receptor abnormalities e) DM associated with genetic syndromes f) DM of other causes. 43
  62. 62. Kaphakara ahara and vihara(Apathya Nimittaja) Margavarana of vayu Bahu Shleshma Dushti abadha & Vapavahana Shareera medas Ojo kleda Vata Vriddhi dusti Dhatu. mamsa aparipakva increase Agnimandya etc. Basti Mootra Beeja Upatapa (Sahaja) Dhatukshaya Madhumeha Illustration 4.1: Samprapti of Madhumeha

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