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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

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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  • 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. 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. 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. 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. 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. DEDICATION I Would Like to Place This Dissertation on the Lotus Feet of My ParentsDate: Signature of the CandidatePlace: Anil kumar.G VI
  • 7. ACKNOWLEDGEMENTSI am Ever Indebted To Lord Almighty, My Venerated Parents, Respected Teachers And Affectionate Friends VII
  • 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. IX
  • 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. 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. 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. 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. 28 28 Effect on PPBS 13329 29 Effect on Urine Sugar 133 XIII
  • 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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
  • 63. Review of Literature Poorva roopa POORVAROOPA Poorvaroopa are indications of impending diseases. They occur prior to completemanifestation of disease and may suggest the forthcoming illness. During the course ofthe Samprapti of an illness, the morbid Doshas circulating ubiquitously in the body tendto localize in an area and produces some of the unique symptoms and is referred by thename Poorvaroopa. Diagnosis at this stage of the illness gains paramount importance, asthe effective treatment at this stage definitely reduces the possible organic damage aswell as degree of morbidity. As Madhumeha is classified under the Vatika type of Prameha, Purvarupa ofPrameha can be taken as Purvarupa of Madhumeha. If all the Pramehas are neglectedthen it results in to Madhumeha. This may be the reason for not mentioning the specificpoorva roopa by our Acharyas for Madhumeha and most of the poorva roopa mentionedin our classics are the clinical features and complications of Diabetes Mellitus. So, thepoorva roopas of Prameha in general is discussed in this context. Our Acharyas havegiven more importance to poorva roopas. According to Sushrutacharya, if all the poorvaroopas are clearly exhibited and if the patient notice a slight increase in mootra, then onecan infer that patient may suffer from Prameha in the near future. If half of thepoorvaroopa are exhibited clearly and patient notice adhikamootra pravritti, then it is theclear indication of the presence of Prameha. In olden days vaidyas used to detect the presence of sugar in urine bypipeelikaabisarana. A patient use to approach a vaidya only when he suffered fromprabhoothamootrapravritti . But he neglected the symptoms like snigdhata of the body,atinidra etc. which occur much more earlier than the above mentioned cardinal feature. 44
  • 64. Review of Literature Poorva roopaThat is why our Acharyas have considered these early stages as poorva roopa. From the above description it is clear that the Acharyas were able to diagnoseMadhumeha only at a later stage. In the present era due to the advanced technologies thesame can be diagnosed well in advance by examining the sugar level in blood and urine.Thus we can say that, most of the poorvaroopa mentioned in our classics are actually theclinical features and complications developed due to Diabetes Mellitus. Pre-Diabetic States53 Sometimes a patient with abnormal hyperglycemia may not have full clinicalsymptoms of Diabetes mellitus and often pre-diabetic states are asymptomatic. Mildsymptoms if manifested go unrecognized but the identification of such stages can go along way in prevention of an overt disease. The British Diabetic Association hassuggested a classification that is accepted by W.H.O. expert committee on Diabetes. Theyare as follows:Potential Diabetes: These are persons who have high probability of developing Diabetes.They do not show any evidence of impaired glucose tolerance. They include, a) Identicaltwin of a diabetic, b) Persons with both the parents diabetic, c) Persons with one parentdiabetic, the other non-diabetic parent having a diabetic parent or a diabetic sibling ortheir offspring having Diabetes.Latent Diabetes: a) Persons with a normal G.T.T. at present, but had an abnormal G.T.T.sometime in the past viz. during pregnancy, infection when under stress or when obese,b) Persons with a normal G.T.T. under standard conditions but an abnormal one withprovocative tests. 45
  • 65. Review of Literature Poorva roopaAsymptomatic Diabetes: This stage is variously known as chemical, subclinical orsubliminal Diabetes. They always show an abnormal G.T.T. but the fasting blood levelsmay be normal in the early stage. Later on, even these levels may be raised. 46
  • 66. Review of Literature Poorva roopa Table No. 3 - Poorva roopa54, 55,56 Sl. Poorvaroopa Charaka Sushruta Ashtanga No. Samhita Samhita Hridaya 1 Sweda + - + 2 Angagandha + + + 3 Angashaithilya + - + 4 Angasada - + - 5 Shayya sukherati + - + 6 Swapna sukherati + - + 7 Asana sukherati + - + 8 Hridayopadeha + - + 9 Netropadeha + - + 10 Jihwopadeha + + + 11 Shravanopadeha + - + 12 Taluni malotpatti - + - 13 Danteshu malotpatti - + - 14 Ghanangata + - + 15 Kesha ativruddhi + - + 16 Kesha jatilibhava + + - 17 Nakha ativruddhi + + + 18 Sheeta priyatwam + - + 19 Galashosha + - + 20 Talushosha + - + 21 Asya madhurya + - + 22 Kara daha + + + 23 Pada daha + + + 24 Mootrapipeelika abhisarana + - + 25 Madhura mootrata - + - 26 Shukla mootrata - + - 27 Snigdha gatrata - + - 28 Picchila gatrata - + - 29 Guru gatrata - + - 30 Pipasa + + - 31 Shwasa dourgandhya - + - 32 Tandra + + - 33 Kara suptata + - - 34 Pada suptata + - - 35 Anga suptata + - - 36 Alasya + - - 37 Mukha shosha + - - 38 Kayachidreshu upadeha + - - 39 Sarvakale nidra + - - 40 Shatpada pipeelika + - - abhisarana on shareera 41 Shatpadamootra abhisarana + - - 42 Pipeelika shareera + - - abhisarana 47
  • 67. Review of Literature Roopa ROOPA Under the heading Roopa the signs and symptoms produced in an individual as aresult of sequential changes in the disease process can be studied. Roopa of a disease willbe produced in the fifth stage of samprapthi i.e. vyaktavasta. In this stage doshadooshyasammurchana will be capable to produce its laxana. In classics, laxana of Madhumeha are only ascribed to mootra and mootrapravrutti which remains incomplete without the study of sarvadaihika laxana explained inthe contexts of aapatyanimitaja and sahaja madhumeha by Sushruta. Hence the laxana ofMadhumeha are mainly grouped under two categories, that is 1.mootra sambandi laxana2.sarvadaihika laxana.MOOTRA SAMBHANDI LAXANA:The laxana in relation with mootra are to be studied under two heads A. samanya laxanaB. vishesha laxana.A. SAMANYA LAXANA: 1. Prabhootha mootrata: This is the cardinal sign described by all Acharyas. Vagbhata mentioned Prameha as the disease of Mutraatipravrtija Patient Voids urine more in quantity and frequency57. Gayadasa opines that this excess urine quantity is because of liquification of the Dushyas and their amalgamation58. 2. Avilamutrata: Patient voids urine having hazy consistency or having turbidity.Gayadasa and Dalhana both opine that, this characteristic feature of urine is because ofthe nexus between mutra, Dushya and Dosha59 Vagbhata also emphasized that thisturbidity of the urine is because of its annexation with the dhatus60. 48
  • 68. Review of Literature RoopaKashyapa61 mentioned following symptoms of Prameha to be observed in pediatricpatientsAkasmat Mutra Nirgama: Child excretes urine suddenly with no intention.Makshika Akranta: Flies get attracted towards the urine.Shweta and Ghana Mutra: Child excretes urine having Shweta colour and solidconsistency i.e. turbidityB. VISHISTA LAXANA62:1. Madhurata: Here Madhurata refers to madhura rasa that is entirely due to Apakva ojas.The Rasa of Ojas is Madhura and hence also of the Mootra as is evidenced by theattraction of Shatpadapipeelika towards the Mootra.2. Rooksha: Refers to the Guna and Rooksha guna is due to vriddhavata.3. Pandu: Refers to the Varna of urine. The urine would have lost its normal varna as aresult of abnormally increased Shareera kleda.4. Kashaya: The term Kashaya denotes both Rasa as well as Kashaya kalpana which areusually dark brown to black in colour. Bhavaprakasha in his description of the conditionmentions that the word Kashaya should indicate the Varna of Kashaya i.e. dark brown toblackish. But when we analyze this description, it becomes evident that the Rasa of urinecannot be Madhura and Kashaya at the same time. Moreover, if the Kashaya rasa hadbeen an accompaniment of Madhura rasa, it must have been less predominant because,the Pipeelikas or ants are drawn towards only Madhura rasa. If we consider Kashaya asVarna in Madhumeha it is almost a non-occurrence in cases of Madhumeha, as weunderstand it in the form of Diabetes. The Kashaya varna can be an occurrence inconditions of Nephropathy as a sequel of DM. Hence, this speculation can be clarified 49
  • 69. Review of Literature Roopawith an argument that does not nullify the opinion of Bhavamishra and therefore theKashaya varnata could be understood as a terminal manifestation of DM.5. Madhusama mootra63: Varna, gandha, rasa of mootra will be similar to that of madhu.It is due to the ojonissarana in mootra. This situation is similar to the previous one thatcan be analyzed on the basis of Vagbhata’s statement, that the Samanya roopas ofPrameha are Prabhoota and Avila mootrata and the other Vishesha roopas are seendepending on the Dosha and Dushya samyoga where, the urine assumes the respectivecharacter in terms of Varna, Rasa, Sparsha and Gandha. When this is applied toMadhusamam, it can mean that urine resembles honey in taste, colour, touch and smellbut clinically and literally the disease favors more towards resemblance of urine withhoney in its taste rather than other qualities, Nevertheless the Varna of honey is alsodarkish brown and can be understood as discussed earlier under the previous heading ofKashaya.SARVADAIHIKA LAXANA64:Apathyanimittaja madhumeha:1) Sthoulya, 2) Bahvashee, 3) Snigdha, 4) Shayya asana swapna sheela.Sahaja Madhumeha:1) Krisha, 2) Alpasheela, 3) Rooksha, 4) ParibhramanasheelaOther than these, some other laxana are found in different context in Ayurveda. They are1. Tanumaduryata65: Due to the circulation of madhura, snigdha, bahudravashleshmaalong with aparipakwa rasa dhatu through out the body because of shareera shithilata onecan notice tanumaduryata.2. Vranaha kruchrena sidyanthi: Delayed healing of wound is seen in Madhumeha. For 50
  • 70. Review of Literature Roopathis Chakrapani gives reasoning as Dustadushyataya.3. Sushruta explains the nature and the extent of klama of a Madhumehi by the followingversion. He says that Madhumehi prefers to stand instead of walking , he likes to sitinstead of standing, he desires to lie down instead of sitting and he prefers more to sleepthan all the above Apart from these Pratyatma roopa, the mootrasambadhi roopa Kaphaja,Pittaja and Vataja Prameha are described as follows66, 67, 68Kapha Pradhana Vatanubandha Madhumeha (Kaphaja Prameha): Prameha Mootra lakshana1) Udakameha : Accha, Bahusita, Sheeta, Nirgandha, Udakopama2) Ikshuvalika rasa meha : Atyartha madhura, Sheeta ,Ishatpicchilam, Avilam, Kandekshu rasa sankasham.3) Sandrameha : Paryushita, Sandribhavati bhajane4) Sandraprasadameha : Samhanyante mootram5) Shuklameha : Shukla, Pishtanibham, Abhikshnam6) Shukrameha : Shukrabham, Shukramishram, Muhurmehati.7) Sheetameha : Atyartha madhuram, Sheetam8) Sikatameha : Katina mootrata9) Shanairmeha : Mandam, Mandavegam, Kruchram10) Alalameha : Tantubaddha iva, Alalam, Picchilam11) Surameha : Suratulyam 51
  • 71. Review of Literature Roopa12) Lavanameha : Vishada, Lavana tulyam13) Pishtameha : Pishtarasa tulyam14) Phena meha : Stokam stokam, SaphenaPitta pradhana Vatanubandha Madhumeha (Pittaja Prameha):1) Ksharameha : Kshara tulya varna-rasa-sparsha2) Kalameha : Masi varna, Ajasram, Ushnamootra3) Neelameha : Chashapakshi nibham, Amlam4) Raktameha : Visra, Lavanam, Ushnam, Raktam5) Manjistameha : Manjistodaka sankasha, Visra6) Haridrameha : Haridrodaka sankasha, Katuka7) Amlameha : Amla rasa, Amla gandhaVata Anubandhya Madhumeha (Vataja Prameha):1) Vasameha : Vasamishram, Vasabham2) Majjameha : Majjanam3) Hastimeha : Hastimatta iva ajasram, Lasika.4) Madhumeha/Kshaudrameha : Kashaya,Madhura, Pandu varnata, Ruksha5) Sarpimeha : Sarpiprakasham 52
  • 72. Review of Literature Roopa CLINICAL FEATURES69 The manifestations of symptomatic diabetes mellitus vary from patient to patient.Most often, symptoms are due to hyperglycemia (polyuria, polydipsia, polyphagia), butthe first event may be an acute metabolic decompensation resulting in diabetic coma.Occasionally, the initial expression is a degenerative complication, such as neuropathy, inthe absence of symptomatic hyperglycemia. The metabolic derangements of diabetes aredue to a relative or absolute deficiency of insulin and a relative or absolute excess ofglucagon. Normally, a rise in the molar ratio of glucagon to insulin leads to metabolicdecompensation. Changes in this ratio can be caused by a fall in insulin or a rise inglucagon concentration, separately or together. Alteration in the biologic response toeither hormone would have the same effect. Thus, insulin resistance could cause themetabolic effects expected of an elevated glucagon/insulin ratio, even if the ratio foundby immunoassay of the two hormones in plasma were normal or even decreased (theglucagon being biologically active, the insulin relatively inactive). Typically, the clinicalfeatures of IDDM and NIDDM are distinctive.Insulin-Dependent Diabetes IDDM usually begins before age 40; some patients developtype 1 diabetes late in life, with a first episode of ketoacidosis occurring at age 50 or evenlater in rare instances. These patients, who on the basis of age should have type 2NIDDM, are usually not obese. Onset of symptoms may be abrupt, with thirst, excessiveurination, increased appetite, and weight loss developing over several days. In somecases, the disease is heralded by the appearance of ketoacidosis during an intercurrentillness or following surgery. As outlined in type 1 patient may have normal weight ormay be wasted, depending on the length of time between onset of symptoms and start of 53
  • 73. Review of Literature Roopatreatment. Characteristically, the plasma insulin level is low or immeasurable. Glucagonlevels are elevated but are suppressed by insulin administration. Once symptoms develop,insulin therapy is required. Occasionally, an initial episode of ketoacidosis is followed bya symptom-free interval (the "honeymoon" period), during which no treatment isrequired.Non-Insulin-Dependent Diabetes: NIDDM usually begins in middle life or later. Thetypical patient is overweight. Symptoms begin gradually, and the diagnosis is frequentlymade when an asymptomatic person is found to have an elevated plasma glucose level onroutine laboratory examination. In contrast to IDDM, plasma insulin levels are normal tohigh in absolute terms, although they are lower than predicted for the level of the plasmaglucose; i.e., relative insulin deficiency is present. Stated in another way, if plasmaglucose concentrations in nondiabetic subjects were raised to levels equivalent to thosefound in NIDDM patients, insulin values would be higher in the normal group. Thisrelative deficiency reflects the previously mentioned insulin secretory defect in NIDDM.Glucagon metabolism in NIDDM is complex. While the elevated fasting plasmaconcentrations can be lowered by large amounts of insulin, the exaggerated glucagonresponse to ingested nutrients cannot be suppressed; i.e., alpha cell function remainsabnormal. For unknown reasons, patients with NIDDM do not develop ketoacidosis butare susceptible to development of hyperosmolar, nonketotic coma. 54
  • 74. Review of Literature Upadravas UPADRAVA Upadrava are manifestations of severe forms of the Roga, and are Rogashraya.They occur alongside the disease or as a sequele. In either form, they mark the beginningof fatality. Unless so severe as to warrant a special attention, they subside with disease. The disease Madhumeha, when severe, involves almost all Dhatu and therespective Srotas. Accordingly, Upadravas appear as and when a particular Srotas isaffected. The Upadravas of Madhumeha can be studied under the following headings. 1.Samanya upadravas 2. Vishishta upadravas. The classification of Upadravas asSamanya and Vishishta has not been done in any of the Granthas. Charaka and Bhelahave listed and described common Upadravas at random. Sushruta, Vagbhata andBhavaprakasha have described them separately as Kaphaja, Pittaja and Vataja1. Trushna: Person will not satisfy even after drinking water continuously is known astrushna70, Pipasa is its synonym. Trushna will manifest as a upadrava due to excessiveloss of kleda through mootra. Pitta with its Ushna guna is the main Dosha here71. Trushnamay manifest as a poorvaroopa where the degree of vitiation is comparatively less.2. Atisara: The long standing vitiation of vata affects its sthana that is pakwashaya whichin turn causes atisara. Westerners have also observed atisara as an upadrava inMadhumeha and they have termed it as diabetic diarrhea. Intermittent or persistentpainless diarrhea has been observed in long standing severe diabetics. The stools arewatery and large. Typically diarrhea is nocturnal it may last for a few hours to few days.3. Paridhupana/Daha: Daha may manifest in kara and pada or savanga. It is a Pittajananatmaja vikara and is described as Sarvanga dahanamiva santapa72 and develops in 55
  • 75. Review of Literature Upadravasconditions of Pitta pradhanyata in Madhumeha. It can be appreciated as diabeticperipheral neuropathy.4. Jwara: is mainly due to Pitta pradhanya and the manifestation seen is that of Jeernajwara. Pitta pradhanyata is usually seen in the second stage of the disease where there isrelatively more involvement of Medas and Rakta. Here, as a result of Dhatu kshaya andreduced Vyadhikshamatva, Jwara develops.5. Dourbalya: It is because of dhatvagni mandya, which later results in ojokshaya, henceojokshaya leads to dourbalya.6. Arochaka: Is a condition where there is Virasa mukhata and the patient experiencesdisinclination in swallowing the food which is already in the mouth as described by thesentence Mukhapravishtasyapi nabhyavahara. The main dosha involved is Kapha butPitta also causes Arochaka.7. Avipaka: Is the Ajeerna occurring as a result of Agnimandya by Kapha.8. Pootimamsa pidaka73, 74: These pidakas manifest due to the vitiation of mamsa, meda,shonita with increased kleda results in development of Pidakas, which develop Shotharesulting in Pooya vriddhi. The Shopha may or may not burst. If not treated, the Pooyaattains Abhyantara prapti and Utsanga, resulting in Asadhyata. The development ofPidakas has been described as limited only to the lower limbs as the Rasayanis there areDurbala. Clinically also, the incidence of diabetic ulcers occurring in the lower limb ismaximum. The Pidakas are the most important Upadravas of Madhumeha as negligencein treating them renders the disease Asadhya.9. Brama: Is the condition where the patient feels Chakravat bramana of gatra (as if thebody is being rotated like a wheel). And whenever he gets brama usually falls down 56
  • 76. Review of Literature Upadravas(bhoomau patati) 75. It is mainly due to Pitta or Vata or both and due to Raja dosha ofManah76. This Upadrava is produced when Gambhira dhatus like Majja are involved.10. Tama: Tamah can be caused by Pitta77 causing Rakta prakopa78 and Vata causingRasa samvahana abhava. This can occur during the course of the illness as a transientphenomenon or during the terminal stage leading to death.11. Shoola: It is due to Vata along with Gambira dhatus like Majja involvevment79. Apartfrom this, Shoola can be understood as udara shoola which is due to badda purishata andudavarta, which is also an Upadrava of Madhumeha.12. Kandu: This is mainly a due to Kapha80 which has attained Bahudrava avastha anddue to excess Sweda as a result of Dushta medas. The patient is hence susceptible to skindiseases. Clinically, the incidence of Yoni kandu and Medra kandu are more inMadhumeha Besides, Kapha pradhana kushta have Kandu as a predominant symptom,which is not uncommon in Madhumeha.13. Alasya: Means anutsaha81 this is due to Kapha and meda.14. Pratishyaya: This is due to Kapha, Vata and Oja kshaya and Pranavaha srotodushti.15. Shaithilya: The Dhatu kshaya leads to Anibida samyogata (loss of compactness)leading to Dourbalya82.16. Mamsopachaya: Is characterized by Mamsa sanghata83 due to Mamsa pradosha andhence a Madhumehi can develop Adhimamsankura vikaras.17. Makshikopasarpana: This condition is the result of Tanu madhuryata and subsequentMadhura bhava of Sweda84. This attracts more Makshikas as this Laxana has been alsomentioned in Poorvaroopavastha. This condition should be considered as a symptom 57
  • 77. Review of Literature Upadravasindicating Asadhya avastha, which is likely to be preceded or succeeded by Murccha adiupadrava.18. Kapha praseka: Means excess Lalasrava due to Kapha bahudrava.19.Chardi: This can also be a symptom of Marma85 which is an occurrence inMadhumeha.20. Nidra: It is due to Kapha dushti and Tamoguna.21. Kasa & Shwasa: Are result of Prana vaha srotodushti by Vriddha kapha and vata.22. Vrushana avadarana: It may be a result of Kandu or Kushta affecting Vrushana.23. Bastibheda / Medratoda: This is due to Vata dushti.24. Hritshoola: is due to Vayu dushti as a result of Avarana by Kapha and Pitta and isalso a symptom of Hridroga due to Madhumeha.25. Amlika: Means Amlodgara as a result of Shuktapaka due to Agnimandya caused bypitta.26. Moorcha: It is also called as moha and defined as Chetanachyuti86 where there isKashtavat patana of the patient and he is unable to experience Sukha and Dukha. This ismainly due to Pitta, Rakta and Tamo guna dushti.27. Nidranasha: It is due to Vata and Pitta vriddhi.28. Panduroga: This is a Pittapradhana vyadhi where due to Dhatvagnimandya, there isRakta dhatu poshaka sara bhaga kshapana leading to Panduroga87.29. Hridgraha: A condition where patient experiences as if his heart is being pulled out itis mainly due to Vata dushti or due to Kaphapitta avarana. 58
  • 78. Review of Literature Upadravas30. Loulya: Is abnormal desire to have all rasa, described as Sarvarasa abhi kanksha likevataja grahani where it is mentioned that guddihi savarasanam88. And it is due to vyadhiprabhava and dathu kshaya.31. Sthambha89: Means Nischalikarana it is due to Vata vriddhi.Gatra stamba is due toojo kshaya.It can be correlated with diabetic neuropathy.32. Kampa: It is due to Vata vriddhi where there is Gatrakampana especially ofHastapada tala.33. Baddha pureeshata/udavartha: Though there is difference between in baddapurishatvaand udavartha the mechanism of manifestation in Madhumeha one and same. Apanavayuin normal course controls the mechanisms of vata, mootra and purisha pravritti. Thusvitiated vata produces badda puishatwa and it further leads to udavartha. The mechanismof constipation is attributed to diabetic autonomic neuropathy.34. Shosha: Occurs due to Dhatu kshaya and vata prakopa.35. Atiprasruta: Is described as Atisrushtam mootram (excessive urination).9036. Angamarda: Udweshtanamiva vedana(Squeezing or twisting type of pain) due toVyana vata dushti.91 Complications of Diabetes mellitus92The complications of Diabetes mellitus can be acute or chronic. Acute complications arethe medical emergency and need immediate medical management, otherwise the patientmay go into coma and ultimately death may occur. Among the acute complications,hypoglycemia is the most serious one encountered in the medical field.They can be classified as follows: 59
  • 79. Review of Literature UpadravasI. Acute metabolic complications:1. Diabetic ketoacidosis 2. Hyperosmolar coma 3. HypoglycemiaII. Chronic complications:A) Angiopathic complications1. Microangiopathic: Retinopathy, Cataract, Glaucoma, Nephropathy, Neuropathy.2. Macroangiopathic: Coronary artery disease, Cerebrovascular disease, Peripheralvascular disease.B) Infections: Skin infections, Pulmonary Koch’s, Urinary tract infections, VaginalCandidiasis, Balanitis, Gangrene of the feet etc.C) Others: Gastro paresis, Diarrhea, Sexual dysfunction.I. Acute metabolic complications:1. Diabetic ketoacidosis: it is seen primarily seen in individuals with Type 1 DM due tothe insulin deficiency. The patient complains of nausea, vomiting, abdominal pain,associated with tachycardia, hypotension, glycosuria, ketonuria, kussmauls respiration,acetone breath, lethargy, central nervous depression followed by coma and death.2. Hyperosmolar coma: It is most commonly seen in elderly individuals with Type 2 DM.Its clinical features include polyuria, orthostatic hypotension, altered mental status,lethargy, seizure and coma. Insulin deficiency and inadequate fluid intake are theunderlying causes of hyperosmolar coma.3. Hypoglycemia: Among the acute complications, hypoglycemia is the most serious oneencountered in the medical field. 60
  • 80. Review of Literature UpadravasII Chronic complications: Blindness is the primarily the result of progressive diabetic retinopathy andclinically significant macular edema. Duration of the DM and the degree of glycemiccontrol are the best predictors of the development of retinopathy. Diabetic nephropathy isthe leading cause of DM related morbidity and mortality. Diabetic neuropathy occurs in approximately 50% of individuals with longstanding Type 1 and Type 2 DM. Diabetic peripheral neuropathy presents with distalsensory loss, hyperesthesia, paresthesia and pain also occurs. Paresthesia ischaracteristically perceived as a sensation of numbness, tingling, burning that begins inthe feet and spreads proximally. Autonomic neuropathy affecting the cardiovascular system causes a restingtachycardia and orthostatic hypotension. Reports of sudden death have also beenattributed to autonomic neuropathy. The most prominent GI symptoms due to autonomic neuropathy are delayedgastric emptying (gastroparesis) and altered bowel motility (constipation or diarrhea).Gastroparesis may present with symptoms of anorexia, nausea, vomiting, early satietyand abdominal bloating. Diabetic autonomic neuropathy may lead to genitourinary dysfunction includingcystopathy, erectile dysfunction, and female sexual dysfunction (reduced sexual desire,dyspareunia, reduced vaginal lubrication).Infections diabetics have increased susceptibility to various infections, such astuberculosis, pneumonia, pyelonephritis, carbuncles and diabetic ulcers. This may due topoor blood supply, reduced cellular immunity or hyperglycemia. 61
  • 81. Review of Literature Upadrava Table No.4 : Samanya Upadrava93,94 Upadravas Charaka Bhela1) Trushna1 + +2) Atisara1 + -3) Jwara1 + -4) Daha1 + -5) Dourbalya1 + -6) Arochaka1 + -7) Avipaka1 + -8) Pootimamsa pidaka2 + +9) Angamarda2 - +10) Kasa2 - +11) Bhrama2 - +12) Tama2 - +13) Shoola2 - + Table No. 5: Vishishta Upadravas95,96,97 Upadrava Sushruta Ashtanga hridaya BhavaprakashaA. Kaphaja Prameha upadrava 1) Makshikopasarpana + - - 2) Alasya + - - 3) Mamsopachaya + - - 4) Pratishyaya/peenasa + + + 5) Shaithilya + - - 6) Arochaka + + + 7) Avipaka + + + 8) Kapha praseka + - - 9) Chardi + + + 10) Nidra + + + 11) Kasa + + + 12) Shwasa + - - B. Pittaja prameha upadravas 1) Vrushana / mushka avadarana + + + 2) Bastibheda + + + 3) Medratoda + + + 4) Hritshoola + - - 5) Amlika + + + 6) Jwara + + + 7) Atisara + + + 8) Arochaka + - - 9) Vamana + - - 10) Paridhupana + - - 11) Daha + + + 12) Moorcha + + + 13) Pipasa / Trushna + + + 14) Nidranasha + - - 15) Panduroga + - - 62
  • 82. Review of Literature Upadrava 16) Peeta vit + - - 17) Peeta mootra + - - 18) Peeta netra + - - C. Vataja prameha upadravas 1) Hridgraha + + + 2) Loulya + + + 3) Anidra + + + 4) Sthambha + - - 5) Kampa + + + 6) Shoola + + + 7) Baddha purushata + - - 8) Udavarta - + + 9) Shosha - + + 10) Kasa - + + 11) Shwasa - + + Table No. 6 : Prameha Pidakas Pidaka Charaka Sushruta Vagbhata (i) Sharavika + + + (ii) Kacchapika + + + (iii) Jalini + + + (iv) Vinata + + + (v) Alaji + + + (vi) Vidradhi + + + (vii) Sarshapika + + + (viii) Masoorika - + + (ix) Putrini - + + (x) Vidarika - + + 63
  • 83. Review of Literature Arista laxana ARISTA LAXANAArista laxana are those signs and symptoms which herald the oncoming death, just as theflowers indicate the next coming fruit, the smoke indicates the fire and clouds the rain.There is no death without arista laksanas and there will be no life after their appearance.Hence the physician should acquire the knowledge of the asrista lakshanas.In Madhumeha the following forms of Lakshanas signal imminent death.1. If a person dreams of drinking various types of sneha in association with chandalas(out cat men) he dies of Prameha.982. If a Madhumehi dreams of consuming water then he dies of Prameha.993. The meeting of the messenger and the physician near the pond or along with waterthen the progress will be bad.4. In spite of regular bath and the application of perfumes if the flies attach concurrentlyon a Madhumeha rogi, then he will die soon.1005. If Madhumeha present with the upadravas it is to be considered as arishta.1016. If he is lethargic, obese, atisnigdha and is a voracious eater, then death impends in theform of Prameha.1027. A person who likes Abhyavaharana and hates Snana and Chankramana will fall victimto the disease Prameha just like the eggs of a Pakshi in its Vasavruksha (Needadruma)that falls prey to its predators, as it is unable to move and rescue itself due to the inherentinertia of the egg.103 64
  • 84. Review of Literature Sapeksha Nidana SAPEKSHA NIDANA Sapeksha nidana plays a vital role in establishing the exact identities of thedisease wherever identical signs and symptoms prevail in two or more diseases making itvery difficult in arriving at a true diagnosis.Regarding diagnosis of Prameha Charaka acharya says that Madhura Mutrapravritti likehoney is manifested in both i.e. Vataja Prameha and Kaphaja Prameha. To differentiateboth these Prameha, knowledge of Nidana Sevana is proper way to reach the diagnosis. IfNidana sevana is Kaphakara, the Mutramadhurya is definitely the manifestation of KaphaPrameha. On the other hand, if etiological factors favor Vata dosha then Vataja Prameha(Madhumeha) may be diagnosed.Until and unless Haridra and Rudhira coloured Mutrapravritti is not associated with thepremonitory symptoms of Prameha, the disease can not be diagnosed as Prameha, but itgoes more in favor of Raktapitta. Here more importance is given to Poorvaroopa ofPrameha and not only to Mutra Pravritti. Regarding Madhumeha, it is to be speciallyemphasized that instead of only Mutra Madhurya, ‘Sharira Madhurya’ is also foundwhich is not present in other types of Prameha. Apart from Mutramadhurya othercharacters of urine are also helpful in differential diagnosis among various Doshikavarieties of Prameha.Here one should essentially consider Madhumeha as a consequence of Vata vriddhi as aresult of Dhatukshaya where Vata is the Anubandhya dosha or Madhumeha as a result ofMargavarana janya vata vriddhi where Vata is an Anubandha dosha and is directlydependent upon Kapha, which has undergone Vriddhi because of Santarpana. The factorsfor differentiation are as follows. (Table no.7) 65
  • 85. Review of Literature Sapeksha Nidana Table No. 7: SAPEKSHA NIDANA Vyadhi bodhaka Madhumeha Madhumeha Nidana (Anilatmaka) (Kaphasambhava) Rogi Krusha, Durbala Sthoola, Balavan Nidana a) Vatakara ahara vihara Kaphakara ahara vihara along with Vata vriddhi as a result of Deerghakaleena madhumeha Rogi avastha b) Beeja uapatapa Madhyama to vriddha Roopa Bala to madhyama vaya Kapha pradhana Samprapti Vatapradhana Kaphamedodushti leading to Madhumeharambhaka dosha Madhumeha arambhaka dushti leading to Vapavahana dosha dushti in Vapavahana dushti especially in Sahaja madhumehi Vyadhiswaroopa Ashukari Chirakari Sadhyasadhyata Asadhya Sadhya in the beginning Upadrava Vata pradhana upadravas Kapha pradhana upadravas Chikitsa Santarpana ApatarpanaMadhumeha is primarily a Medovaha srotodushtijanya vikara but its Pratyatma lakshanasbecome Vyakta in the Mootravaha srotas with abnormal change in the Rasa, Varna, 66
  • 86. Review of Literature Sapeksha NidanaGandha, Sparsha of the Mootra and it is characterized by Prabhoota and Avilamootrata.104 Prabhoota mootrata means Atipravrutti of mootra. It goes without saying that thereis also increased frequency of micturition along with increased quality of urine and Avilamootrata means Atyartha Kalusha Samalam105 or Malinam akulam which means thatthere is a considerable change in the quality of urine as per the above mentioned factors.Considering these factors, it becomes contextual to enumerate the conditions where thereis increased frequency of urine and abnormality in its quality (Table No.9). Most of thetimes these symptoms are associated with Mootravaha srotodusti and other diseases atdifferentiating Madhumeha is not a problem for evident reasons.Differential Diagnosis:106Differential diagnosis between the following types are listed below, Table No. 8: Differential DiagnosisCharacteristics Juvenile or growth Adult or maturity J type onset type I (IDDM) onset type II (NIDDM)Age of onset Childhood or young Middle age or later Young age ageSex incidence Equal More in males -Mode of onset Acute or rapid Incidence IncidenceSymptoms Present Often absent PresentBody weight Often lost Often gained Very leanKetosis Occurs easily Absent Absent 67
  • 87. Review of Literature Sapeksha NidanaInsulin sensitivity High Low LowPlasma insulin Low Normal or increasedResponse to sulphonylurea Poor Good Poor It becomes relevant to consider the following conditions where hyperglycemia isa common manifestation under the heading of differential diagnosis.I. DM & Endocrine disorders:a) Pituitary gland: 1) Pituitary diabetes due to growth hormone, 2) Acromegaly,3) Diabetes insipidus.b) Adrenal Cortex: 1) Cushing’s syndrome, 2) Steroid diabetes due to administration ofsteroids, 3) Primary Hyperaldosteronism.c)AdrenalMedulla: 1)Phaeochromocytoma, 2)Addison’sdisease, 3) Adrenalectomy.d) Thyroid: 1) Hyperthyroidism, 2) Myxoedema.II. Pancreatic Diabetes: 1) Acute pancreatitis, 2) Mumps (rarely), 3) Chronicpancreatitis, 4) Haemochromatosis, 5) Total pancreatectomy, 6) Carcinoma of pancreas.III. Diabetes and Liver: 1) Cirrhosis of liver, 2) Gall Stones.IV. Drugs & Diabetes: 1) Thiazide, Chlorthalidone, frusemide, oestrogen containingoral contraceptives, β blockers & catacholaminergic drugs.V. Miscellaneous: 1) Type I glycogen storage disease, 2) Down’s syndrome,3) Turner’s syndrome, 4) Huntington’s chorea, 6) Burns. 68
  • 88. Review of Literature Sapeksha NidanaConditions where there is polyuria: The Polyuria of DM should not be confused with prostatic hypertrophy or cystitiswhere it is only increased frequency of micturition & not increased quantity.I Polyurea due to water diuresis:a) Cranial or neurogenic Diabetes insipidus: This is due to an identifiable lesion in thehypothalamus, pituitary or both, leading to failure of A.D.H.2) Nephrogenic Diabetes insipidus: Familial form seen in males only, also as anaccompaniment of Fanconi syndrome.3) Psychogenic polydipsia or compulsive water drinking: This is a hysterical condition.There is clinically marked fluctuation here.II Polyurea due to increased solute load: Diuretic therapy and Chronic renal failure. 69
  • 89. Review of Literature Sapeksha nidana Table NO. 9: SAPEKSHA NIDANA Mootra Lakshana (Varna Nimitta) Vikara 1) Avila mootra/mootra dosha/prakupita Ashmari poorva roopa108 mootra Ashmari109 2) Bhasmodaka pratikasham Mutra shukra110 3) Bastagandhitvam Ashmari poorvaroopa111 4) Gomeda prakasham Ashmari 5) Guru a) Kaphaja arsha112 b) Vata kundalika113 6) Haridram a) Paittika gulma114 b) Pattika arsha115 c) Vishamasannipata jwara116 d) Kamala117 e) Paittika mutrakrichra118 f) Rakta pitta poorva roopa119 g) Paittika udara120 h) Ushna vata121 i) Nanatmaka pitta vikara122 7) Krishna a) Vatika arsha123 b) Vatika gulma124 c) Asadhya kamala125 d) Paittika mutrakrichra126 8) Picchilam a) Kaphaja arsha127 b) Kaphaja mootra krichra128 c) Kaphaja mootraiikasada129 9) Pita a) Paittika arsha130 b) Halimaka131 c) Paittika Jwara132 d) Kamala133 e) Kshiralasaka134 f) Mutrasada135 g) Paittika mutrakrichra136 h) Pandu purvaroopa137 i) Paittika pandu138 j) Paittika trushna139 k) Paittika udara140 l) Ushna vata141 m) Basti vidradhi142 10) Rakta (Sarakta, Sasruk, Sarudhira, a) Rakta vruddhi143 Raktabham) b) Ashmari144 c) Sannipata jwara145 d) Asadhya kamala146 e) Ksata kshina147 f) Mutrasada g) Mutrotsanga148 h) Paittika mutra krichra i) Raktaja mutra krichra149 j) Raktapitta poorva roopa150 k) Ushna vata151 11) Sarkara saha Sarkarashmari 70
  • 90. Review of Literature Sapeksha nidana 12) Sita (Sitalam) Sannipatika mutra krichra 13) Sasikatam (Sikatanuviddam matam) Ashmari 14) Snigdha a) Kaphaja arsha152 b) Kaphaja mutra krichra153 c) Kaphaja basti kundala154 15) Shukla (Shweta, sita) a) Kaphaja arsha155 b) Kaphaja gulma156 c) Kaphaja jwara157 d) Mutra sada158 e) Kaphaja mutrakricchra159 f) Kaphaja pandu160 g) Kaphaja udara161 h) Kaphaja unmada162 i) Kaphaja bastikundala163 16) Shyava a) Vatika arsha164 b) Vatika udara165 Mootralakshana (Pravartana Nimitta) Lakshana1) Abhikshnam (Muhuh muhuh, Punah punah a) Ashmari166subahushah, vikiranam b) Mutratita167 c) Vatika mootrakricchra168 d) Ushna vata1692) Atipravrutti a) Amavata170 b) Arsha poorvaroopa171 c) Sahaja arsha172 d) Kaphaja arsha e) Mutra praseka173 f) Upasthita prasava174 g) Chidrodara175 h) Asadhya masurika176 i) Ama jwara177 71
  • 91. Review of Literature Sadya asadyata SADHYASADHYATHA A forecast of the probable course and termination of a disease is prognosis orsadhya asadhyatha. Madhumeha has been described as Anushangi, which meansPunarbhavi. Therefore, one should make all efforts to prevent and control it.Sadhyata of Kaphaja Prameha178: The ten Kaphaja pramehas are described as Sadhyabecause of the following reasons.179 a) Samakriyatvat b) Atishayena medo dushitam nabhavat.A. Samakriyatvat: Tulya dushyata180 is a determinant of Sadhyata in Madhumeha, whichmeans the Guna of the Dosha and Dushya involved are the same. This makes thetreatment easier because the Katu, Tikta, Kashaya rasa and Tikshna, Ushna guna, whichare antagonistic to Kapha, are the same for Medas, Mamsa, Kleda, Lasika, and Rasa etc.Dhatu. Hence due to Samakriyata, Kaphaja meha are Sadhya. This is the early stage ofMadhumeha.B. Atishayena medo dushitam na bhavat: Kaphaja mehas are characterized by lessinvolvement of Dhatus. Here, predominant symptoms of only Kapha are only seen;therefore, Madhumeha is Sadhya in this stage. Moreover other Dhatus are not muchinvolved in this stage and Upadrava are not manifested.Yapyata of Pittaja Prameha: The six Pittaja mehas are described as Yapya because ofa) Vishamakriyatva, b) Atrapi atishayena medo na dushtava and c) Samsrushta doshameda sthanatvat181.a) Vishamakriyatvat: The Dosha Pitta and the Dhatu Medas, Rasa, and Mamsa haveViruddhaguna, which makes the Chikitsa Vishama i.e. if Pitta is treated with Sheeta andMadhuradi dravya, they are antagonistic to Pitta but are Medo- rasadi dhatukara and if 72
  • 92. Review of Literature Sadya asadyataMedo-rasadi dhatu are treated with Tikshna Ushnadi dravyas, they cause Pitta vriddhihence defeating the purpose of Shuddha chikitsa. Hence Pittaja Prameha are Yapya.b) Atrapi atishayena medo na dushtatvat: Pittaja prameha also are characterized byrelatively less involvement of Dhatu as suggested by the term “Atrapi” which means thatthe involvement of Medas and other Dhatu is too severe for it to be Sadhya, yet notsevere enough to be Asadhya. Therefore this stage of the disease is Yapya.c) Samsrushta dosha meda sthanatva: Means “Sannikrushtam doshasya Pittasyamedashcha sthanam yasmat” i.e. proximity in the Sthana of Medas and Pitta hence Pittajapramehas have been called Durjaya. The Sthana of Pitta is Amashayam and that ofMedas is Vapavahana. There is proximity or Pratyasannata of these Sthanas in the Koshtaas described by the term Ekadesha. Hence there is a mutually contradictory environmentin Ekadesha; the result is Vishama kriya of the Chikitsa and therefore Pittaja pramehasare Yapya.Asadhyata of Vataja Prameha: The four Vataja Prameha are considered Asadhya dueto a) Mahatyayatvat, b) Viruddhopakramatvat.a) Mahatyayatvat: means Majja prabhrutisarabhoota dhatukshaya or ashukariDue to this guna all the Dhatu including the Gambhira dhatus undergo Nasha, Kshaya &Apakarshana.This process involves multiple Srotas producing Upadrava and is henceMahavyapattikara, which means that the disease is much too savere to sustain life.b) Viruddhopakramatvat182: The Chikitsa of Vataja Prameha involves Viruddhopakramawhich means there is a mutual contradiction in the treatment modalities as use of Snigdhaetc. are Pathya for Vata but Apathya for Medas. Hence the disease is Asadhya. 73
  • 93. Review of Literature Sadya asadyataOther situations determining Asadhyata of Madhumeha:1) Madhumeha with all Poorvaroopa183 : It has been said by Charaka that if a disease inRoopavastha has all the Poorvaroopa manifested then the disease becomes Asadhya184 .Based on this principle, the inherent nature of Sadhya Asadhyata of Kaphaja, Pittaja andVataja meha undergoes modifications as follows.a) Sadhyata of Kaphaja meha attains Asadhyata when associated with all Poorvaroopas.b) Yapyata of Pittaja meha attains Pratyakhyeyata when associated with all poorvaroopa.c) The severity of Asadhyata increases when associated with Poorvaroopa. Vataja Prameha has already been described as Asadhya but this term has to beanalytically interpreted in the two clinical types of Vataja mehas viz. Dhatukshaya janyaand Margavarana janya.2) Jatah Madhumeha is Asadhya due to Beeja dosha as there is an irreversibleMadhumeharambhaka dosha dusti since the birth itself185.3) Madhumeha with Pidaka is Asadhya4) Madhumehi who has Bala mamsa kshaya can be left untreated186.5) All Pramehas if left untreated terminate into Madhumeha which is Asadhya187.6) Prameha with Gadha upadravas and Atiprasruta mootra is Asadhya.7) Pramehas with Arishta laxana is Asadhya.8) A patient who hates hygienic habits like Snana, Chankramana and one who hasMandotsaha, who is Atisthoola, Snigdha and Mahashana dies of Prameha188. 74
  • 94. Review of Literature Sadya asadyata Prognosis189 The prognosis in diabetes has improved steadily since the introduction of insulin,but even with its use the average exception life of diabetic is still less than that of nondiabetics. It may be difficult to estimate the prognosis of an individual patient because somany variable factors have to be considered. The working capacity and longevity of adiabetic patient to a great extend depends on the timely recognition of the disease, itsseverity, complications, the age of patient and proper treatment. If diabetes develops atearly age shorten is the patients life span. The prognosis of diabetes mellitus is mainlydetermined by the degree of affection of the cardio-vascular system. The commonestcause of the death in diabetes mellitus are pathological conditions of vessels. (Myocardialinfarction, thrombosis of cerebral vessels etc.) in the neuropathy at young age.The patients having mild diabetes are capable in their works. In moderate and severeforms of the diabetes the working capacity is assessed individually depending on thecourse of diabetes mellitus and concomitant diseases. 75
  • 95. Review of Literature Chikitsa CHIKITSA In general Chikitsa is the method adopted for eradication of the disease from thebody. The aim of treatment is to restore swasthya. That means to restore normal functionsof agni, dosha, dhatu, mala and maintain mental health. The primary importance ofChikitsa lies in samprapti vighatana.SAMANYA CHIKITSA:Nidanaparivarjana in Margavarana janya Madhumehi: An pathyanimittajamadhumehi usually Sthoola, who likes Abhyavaharana & hates Chankramana is in asituation just like of the helpless eggs on a tree, they cannot move to avoid their predators& hence fall victim to them. Here, the patient should be made to avoid all Kaphakaraahara vihara either to prevent the occurrence or to cure the disease.Nidana parivarjana in Dhatu kshaya janya Madhumehi190: Nidana parivarjana insuch Madhumehis is studied with special reference to Sahaja madhumeha. It lies entirelyon the Mata or Pita as to how best they act to prevent the occurrence of the disease inthem. They should avoid the Beeja, Beeja dhaga or Beeja bhaga avayava upatapa leadingto Madhumeharambhaka dosha dushti.Apakarshana & Prakruti Vighatanana: The Apakarshana of Doshas are mainly donethrough Samshodhana but only when Roga & Rogi bala are in Pravaravastha and wheneither one or both are Avara, then it is done through Langhana and Langhana panchana,which constitutes Samshamana chikitsa, in other words Prakruti vighatanana.Apakarshana in Margavarana janya Madhumeha: Shodhana especially Vamanashould be preferred in a Madhumehi if the Dhatukshaya is minimum & there are Kapha& Medodushti lakshanas. If there are Pittaja lakshanas & Dhatu kshaya does not render 76
  • 96. Review of Literature Chikitsathe patient Durvirechya, then Virechana can be performed. Similarly, if the Anubandhavata lakshanas are more and the patient is Samshodana arha then Basti can be performed. Madhumeha is a Swedana anarha vyadhi191 but Niragni sweda in the form ofVyayama is indicated. The selection of Yogas for Samshodhana & Snehana should beselected as per the recipes prescribed in Kalpa sthana. After Shodhana, Shamana chikitsacan be done by Kaphamedohara dravya.Prakruti vighatana in Dhatu kshaya janya Madhumeha: Dhatu kshaya avastha is theresult of Beeja dushti in Sahaja madhumeha & due to a state of Atikarshita dhatus as aresult of continued Dhatu kshaya, which in fact is the progressed stage of Margavaranajanya madhumeha. Both the situations are considered Samshodhana anarha192. In suchcases, Samshamana chikitsa is advised, whereas Madhumeha in both these cases areAsadhya and hence need not be treated. Notwithstanding this, the principles of chikitsafor Vataja pramehas are for Vata anubandhadoshatva, which is still dependent on theKapha & Pitta doshas and not for Vvata anubandhya dosha janya madhumehacharacterized by Atishaya karshana of Dhatus. Hence Samshamana chikitsa should beappropriately adopted in such patients.AVASTHA ANUSARA CHIKITSA OF MADHUMEHA193: Sushruta in the chapter of Prameha pidaka chikitsa has identified the stages ofMadhumeha & accordingly advised the treatment, which can be discussed as follows:Stage I: Is the Poorvaroopa avastha where the Dosha dushya sammurchana has justbegun, the disease should be treated with Apatarpana, Vanaspathi kashaya andChagamootra. If left untreated, Madhumeha proceeds to the II stage. 77
  • 97. Review of Literature ChikitsaStage II: This is the Vyakta avastha of Madhumeha where, due to continued Madhuraahara sevana, the Sweda, Mootra and Sleshma attain Madhura bhava & hence should betreated with Ubhaya samshodhana i. e. Vamana, Virechana & Basti. If left untreated, thedisease progresses to stage III.Stage III: In this stage, the Mamsa & Shonita undergo Pravruddha dushti causingShopha & other Upadravas and these should be appropriately treated as mentionedaccordingly, like Siramokshana in Shopha. If left untreated, the disease progresses tostage IV.Stage IV: In this stage, the Upadravas like Shopha would have attained Ativruddhaavastha, manifesting symptoms like Ruja & Vidaha, where Shastra chikitsa andVvranakriya should be performed. If neglected, the disease proceeds into Asadhyaavastha, which is the V & final stage.Stage V: In the Asadhya avastha, the Upadravas become Mahantha & makes the diseaseAsadhya, like here when the Pooya of Pidakas attain Abhyantaraprapti and becomeUtsanga.Analysis: Though explained as Prameha pidaka avastha chikitsa, description of stagewise progression of the disease and the treatment has been done by Sushruta on thepretext of explaining the Prameha pidaka chikitsa. This description seems to be Chikitsain case of Apathyanimittaja madhumeha, the course of this illness has been discussedalready under Samprapti & accordingly in the Poorvaroopavastha, Sushruta advisesApatarpana & other Shamana dravyas as there is Alpadosha & Alpa dhatu dushti. Hence,unless the need arises, Samshodhana is not the treatment of choice and as the Lakshanasare predominantly due to Kapha, Kaphahara chikitsa should be done & this seems to be 78
  • 98. Review of Literature Chikitsathe logic behind prescribing Apatarpana & Tikshna dravyas like Chaga mootra. Whereasin Vyakta avastha there is Bahu dosha & a relatively Alpa dushti of dhatu like Medas &Rakta which warrants Shodhana, accordingly Vamana, Virechana & Basti have beenadvised as the Rogi is still Balavan & Sthoola & so, Shodanarha. In the next stages, there is a progressive Dhatu kshaya & production ofUpadravas. The patient is Shodhana anarha & there is Vata pradhanyata. Hence, onlyShamana chikitsa & respective Upadrava chikitsa should be done. Sushruta has stressedthe importance of timely intervention in Madhumeha because in case of negligence, thedisease progresses involving Gambhira dhatus & the Upadravas pervade the entire bodymaking it Asadhya.SANTARPANA APATARPANA CHIKITSA IN MADHUMEHA: Madhumeha has been described as Santarpanotha vyadhi as well asApatarpanotha vyadhi. The former is Apathya nimittaja madhumeha & latter is Sahajamadhumeha or Madhumeha due to Dhatu karshana due to long standing Prameha.Accordingly, two forms of Madhumehis are encountered, one who is Sthoola & Balavanfor whom Apatarpana is the best & the other who is Krusha & Paridurbala for whomSantarpana is the best.I. Apatarpana chikitsa194: is done in the form of Langhana, Langhanapachana &Doshavasechana.a) Langhana this is done in Alpadoshavastha where only Upavasa, Pipasa, Maruta, Atapasevana, Rooksha udvartana, Pragadha vyayama, Nishi Jagarana & so on, which areKaphamedohara are helpful. 79
  • 99. Review of Literature Chikitsab) Langhanapachana: This is done in Madhyamadoshavastha where along withLanghana, Ama pachana is done with Tikshna, Ushna dravyas.c) Doshavasechana: This is done in Bahudoshavastha where the Shodhana of Doshas isdone from Ubhaya margas.II. Santarpana Chikitsa: Laghusantarpana chikitsa is Prashastha for Krusha andDurbala rogis195. The following can be administered in Madhumehi. a) Mantha b)Kashaya c) Yava d) Churna e) Lehya f) Laghu Bhakshya. These formulations should beprepared such that they cause Santarpana without causing Vriddhi of Kapha & Medas.Among all these, Yava is considered as best for Madhumehi, which will be discussed inthe chapter of Pathya apathya.Shreshta Aushadha prayoga in Madhumeha:Shilajatu, Guggulu, Loharaja: These Dravyas are medicines par excellence inMadhumeha, either in Krusha or Sthoola, as they are Virukshana & Chedaneeya, which isgood for Kapha, as well as Rasayana, which is good for Dhatukshaya & Vatavriddhi. TREATMENT196(A) Goals of treatment of diabetes: Diabetes mellitus requires ongoing medical care as well as patient and familyeducation both to prevent acute illness and to reduce the risk of long term complications.The therapeutic objective is to restore known metabolic derangements towards normal inorder to prevent and delay progression of diabetic complications. The management ofdiabetes patient is not aimed solely at glycaemic control various aspects requiringassessment and control. The aims of treatment have been varied according to an arbitrarydivision of patients into three categories ranging from those in whom symptomatic relief 80
  • 100. Review of Literature Chikitsadone seems the most appropriate or any attainable goal to those in whom an attempt atmaximal prophylaxis against future tissue damage seems desirable and possible(B) Treatment regimens:(i) Diet: A well-balanced nutritious diet remains a fundamental element of therapy. Inobese patient with mild hyperglycemia the major goal of diet therapy is weight reductionby caloric restriction.1. Intake of protein and carbohydrate according to the recommendation of Americandiabetes association.2. Dietary fibres: Food such as oatmeal cereals and beans with relatively high solublefibre content as staple component of the diet in diabetes. These tend to retard nutrientabsorption rates so that glucose absorption is slower and hyperglycemia may be slightlydiminished high soluble fibre content in the diet may also ha favorable effect on bloodcholesterol levels.3. Artificial sweeteners: Diabetes can use artificial sweetness like aspartame, sucralose,acesulfame.(ii) Oral anti diabetic agents: oral drugs are used to lower Blood glucose level by achieving following goals.1. Drugs that primarily stimulate insulin secretion.2. Drugs that alter insulin action.3. Drugs that principally affect absorption of glucose. 81
  • 101. Review of Literature Chikitsaa) Sulphonylureas:Mode of action: Stimulate production of insulin by increasing number of insulinreceptors.Indications: 1) Maturity onset (Insulin dependent) diabetes of average wt. not controlled by diet. 2) Diabetes or normal weight stabilized on insulin dosage not more than 30 units per day who have never been ketotic. 3) Failure to lose weight when this is indicated.Contra-indications: 1) Juvenile diabetes. 2)Patients with ketosis. 3)Obese adult-onset uncontrolled diabetics (Biguanides can be used). 4)Insulin taking diabetics. 5)Presence of renal, hepatic or cardio respiratory disease or alcoholic abuse (because of increased risk of lactic acidosis)Adverse effects: 1) Hypoglycaemia: Most frequent with glibenclaimide also chlorpropamide. Increase in hypoglycaemic effect if concomitant use of sulphonamides, salicylates, phenylbutazone, Monoamine oxidase inhibitors. 2) Dyspepsia. 3) Skin rash including photosensitivity, rarely exfoliative dermatitis. 4) Facial flushing after ingestions of alcohol (mostly chlorpropamide) 5) Cholestatic Jaundice (chlorproppamide) 6) Blood dyscariasis (rare). 82
  • 102. Review of Literature ChikitsaDrug Interactions With Sulphonylureas: A) Increased hypoglycaemic action-beta-blockers, sulphonamides, phenylbutazone, chloramphenicol, cyclophosphamide, salicylates, dicoumarol, and monoamine oxidase inhibitors. B) Decreased hypoglycaemic action-Adrenergic compounds, corticosteroids, oestrogen containing oral contraceptives, thiazide, diuretics, and phenytoin.Biguanides:Mode of action: Major effect is to increase peripheral uptake of glucose and in largedoses to dealy or decrease intestinal absorption. Biguanides do not cause hypoglycaemia.Indications: 1) Treatment of maturity onset, diabetic who failed to lose weight on diet. 2) In combination with sulphonylureas-To enchance the inadequate or failing effects of sulphonylurea. 3) As an adjunct to insulin therapy in brittle diabetes whose blood sugar tends to swing unpredictably, one who is prone to ketosis and who develops hypoglycaemia with only slight overdose of insulin.Adverse Effects: 1) Malaise, weakness, drowsiness. 2)Metallic taste in mouth, anorexia, nausea, dyspepsia, diarrhoea. 3)Lactic acidosis. 4)Vitamin B12, malabsorption (after prolonged treatment).(iii) Insulin: Insulin is indicated for type – 1 diabetic as well as for type - 2 diabetic patientswhose hyperglycemia does not respond to diet therapy either alone or combined with oral 83
  • 103. Review of Literature Chikitsahypoglycemic drugs. Insulin injections are very much necessary in severe conditions ofhyperglycemia. There are various preparations are present depending upon their purity, solubilityand species (like Human / Bovine ).Four principle types of insulins are available.1. Ultra - short acting with very rapid onset and short duration2. Short acting with rapid onset of action3. Intermediate acting4. Long - action with slow onset of action. The injection can be given with the help of syringes with half inched ultra fineneedles attached available in 1 ml, 0.5 ml, 0.3 ml and 0.25 ml sizes. For the injection anypart of the body covered by loose skin can be used such as abdomen, thigh, upper arms,flanks and upper buttocks.(iv) Insulin - like growth factor-1 (IGF - I) therapy(v) Aspirin therapySteps in the management of diabetic patients:(A) Diagnostic examination: All necessary examinations should be done for the diagnosis including all systemic examinations and with the help of proper history.(B) Patient education (Self management training): Since diabetes is a lifelong disorder, education of the patient and the family is probably the most important obligation of the physician who provides initial care.Advice:1. To check regular blood sugar level 84
  • 104. Review of Literature Chikitsa2. Maintain diet control The teaching curriculum should include explanations by the physician or thenurse the nature of the diabetes and its potential, Acute and chronic hazards and how theycan be recognized early and prevented or treated.(C) Self - monitoring of blood glucose. Monitoring of blood glucose by patients has allowed greater flexibility inmanagement while achieving improved glycemic control.Initial therapy: Treatment must be individualized on the basis of the type of diabetes and specificneeds of each patient.(1) The obese type 2 patient: The most common type of diabetic patient is obese A) Weight reduction 1.By means of use of prescribed diet and diet control 2.By means of exercise to expand energy. b. Hypoglycemic agents:(2) The non-obese patient Treatment mainly depends upon the blood glucose level. a. Diet therapy: Diet with caloric content sufficient to maintain ideal weight Restrictions of saturated fat and cholesterol are also strongly advised. b. Oral hypoglycemic agentsComplication management: According to the complication and its severity. 85
  • 105. Review of Literature Pathya Apathya Pathya ApathyaGeneral considerations on sthoola and krusha Madhumeha patients Pathya differ from one set of patients to another like the difference of treatment inthem. In sthoola Madhumeha there is marga avarodha of vayu by vriddha kapha andmedas. Hence to rectify the imbalance of the dushyas and to reduce the amaroopi medas,the patient should be advised to follow the following diet. 1) The diet which aims to wards the alleviation of kapha dosha and medodathu. 2) The diet which inhibits the vitiation of vayu. 3) The diet which gives strength to the body. 4) The diet which is having low caloric value and low glycemic index are to be suggested to the patients.Ahara:In general, Ahara, which are Vatamedokara are Apathya in Madhumeha. In other words,Madhumehi should be cautious about taking Ahara, which is Madhura rasa pradhana,Guru and Abhishyandi. It is advised to follow the general principles of food intake as laid down in Ashtavidha ahara vidhi vishesha ayatanas with special emphasis on Matra. One should alwaysavoid Adhyashana, Vishamashana and Atimatra bhojana. In case of Sthoola Madhumehi,Ushna, Tikshna, Lekhana, Virukshana and Chedaneeya aharas can be used liberally,where as in Krusha Pramehi Laghu and Santarpana ahara, which is not Vatamedokara,should be given; which means foods like Yava are ideal. Taila, Ghrita etc Snigdhadravyas, which are basically Vatakara, can be used after Samskara so that they arerendered Tarpaka as well as Vatamedohara qualities. Laghu, Tarpaka Pathya kalpana like 86
  • 106. Review of Literature Pathya ApathyaYusha, Mantha, Yavagu, and Kashaya etc prepared from Kaphamedohara dravyas can beused generously among the Pathya mentioned for Madhumeha. Tikta Rasa, Yava andMadhu are seen to be indicated high in the priority lists of Ayurvedic classics.Importance of Tikta rasa197,198 Madhumeha arambaka dosha is kapha, though the arambaka dosha is vayu here,the vayu is in avrita avastha. Hence tikta rasa pradhana dravyas are beneficial. Tikta islaghu and ruksha where as kapha is guru and snigdha. Tikta rasa is having more laghu quality than other rasa likewise it is having veryless rukshata among kashaya, katu, and tikta rasa. Tikta rasa helps in decreasing kapha,shareera kleda (through shoshana) and meda, which are known as the important factorsinvolved in Madhumeha. It helps in reducing factors involved in the Madhumeha it helpsin reducing the dravatwa of mootra. Dravatwa then leads to the decrease of saratwa hencethe frequency and quantity of mootra will be reduced thorough tikta rasa sevana.Karavella, boomyamalaki, etc., are to be used.Importance of yava199: yava is the best among the diets. In prameha yava is the diet ofchoice, yava can be consumed in different modes of preparation yavana, yavamahada etc.in chikitsa shastra it had been claimed that yava manda increases the quantity of mootra,and yava kshara is known as mootrala. Hence a doubt arises whether yava is advisable inMadhumeha. Infact yava is mootra vriddikaraka. To be precise it reduces, the dravagunaof mootra and hence reduces frequency and quantity of urine. Along with these, yava isrooksha and laghu and helps in bringing the vitiated kapha dosha to normalcy. Susrutahas termed yava as ‘atirooksha and prabhada mootra’ in actions, the person who is 87
  • 107. Review of Literature Pathya Apathyaaffected by santharpanotha Madhumeha must perform vyayama, rooksha udvarthana,ratri jagarana and others which will combat kapha and pitta.Vihara200: Chankramana, Snana and Asana, four Kaya Viharas viz., Vyayama, Mrija,Nishi gamana, and Jagarana are potent Vatamedohara viharas which can be performed inincreased magnitude by a Sthoola Madhumehi as he is Balavan. In a Krusha Madhumehi,these should be advised depending on his Bala. If a Krusha rogi is unable to performVyayama then only Mrija and Chankramana can be advised with some Vishama shareeranyasa. Among Viharas, Vyayama figures prominently in the classics as an effectiveVatamedohara vihara. Pragadha vyayama can be performed depending on one’s owninterest and knowledge. Vishama shareera nyasa can be performed by both Sthoola andKrusha Pramehi in the form of Yogasanas but one should be careful while performingthese as they can be harmful if improperly performed. A regular and sustained exerciseregimen is beneficial.Vyayama201: Any Karma or action of the body that produces Shareera ayasa is Vyayama.Vyayama is Alasyahara, Sthoulya apakarshaka and causes Sthiratva, Laghuta andAgnideepthi; the person becomes Klama, Pipasa, Ushna, Sheeta, Klesha-saha. Vyayamashould be performed to a man’s Ardhashakti. Otherwise, it can be harmful. Vyayama thusis ideal in Madhumeha especially in Sthoola and Balavan.Yogasana202: The severe diabetics can be advised to perform yogasana because inyogasana both the body and mind gets steadiness without any physical exertion or stress. 88
  • 108. Review of Literature Pathya ApathyaPranayama and Meditation: Breathing exercise and meditation techniques are alsoproving as an effective panacea in stress management, thus acting synergistically inDiabetic management. Meditative techniques like transcendental meditation of MaharshiMahesh Yogi, Sudarshana kriya of Pandit Sri Sri Ravishankar are popular innovations inthis field.Vichara203, 204: Manas is among the adhistanas of Vyadhi. Rajas and Tamas are the doshaof Manas, which get aggravated by Udeerana of Dharaneeya vega like Icha, Dwesha,Moha, Krodha, Irshya, Mada, Matsarya and Shrama. The upaya for dharana of these vegais by Indriya Nigraha. Due to Prajnaparadha, Rajo and Tamo dushti occur. This leads tomanifestation of Manasika roga. In milder forms of involvement of dosha leads tohastening of development or aggravation of a Vyadhi. Hence Manasika dosha should bebalanced well by resorting to Jnana, Vignana, Atma Jnana etc. The Manasika dosha areinterrelated to Shareerika dosha. Tamoguna increases Kapha and Rajoguna increasesVata and Pittta. Hence all these should be avoided. Rajo guna is the motivator of mindinto activity under normal circumstances. Hence mind should be motivated into Vyayamaand other activities, which help in reducing Vata and Medas.APATHYA:Apathya Vichara in Madhumeha has been summarised in table.LIFE SYTLE MODIFICATION IN THERAPY OF DIABETES205:Diet: Before the discovery of insulin(1921) the only treatment available for the diabeticswas diet therapy. This meant starvation and no carbohydrates. Over the past few decadesdiet therapy has revolutionized. Present scientific concept is, as a diabetic, one can eatnormal diet and choose variety of food stuff available, provided the quality and quantity 89
  • 109. Review of Literature Pathya Apathyais balanced and total calories are proportionate to ones ideal body weight. Diabetes ismodal disease where proper diet therapy can make wonders.For type 1 diabetes neither diet nor exercise can be regarded as a primary modality oftreatment. In contrast, both are primary therapeutic options for management of type 2diabetes. Their potential however is limited in most instances due to poor compliance.Dietary management of diabetes should not only aim to achieve glycaemic control, butalso to normalise dislipidaemia, commonly associated with diabetes. The carbohydratecontent in the diet, the type of fat, quantity and type of protein has been altered from timeto time to meet these needs.Carbohydrate content of the diet has to provide 50-60% of the calories and most of this isto be in the form of complex carbohydrates with a high fibre content and low glycaemicindex. Fat content of the diet should provide 20-25% of the calories distributed in theratio of 1:1:1 among saturated, monosaturated and poly unsaturated fatty acids (PUFA).PUFA content of less than 10% of the total calories and an EFA content of at least 3% ofthe total calories is advisable with the n6/n3 ratio being less than 10. Protein intake0.8g/kg is recommended, so as to contribute to 12-20% of the total calories. Vegetableproteins are preferred due to their high fibre content and absence of saturated fat that ispresent in animal proteins. A low fat diet also improves the lipid profile.ALCOHOL:Alcohol intake increases the risk of hypoglycaemia, may induce keto-acidosis, lacticacidosis, and may contribute peripheral neuropathy. Alcohol is also an additional sourceof calories, each ml provides 7k.cal and should therefore be avoided as per as possible. 90
  • 110. Review of Literature Pathya ApathyaCESSATION OF SMOKING:Smoking in addition to being an independent risk factor for development of type 2diabetes mellitus also contributes to the development and progression of the macro andmicro vascular complications of diabetes. Cigarette smoking is associated with anadverse effect on the serum lipids and lipo-proteins. Increase in the platelet reactivity isseen in hyper cholestrolaemic patients who smoke cigarettes. The effect of cigarettesmoking on the lipid profile is not limited only to smokers. A reduction in HDLcholesterol levels is noted even in children passively exposed to cigarette smoke at home.There is also evidence that smoking cessation reduces the risk of morbidity and mortalityfrom coronary artery disease.EXERCISE:Exercise constitutes the first step in the treatment of type 2 diabetes along with diet. Itimproves the condition of a diabetic patient due to several factors. There is an increase inthe number of insulin receptors as well as the sensitivity of insulin receptors. In additionthere is an elevation of 2-3 DPG levels in the RBC and reduction in HbA1C. Thesepromote the delivery of oxygen to the peripheral tissues, which result in the improvedefficiency of the diabetic. The best form of exercises recommended to a diabetic is stepwise increase of aerobic exercise. On the other hand isometric exercise like weight liftingsustained hand grip are to be avoided in diabetics as they increase arterial pressure.YOGIC PRACTICES:Recently several well planned studies have demonstrated the beneficial effects of yogicpractices in diabetics. Patients with diabetes demonstrated a significant fall in fasting and 91
  • 111. Review of Literature Pathya Apathyapost prandial blood sugar values and HbA1C with reduction in the requirements of oralhypoglycemic agents and insulin. Patients with type 1 diabetes, with brittle diabetesshowed marked improvement with practice of yoga. There was a salutary affect on thelipid profile with fall in serum cholesterol, triglycerides and HDL cholesterol fraction.Certain asana have been identified as useful in the control of diabetes. 92
  • 112. Review of Literature Pathya Apathya 206, 207, 208,209 Table No. 10: Pathya in Sthoola Madhumehi Sl. Ahara Sl. Vihara No. No. 1) Patha 1) Vividha vyayama yoga 2) Haritaki & Madhu 2) Niyuddha 3) Chitraka 3) Kreeda 4) Mridvek 4) Gajaturaga charya 5) Kapitha + Maricha + Madhu annapana 5) Ratha charya 6) Ustra,Ashwa, khara pureesha churna 6) Padaticharya ashana 7) Parikramana 7) Shyamaka 8) Padaticharya 8) Neevara 9) Astropastrabhyasa 9) Amalaka 10) Mrugaihi saha vaset 10) Tinduka 11) Apatarpana 11) Ashmantaka phala 12) Samshodhana 12) Mudgayusha 13) Pragada udvartana 13) Triphala 14) Snana jalavasekaihi 14) Trikatu Sl. Vichara 15) Trimada No. 16) Draksharista 1) Chinta 17) Yava Bhakshya 18) Arishta Kashaya Avalehya 19) Jangala Rasa 20) Shulya mamsa. 93
  • 113. Review of Literature Pathya Apathya 208, 210, 211 Table No. 11: Pathya in Krusha Madhumehi Sl. Ahara Sl. Vihara No. No. 1) Aviruddha annapana 1) Padratrana 2) Rasagandhavathi annapana 2) Atapatrarahito 3) Hingu yukta yusha 3) Brikshyashi 4) Saindhava yukta yusha 4) Gramaikatravasi 5) Sarshapa yukta yusha 5) Krushet 6) Mudgadi yusha & Odana 6) Khanet Kupam 7) Mantha of all Dravyas mentioned as Pathya for Krusha 7) Shilonchavruthihi 8) Kashaya 9) Yavadi churna Sl. Vichara No. 10) Lehya of Yavadi 1) Muniriva samyatatma 11) Odana of Laghu tarpaka dravyas 2) Brahmarathamuddreth 12) Vatya of Laghu Tarpaka dravyas 13) Madya of Yavadi 14) Saktu of Yavadi 15) Apoopa of Yavadi 16) Vishkira mamsa 17) Pratuda mamsa 18) Yava churna soaked in Triphala Kwatha overnight, next day taken with Madhu & Saindhava19) Yava saktu mixed with Haritaki, Amalaki etc. kwatha along with Guda, made into Apoopa 20) Purana shali odana 21) Tikta shakha odana 94
  • 114. Review of Literature Pathya Apathya Table No. 12: Apathya Ahara, vihara, vichara212, 213, 214,215 Ahara Ahara Vihara 1) Picchila 30) Nava Madya 1) Divaswapna 2) Sheeta 31) Gramya mamsa 2) Avyayama 3) Guru 32) Anupa mamsa 3) Alasya 4) Snigdha 33) Matsya 4) Mrija tyaga 5) Drava 34) Nava Hayanaka 5) Asana sukha 6) Abhishyandi 35) Nava Yavaka 6) Anya slesha meda 7) Atipramana 36) Nava Chinaka mutra kriya 8) Adhyashana 37) Nava Uddalaka 7) Snana tyaga 9) Virudhashana 38) Nava Naishadha 8) Chankramana Tyaga 10) Madhura 39) Nava Itkata 9) Rakta Mokshana 11) Amla lavana 40) Nava Mukunda 10) Swedana 12) Kaphakara 41) Nava Mahavrihi 11) Dhoomapana 13) Medokara 42) Nava Pramodaka 12) Mootravegadharana 14) Mootrakara 43) Nava Sugandhaka 13) Sheetala Jalasnana 15) Sauvira 44) Nava Kalaya 14) Pushpa sugandha 16) Tushodaka 45) Masha 15) Snehana 17) Shakti 46) Tila 16) Dushtambu snana 18) Maireya 47) Palala 17) Shareerika Ashrama 19) Sura 48) Dadhi 18) Vidhivarjita shayana 20) Asava 49) Nava Annapana 19) Vyavaya 21) Toya–Dushta 50) Kshara Vichara 1. 22) Paya 51) Nishpava Bhaya 23) Taila 52) Dushtambu 2. Krodha 24) Ghrita 53) Kushmanda 3. Shoka 25) Ikshuvikara 54) Bhojanante 4. Alasya 26) Dadhivikara Jalapana 5. Loulya 27) Pistanna Souhitya 6. Mandotsaha 28) Amlayavagu 7. Abhyavaharyeshu 29) Amlapanaka Grudhnus 8 Asatam Sanga 95
  • 115. Drug Review Asanadi Kwatha DRUG REVIEW Drug plays a vital role in the management of the disease. Due to this reason; it hasbeen placed next to physician in the Chatushapada. The comprehensive knowledge of thedrug is very important to physician because without knowledge of the drug, the patientcan not be treated properly. It has been well said by Acharya Charaka ‘a drug that isnot understood perfectly is comparable to poison, weapon, fire and the thunderbolt;while, the perfectly understood drug is comparable to ambrosia.The best drug is that which cures the disease promptly and also preserves or sustains thehealth of an individual.ASANADI KWATHA: Asanadi Kwatha is anubhuta yoga which is been prescribing in S.D.M. Ayurvedahospital, Udupi, Karnataka Since 20 yrs. It contains 14 ingredients Properties of eachdrug are mentioned in Table number 14. Most of these drugs have tikta, kashayarasa,laghu, rooksha guna and katuvipaka.These are said to be kaphagna, mehagna, medognaand mootrasangrahaneeya. Tikta, kashayarasa, laghu, rooksha guna produces rookshana effect and they arehaving opposite qualities to that of kapha and medas. Hence they act as mehagna andkaphagna. When medas is reduced then the pressure on vapavahana is also diminished asit is the moolasthana of medovahasrothas. Bahudravata will be present in Madhumeha.Tikta, kashayarasa present in this yoga produces shoshana effect. Bahudravata will bereduced by the absorption of excessive fluid from the body cells. when bahudravatareaching basthi reduces then prabhoothamootrata, pratyatmalakshana of Prameha alsoreduces. Pipasa which is dependent on prabhoothamootrata also subsides. Asanadi 96
  • 116. Drug Review Asanadi KwathaKwatha reduces medas thereby Sthoulya and as it is mootrasangrahaneeya, absorbsbahudrava and hence reduces polyuria, and polydipsia and thereby checks thepathogenesis of Madhumeha. So, this kashaya considered to be Mehagna.Ingredients217,218: Table No.13: Ingredients of Asanadi Kwatha Asana – 1 part Vibhitaki - 1part Khadira – 1part Amalaki - 1part Sariva - 1part Punarnava - 1part Manjishta -1part Ashwaganda – 1part Ushira - 1part Haridra – 1 part Chandana - 1part Gokshura – 1 part Haritaki - 1part Saptarangi - 2 partMethod Preparation: All the raw materials were procured and checked for genuinitythen dried and subjected to pulverization for the desired particle size viz. Kwatha churna.1. ASANA ( Pterocarpus marsupium):Chemical Composition : Tannin, kinotannic acid (70 to 80%) usually believed to beidentical with catechu tannic acid and distinct form gallo-tannic acid other constutents ofkino are pyrocatechin, gallic acid and gum. 97
  • 117. Drug Review Asanadi KwathaKarma: Due to Rasa it acts against Kapha, Meda and Kleda. Due to Veerya it actsagainst Vata. Bhavprakasa mentioned it as Mehaghna and Rasayana. It is also helpful inblood disorders.Pharmacological studies:1. Extract of heart wood showed significant hypoglycemic action in fasting rabbits 3& 5hrs. after oral administration (I.J.M.R,1967,55,166).2. Alcoholic extract of stem significantly lowered blood sugar and improved glucosetolerance of rabbits (J.Res.Ind.Med.1971, 6,205).3. Administration of ethyl acetate extract for 14 consecutive days to rats producedsignificant reduction in levels of triglycerides, total cholesterol and LDL (J. Nat. Prod1993, 56, 989).4. A flexible dose open trial was undertaken in 4 centers in India to evaluate the efficacyof an ayurvedic drug asana in the management of newly diagnosed or untreated type 2DM. By 12th week, control of blood sugar had been attain in 67 out of 97 patientsstudied, and the dose at which control was attained was 2 g of the extract in about 73% ofthe patients 3 g in about 16% and 4 g in 10% of patients. Mean HbA1c decreasedsignificantly (p<0.001) to 9.4%; no side effects were reported (Seshaiah, v.sundaram etal, .1998).2. SAPTARANGI (Salacia reticulate):Chemical composition: Roots contain 1, 3 – diketones, fat, rubber, dulcitol, mangiferin,phlobatannin, glycosidal tannins, leucopelargonidin.Karma: Mutrasanghrahani, Madhumehara, Shothahara, Deepana, Anulomana,Raktashodaka, 98
  • 118. Drug Review Asanadi KwathaPharmacological studies:1. Roots have been used as an ant diabetic drug in the indigenous system of medicinesand clinical tests are said to have substantiated their efficacy. (The wealth of India, CSIR,New Delhi).2. Methanolic extract from the stems of Salacia chinensis (Hippocerateaceae) showedpotent anti-hyperglycemic effects in oral sucrose or maltose-loaded rats, inhibitoryeffects on intestinal alpha-glucosidase, rat lens aldose reductase, formation of Amadoricompounds and advanced glycation end-products, nitric oxide production fromlipopolysaccharide-activated mouse peritoneal macrophage, and radical scavengingactivities.(Yoshikawa M et. al. Yakugaku Zasshi. 2003 Oct).3. In a detailed study, the aqueous extract of the root bark showed a significanthypoglycemic activity in the streptozotacin induced diabetes albino rats. The plasmaglucose concentration was determined at regular intervals following administration. Thedrug was effective as a hypoglycemic agent at all doses tested (0.5g/kg, 1.0 g/kg and5.0g/kg). The maximum decrease in plasma glucose was observed between 1-5hrsfollowing the administration of the drug. The maximum hypoglycemic activity of 30%was observed 3hrs after administration. (Karunanayake, et al.1984).3. HARIDRA (Curcuma longa):Chemical composition: It contains 5-8% of volatile oil & yellow colouring matter-Curcumin. In addition to this it contains Vit. A, Protein 6.3%, Fat 5.1%, Minerals 3.5% &Carbohydrate 69.4%. Curcumin, curcuminoids, Germacrone, Tumerone, Curcumenol,Turmeronol A & B, curlone, stigmasterol, beta tumerones, beta bisabolene, alphacurcumene, Zingiberine, betasesquiphellandene, bisacurone, curcumene, 99
  • 119. Drug Review Asanadi Kwathadehydrocuridione, procurdione, procurcumadiol, bis-acumol. The essential oil from therhizome contains d-a-phellandrene, d-sabinene, cineol, borneol, Zingiberene,sequisterpenes (tumerones). The crystalline coloring matter, curcumin is diferuloylmethane. The antioxidant properties of curcuma powder are probably due to the phenoliccharacter of curcumin. (The wealth of India).Karma: Shothahara, Vranaropana, Vranashodana, Kusthagana, Raktaprasadan,Mutrasanghrahani..Pharmacological studies:1. In a research study administration of turmeric or curcumin to diabetic rats reduced theblood sugar, Hb & HbA1c levels significantly. (ArunN, NaliniN. Plant Foods 2002)2. Curcuma longa rhizome extracts showed blood glucose lowering activity inexperimental induced diabetic rats. After 3 & 6 hrs. Of curcuma injection (10 mg), 37.2%& 54.5 % fall was observed respectively in glucose levels.(Tank R. et al, Indian Drugs1990, V-27 (11), 587- 589)4. Streptozotocin-induced diabetic rats were maintained on 0.5% curcumin containingdiet for 8 weeks. Blood cholesterol was lowered significantly by dietary curcumin inthese diabetic animals. Cholesterol decrease was exclusively from LDL-VLDL fraction.Significant decrease in blood triglyceride and phospholipids was also brought about bydietary curcumin in diabetic rats. (Babu PS, Srinivasan K. Mol Cell Biochem. 1997 Jan;166(1-2):169-75.)5. Curcumin from Curcuma longa was screened for neuroprotective activity .Oraladministration of curcumin to ethanol intoxicated rats revealed that the antioxidative and 100
  • 120. Drug Review Asanadi Kwathahypo lipidaemic action of curcumin is-responsible for its protective role against ethanolinduced brain injury. (Rajakrishnan V, et.al. (Phytotherapy, 1999 Nov; 13(7):571-4])4. KHADIRA (Acacia catechu)Chemical Composition: Heart wood contains catechin, catechu tannic acid. Woodcontains 1-epicatechin, ± Afzelchin, gossypetin, procyanidin Ac, taxifolin.Karma: Kapha-Pittahara, Medogna, Deepana, Dantya.Pharmacological studies:1. A flavoniod isolated from ethonolic extract of central wood of A. catechu showedhypoglycaemic activity (chakravarthy et al., 1983)2. Seeds exhibited marked hypoglycaemic activity in normal rats but not in alloxaninduced rats (I.J.M.R.1976).5. SARIVA (Hemedismus Indicus):Chemical Composition: Hyperoside, rutin, desinine, hexatriacontane, β-sitosterol;hemidesminine, hemidesmin-1 and hemidesmin-2, P-methaxi salycilic aldehyde.Karma: Tridoshara, Grahi.Pharmacological studies:1. A Saponin from it was found to have anti-inflammatory activity (ICMR, 1968-69)2. It showed immunomodulator activity and immunosuppressant activity. It decreases thephagocytosis in experimental studies (Atal et al., 1986).6. MANJISHTA (Rubia cordifolia)Chemical Composition: Antitumour cyclic hexapeptides, RA-V and RA-VII along withRA-I-IV; anthraquin-ones munjistin, purpuroxanthin, rubiatriol, rubicoumaric acid, rubi 101
  • 121. Drug Review Asanadi Kwathafolic acid, pseudopurpurin, alizarin, M rubiadin, rubimallin, purpirin, xanthopurpurin,ruberythric acid etc.Karma: Kapha pitta hara, varnya, vishagna.Pharmacological studies:1. The blood purification effect of the partially purified fraction of the whole plant hasbeen studied on rabbit platelets. It inhibits the platelet aggregation-induced by PAF(platelet aggravating factor) but not thrombin. It also inhibits the binding of 3H-PAF tothe platelets in the dose-dependent manner. Thus it appears that R.cordifolia inhibitsaction of PAF at its receptor level either by its blocking or by desensitization (Tripati etal., 1993).2. Crude extract of R.cordifolia exhibited spasmolytic activity similar to that of verapamilsuggesting presence of calcium channel blocker like constituent(s) in this plant (Gilani etal, .1994)7. AMALAKI (Embilica officinalis)Chemical Composition: Fruit contains gallic acid, tannic acid, sugars, albumin, celluloseand minerals. The fruit is one of the richest natural sources of vitamin C, containing up to720 mg/100g of fresh pulp and 921 mg/100cc of pressed juice. Other contents are asfollows: Moisture 81.20, protein 0.5, fat 0.1, minerals 0.7, fibre 3.4, carbohydrate 14.1,calcium 0.05, phosphorus 0.02 % and iron 1.2 mg, nicotinic acid 0.2 mg per 100gms. offruit.Karma: Daha prashamana, Chakshushya, Medhya, Rochana, Deepana, Anulomana,Vrishya, Rasayana, Pramehagana..Pharmacological studies: 102
  • 122. Drug Review Asanadi Kwatha1. Emblica fruit powder reduced blood sugar level in normal rabbits, as well as inhyperglycemic rabbits proving the hypoglycaemic activity (Tripati et., 1979).2. A clinical study on nisha amalaki churna in diabetes proves the efficacy of thecombination (Gopal Kumar et al; 1995 & Nagrjuna. Jan, 1983 p.105- 107)3. hypo-lipidemec and anti atherosclerotic activity five groups of rabbits were studied for16 weeks to determine the effect of emblica fruit and vit.c (6 mg/kg) on cholesterolinduced hypercholesterolemia and atherosclerosis. Both reduced the serum cholesterol(Thakur & Mandal, 1984).4. Amlaki Rasayana is said to have growth promoting effect. The drug has significanteffect on the levels of serum protein fractions, yet raises the total protein level.(Tewariet.al; 1968).5. Methanolic extract (75%) of Terminalia chebula, Terminalia bellerica, Emblicaofficinalis and their combination named Triphala are being used extensively in Indiansystem of medicine. Oral administration of the extracts (100 mg/kg body weight) reducedthe blood sugar level in normal and in alloxan (120 mg/kg) diabetic rats significantlywithin 4 hrs. Continued, daily administration of the drug produced a sustained effect.(Sabu MC, Kuttan R. J Ethnopharmacol. 2002 July)8. HARITAKI: (Terminalia chebula)Chemical composition: Myrobalans contains astringent principles; tannin and a largeamount of gallic acid, lacilage. Major tannin constituents are chebulagic acid, chebulinicacid & corilagin. Chebulinic acid when heated in water splits up into tannic acid andgallic acid. 103
  • 123. Drug Review Asanadi KwathaKarma: Vedanasthapana, Vranashodhana, Vranaropana, Deepana, Pachana, Krimighna,Kusthaghna, Medhya, Chakshushya, Brimhaniya, Anulomana, Rasayana.Pharmacological studies:1. The fruits are laxative, stomachic, tonic. Main purgative ingredient of Triphala is T.chebula, the other two only increasing the purgation activity of peristaltic movementsuniformly progressive. The purgative principle in the pericap of the fruit of T. chebulahas been found to be a glycoside which may be similar to sennoside. Chebulin possessantispasmodic activity (The wealth of India Pg. No. 175, Vol. 10)2. T. Chebula is found to possess hypoglycaemic activity on glucose inducedhyperglycaemia in rats (Tripati et. al; 1979).3. Anti oxidant property of T. Chebula is reported (Fu Naiwu et.al; 1992)4. Hypolipidimic action of ethyl acetate soluble fraction of the alcoholic extract of T.Chebula stem in normal and trition-treated rats is reported (Kanna et.al; 1993)9. VIBHITAKA (Terminalia bellerica):Chemical Constituents: It contains gallotannic acid, β-sistesterol, resins, chebulagicacid, glucose, galactose and fructose.Karma: Anulomana, Bhedaniya, Shothahara, Kasaghna, Chakshushya.Pharmacological studies:1. T. bellerica showed significant activity against both gram positive and gram negativebacteria. (Valsaraj et al; 1994).2. A significant hepato protective effect was observed as evident from shortenedhexobarbitone “sleep time” and zaxozolamine “paralysis time” when compared withCCL4 alone.(Anand et al; 1994). 104
  • 124. Drug Review Asanadi Kwatha10. USHIRA (Vetiveria zizanioidis):Chemical Composition: A volatile essential oil, resin, colouring matter, a free acid, asalt of lime, oxide of iron and woody matters.Karma: Dahaprashaman, Trishnanigrahana, Stambhana, Swedapanyana,Raktaprasadana,Pharmacological studies:1 .Khustineol exhibited juvenile hormone activity against mustered aphid(LapaphisErysmi)-(Ind.J.Chem.1985,24B 496).11. CHANDANA (Santalum album):Chemical Constituents: Santalic acid, n-ocacosanol, plamitone.Karma: dahaprashana, Varnya.12. ASHWAGANDHA (Withamnia somnifera)Chemical Constituents: Withaferin A, Withanon, Withanolide WS-1, Withanolide A-Y,Somnitol etc.Karma: vayasthapana, deepana, sothahara.Pharmacological studies1. Its powder provided significant relief from symptoms of anxiety neurosis besides aquantitative reduction anxiety level (Singh et.al; 1977)2. The immunomodulatory and immuno suppressive activity are established (Furmanowaet.al; 2001).13. PUNARNAVA (Boerhavia diffusa):Chemical Constituents: Hentriacontane, β-sitosterol, oxalic acid, D-glucose,punarnavoside, punarnavine-1,punarnavine-2, boeravinones A,B,Cetc. 105
  • 125. Drug Review Asanadi KwathaKarma: sothahara, vayasthapana, deepana.Pharmacological studies:1. The administration of punarnava for a period of 3-6 months showed that the drugdesreased blood urea with a simultaneous increase in serum cholesterol and blood sugar.This is attributed to the rasayana effect of the drug (Apparao et al., 1969)2. The drug in the form of a powder on an aqueous decoction was found to be useful inthe treatment of nephritic syndrome in 22 patients. The drug compared well with knowndrugs like corticosteroids. The drug induced diuresis in the patients. Besides relieve inclinical edema, these patients also showed overall improvement, such as decrease inalbuminuria, rise in serum protein and fall in serum cholesterol level ( Singh & Udupa1972d).3. It produced 50% inhibition of lipid peroxidation at a concentration of 2.28 mg/dl and1.84 mg/ml in Fe++ascorbate system. Through this the anti oxidant property of B.diffusais established.4. The alkaloid fraction of B.diffusa root was found to posses restorative activity againststress induced changes in plasma and adrenal cortisol levels. It also significantlyaugmented the antibody production in stressed rats as compared to control (Mungantiwaret al., 1997)14. GOKSHURA (Tribulus terrestris )Chemical Constituents:Fruits - Chlorogenin, diosgenin, gigenin, rutin, rhamnose.Roots – campesterol, β-sitosterol and stigmasterol, neotigogenin.Karma: Vrushya, Mutrala, Rasayana. 106
  • 126. Drug Review Asanadi KwathaPharmacological studies:1. Nephro protective activity - Nephro protective activity was evaluated in gentamicin-induced nephro toxicity (80 mg/kg/day S.C) in male albino rats, NR-AG-I (containingC.nurvala,T-terrestris, D. biflorus & shilajit) NR-AG-II (C.nurvala,T-terrestris, B.diffusaS.officinarum &B.frondosa)2. A new original preparation “Tribestan” has been obtained from T-Terrestris having astimulatory effect on sexual functions(Tomova, 1987). 107
  • 127. Drug Review Asanadi Kwatha Table No.14: Asanadi Kwatha - Rasa panchakaS. Name L.Name Guna Rasa Virya Vipaka Doshgnata Rogagnatano. Pterocapus Laghu, Kashaya, Kapha Madhumeha,1 Asana sheeta katu marsupium ruksha Tikta pitta hara sthoulya, Tikta, Laghu, Kapha Madhumeha2 Khadira Acasia catachu katu sheeta katu ruksha pittahara kandu,kusta kashaya Hemidismus Guru, Madhura Prameha,jvar3 Sariva sheeta Madhura Tridosara indicus Snigdha Tikta a,kusta,vrana. Prameha,mut Rubia Guru, Madhura Kapha4 Manjista ushna Katu rakrucchra, Cardifolia ruksha Tikta pittahara Kusta. Vetiveria Ruksha, Tikta, Kapha trisna,mutrak5 Ushira sheeta Katu Zizanoides laghu madhura pittahara rucchra,daha Santalum Laghu, Tikta, Kaphapitt prameha,daha6 Chandana sheeta Katu album ruksha madhura ahara jwara,trushna Lavanav Terminalia Laghu, Prameha,vata7 Haritaki arjihtapa ushna Madhura Tridosara Chebula Ruksha rakta,kusta ncharasa Jwara,Kasa Terminalia Ruksha, Kapha8 Vibhitaki Kashaya ushna Madhura trushna,Shwa Belarica laghu pittahara sa. Lavanav Prameha,Mut Emblica Ruksa,9 Amalaki arjithapa sheeta Madhura Tridosara rakrucchra,ku officinalis laghu ncharasa sta,netraroga Madhura pandu, swasa, Laghu, Kapha10 Punarnava Boveria diffusa Tikta ushna Katu hrudroga, ruksha vatahara kashaya sotha, Tikta Mutagata, Withamnia Snigdha Vatakapha11 Aswaganda Katu ushna Katu klibya,hridro Sominefera laghu ra kashaya ga,nidranasa Curcuma Ruksha Tikta Kaphavata prameha,kust12 Haridra ushna Katu Longa laghu katu hara a,pandu Prameha, Tribulus Guru, Vata13 Gokshura Madhura sheeta Madhura mutrakruchra Terrestris snigdha pittahara klibya,kasa Salacia Ruksha Tikta Kapha14 Saptarangi ushna Katu Prameha Retituculata laghu Kashaya pittahara 108
  • 128. Clinical Study Methodology MATERIALS AND METHODSA dissertation entitled “A clnical study on the effect of Asanadi Kwatha in Madhumeha”was carried out on 20 patients who attended the OP & IP sections of SDM AyurvedaHospital, Udupi during April 2005 to December 2005.Aim of study 1) To evaluate the effect of Asanadi Kwatha in Patients suffering from Sthoola & Krusha Madhumeha. 2) To evaluate the effect of Asanadi Kwatha in NIDDM patients. 3) Comprehensive literary study on Madhumeha.Source of Data: Patients of either sex between age group of 30 – 75 yrs who attendedIP & OP section of S.D.M. Ayurveda Hospital were selectedSelection of Patients:Patients fulfilling above criteria were administered Asanadi Kwatha without interfering intheir routine dietary and physical activities.Diagnostic Criteria:Criteria – 1: Patients presenting with Pratyatma Laxana of Madhumeha – Prabhoota & Avilamootrata with Mootra or Tanu madhurya, with or without other Roopa were taken asMadhumehi.Criteria – 2: F.B.S. 120mg/dl to 180 mg/dl P.P.B.S. 160mg/dl to 300 mg/dl 109
  • 129. Clinical Study MethodologyInclusion Criteria: Patients fulfilling the following conditions were included. 1) Patients between 30years to 75 yrs. 2) Sthoola & Krusha Madhumehi 3) Patients of Type 2 DM with fasting blood sugar greater than 120mg/dl & lesser than 180 mg/dl & postprandial serum glucose level of more than 160mg/dl & less than 300 mg/dl.Exclusion Criteria: The following patients were excluded from the study 1) Patients below 30 yrs & above 75 years. 2) Jata Madhumehi 3) IDDM patients 4) Gestational diabetics. 5) DM secondary to drugs like corticosteroids or due to secondary disorders.Investigations: The following investigations were done on a mandatory basis.1. F.B.S 2. P.P.B.S 3. Urine SugarResearch Design: A single blind clinical trial with pre & post test design was adopted.Intervention: Intervention was done with Asanadi Kwatha 40 ml twice daily, beforefood, for duration of 30days, with a follow up for every 7 days.Asanadi Kwatha is prepared from Asanadi Kwatha churna and Jala, taken in theproportion of 1:8 (40 grams of Asanadi Kwatha churna and 320 ml of water) Kashaya isprepared by reducing up to chathurtha avashesha(80 ml). Obtained 80 ml of AsanadiKwatha is given in two divided doses i.e. 40 ml in two doses.. 110
  • 130. Clinical Study MethodologyAssessment Criteria: Any change in the following symptoms were noted & taken forassessment (1) Fasting Blood sugar (2) Post Prandial Blood Sugar (3) Post Prandial Urine sugar (4) Sweda Adhikya Sweating after heavy work and fast movement or in hot weather - 0 Profuse sweating after moderate work and movement -1 Sweating after little work and movement (stepping ladder etc.) - 2 Profuse sweating after little work and movement -3 Sweating even at rest or in cold weather -4 (5) Prabhoota Mootrata [Quantity {in liter}] 1.50 to 2.00 - 0 2.00 to 2.50 - 1 2.50 to 3.00 - 2 3.00 and onwards - 3 (6) Avila Mootrata (Turbid urine) Crystal clear fluid - 0 Faintly cloudy or smoky (turbidity barely visible) - 1 Turbidity clearly present but newsprint - easily read through test tube - 2 Newsprint not easily read through test tube - 3 Newsprint can not be seen through test tube - 4 111
  • 131. Clinical Study Methodology (7) Sthoulya (Assessed according to body mass index in Kg/H in m2) Undernourished (less than 20) - 1 Normal weight (18.5 to 24.9) - 0 Overweight (25.0 to 29.9) - 1 Obese (30.0 to 39.0) - 2 Morbid obesity (40 and above) - 3 (8) Dourbalya Can do routine exercise/work - 0 Can do moderate exercise with hesistancy - 1 Can do mild exercise only, with difficulty - 2 Can not do mild exercise too - 3 (9) Suptata (Numbness & tingling sensation) No Suptata - 0 Kara-pada-tala-Supti incontineous - 1 Kara-pada-tala- Supti contineous but not severe -2 Kara-pada-tala- Supti contineous and severe - 3 (10) Daha (Burning sensation) No daha - 0 Kara-pada-tala-daha/Supti incontineous - 1 Kara-pada-tala-daha/Supti contineous but not severe - 2 Kara-pada-tala- Daha contineous and severe - 3 112
  • 132. Clinical Study Methodology (11) Bahvashitva (Polyphagia) No Bahvashitva As usual - 0 Slightly increased (1 – 2 meals) - 1 Moderately increased (3 – 4 meals) - 2 Markedly increased (5 – 6 meals) - 3 (12) Trushna (Polydipsia) Feeling of thirst 7 – 9 times/24 hours - 0 Feeling of thirst 9 - 11 times/24 hours - 1 Feeling of thirst 11 – 13 times/24 hours - 2 Feeling of thirst >13 times/24 hours - 3 113
  • 133. Clinical study Observation OBSERVATIONIn the present study, 24 patients suffering from Madhumeha, fulfilling the inclusioncriteria were registered, out of which, 4 patients failed to complete the study for differentnon-medical reasons. Following are the detailed descriptive statistical analysis of thepatients included in the study. Total patients registered for the study : 25 Completed : 20 Drop outs (LAMA) : 5 Observations1. Age Incidence: The majority of the patients (50 %) were reported in the age group of51 – 60 years followed by 35% in the age group of 61 - 70 years, 15% in the age group of41 – 50 years (Table15 & Graph 1).2. Sex Incidence: Equal incidence of Madhumeha was found in either sex(Table16 & Graph 2)3. Marital status incidence: 100% patients were married. None was unmarried. (Table17& Gaph 3)4. Educational status incidence: 30% of the patients were educated up to Middleschool. While 20% completed primary school, 20% were completed high school. 15%uneducated and 15% Graduated (table18 & Graph 4)5. Religion incidence: Maximum number of patients i.e. 70% were Hindus, 20% patientswere Christians and 10% patients were Muslims(table19 & Graph5) 114
  • 134. Clinical study Observation6. Socio-Economic status incidence: It is observed that maximum patient belongs tomiddle class i.e. 45%, followed by upper middle 30%, lower middle 10% poor 10%. Andrich were 5 %.( Table20 & Graph 6)7. Occupational Incidence: Most of the patients were habituated to a sedentary life stylei.e. 40%, moderate workers were 35%. While the remaining 25% were accustomed toperforming heavy work (Table 21 & Graph 7)8. Incidence of Addictions: Data depicts that maximum number of patients i.e. 45%were taking tea/coffee, however 40% of the patients were Smokers, 10% of the patientswere addicted to alcohol and 5% had habit of chewing tobacco. (Table22 & Graph 8).9. Incidence of Dietary Habits: 80% of the patients were accustomed to mixed type ofdiet while 20% were Vegetarians (Table23 & Graph 9).10. Incidence of Deha Prakruti: A predominance of Pittakapha prakruti was observedin the patients with 45% followed by Vatakapha 35% and 15% of Vatapittala, 5% ofKaphavatala prakruti (Table 24 & Graph 10).11. Incidence of Sara: 65% of the patients were of Madhyama Sara while 25% were ofAvara Sara, 10% were of pravar sara observed (Table25 & Graph 11).12. Incidence in Samhanana: Patients of Madhyama Samhanana were 80% while thoseof Pravara Samhanana were 20% (Table26 & Graph 12).13. Incidence of Satva: Satva analysis of the patients revealed 50% of Madhyama aSatva, 30% of Pravar Satva remaining of avara satva (table 27 & graph 13). 115
  • 135. Clinical study Observation14. Incidence of Rasa Satmya: 55% of the patients were Sarvarasa Satmya while 45%were Madhyama Rasa Satmya i.e. accustomed to more than one Rasa (Table28 &Graph14).15. Incidence of Agni: Teekshna Agni was observed in 55% of the patients, VishamaAgni in 25% and Manda Agni in 20% (Table29 & Graph 15).16. Incidence of Bala: 70% of the patients were of Madhyama Bala, 20 % of Avara Balaand 10% of Pravara Bala (Table30 & Graph 16).17. Incidence of Family History: Majority of the patients were not having any familyhistory (Table31 & Graph 17). 116
  • 136. Clinical Study Observation OBSERVATIONTable 15: Age Incidence Age group No. of Pts % 31 – 40 0 0 41 – 50 3 15 51 – 60 10 50 61 – 70 7 35Graph 1: Age Incidence (in %) AGE INCIDENCE 60 40 20 No of Pts 0 31 - 40 41 - 50 51 - 60 61 - 70Table 16: Sex incidence Sex No. of Pts % Male 10 50 Female 10 50Graph 2: Sex incidence (in %) SEX INCIDENCE 60 40 No of Pts (%) 20 0 M ale Female 117
  • 137. Clinical Study ObservationTable 17: Marital Status Status No. of pts % Single 0 0 Married 20 100Graph 3: Marital Status (in%) MARITAL STATUS 100 80 60 No of pts (%) 40 20 0 Single M arriedTable 18: Educational status Education No of Pts % U 3 15 PS 4 20 MS 6 30 HS 4 20 G 3 15 118
  • 138. Clinical Study ObservationGraph 4: Educational status (in %) EDUCATIONAL STATUS 30 20 No of Pts in % 10 0 U PS MS HS GTable 19: Religion Incidence Religion No of Pts % Hindu 14 70 Muslim 2 10 Christian 4 20Graph 5: Religion Incidence (in %) RELIGION INCIDENCE 80 60 40 No of Pts (%) 20 0 Hindu M uslim ChristianTable 20: Socio - Economic Status Status No of Pts % VP 0 0 P 2 10 LM 2 10 M 9 45 UM 6 30 R 1 5 119
  • 139. Clinical Study ObservationGraph 6: Socio - Economic Status (in %) SOCIOECONOMIC STATUS OF PATIENTS 60 40 No of Pts in % 20 0 VP P LM M UM RTable 21: Occupational Incidence Occupation No of Pts % HW 5 25 MW 7 35 SW 8 40Graph 7: Occupational Incidence (in %) OCCUPATIONAL INCIDENCE 40 30 20 No of Pts (%) 10 0 HW MW SWTable 22: Incidence of Addictions Habits No of Pts in% SM 8 40 TB 1 5 SN 0 0 AL 2 10 T/C 9 45 120
  • 140. Clinical Study ObservationGraph 8: Incidence of Addictions (in %) ADDICTIONS 50 40 30 20 No of Pts in % 10 0 Sm Tb Sn Al T/CTable 23: Dietary Habits Diet No of Pts % Veg 4 20 Mixed 16 80Graph 9: Dietary Habits (in %) DIETARY HABITS 80 60 40 No of Pts in % 20 0 Veg M ixedTable 24: Deha Prakruti Prakruti No. of Pts % VP 3 15 PV 0 0 VK 7 35 KV 1 5 PK 9 45 KP 0 0 T 0 0 121
  • 141. Clinical Study ObservationGraph 10: Deha Prakruti (in %) PRAKRUTITAHA INCIDENCE 50 40 30 No of Pts in % 20 10 0 VP PV VK KV PK KP TTable 25: Sara incidence (in %) Saratah No. of Pts % Pravara 2 10 Madyama 13 65 Avara 5 25Graph 11: Sara incidence SARATAHA INCIDENCE 80 60 40 No of Pts in % 20 0 Pravara M adyama AvaraTable 26: Samhanana (in %) Samhanan No. of Pts % Pravara 4 20 Madhyam 16 80 Avara 0 0 122
  • 142. Clinical Study ObservationGraph 12: Samhanana (in %) SAMHANANA OF THE PATIENTS 80 60 40 No of Pts in % 20 0 Pravara M adhyam AvaraTable 27: Satva incidence Satva No of Pts % Pravara 6 30 Madhyam 10 50 Avara 4 20Graph 13: Satva incidence (in %) SATVATAHA INCIDENCE 60 40 No of Pts in % 20 0 Pravara M adhyam AvaraTable 28: Rasa Satmyata Rasa No of Pts % Sarva 11 55 Madyama 9 45 Avara 0 0 123
  • 143. Clinical Study ObservationGraph 14: Rasa Satmyata (in %) RASA SATMYA INCIDENCE 60 40 No of Pts in % 20 0 Pravara M adhyam AvaraTable 29: Status of Agni Agni No of Pts % Teekshna 11 55 Sama 0 0 Vishama 5 25 Manda 4 20Graph 15: Status of Agni (in %) AGNI PRADHANYATA 60 40 No of Pts in % 20 0 TeekshnaSama VishamaM andaTable 30: Bala incidence Bala No of Pts % Pravara 2 10 Madhyam 14 70 Avara 4 20 124
  • 144. Clinical Study ObservationGraph 16: Bala incidence (in %) BALA INCIDENCE 80 60 40 No of Pts (%) 20 0 Pravara M adyama AvaraTable 31: Family History Relation No. of Pts % First degree 4 20 Second 0 0 degree No history 16 80Graph 17: Family History (in %) Family history 80 60 40 20 No.of Pts in % 0 first second No degree degree history 125
  • 145. Clinical study Results RESULTS1. Effect on Prabootha mutrata: The mean score of Prabhoota Mutrata which was1.155±0.686 before treatment came down to 0.750±0.786 after treatment. Statisticalanalysis of this data proved to be highly significant, ruling out the possibility of chance.(P=<0.001) (Table 32 & Graph 18).2. Effect on Avila mutrata: The mean Avila Mutrata of urine which was 1.050±0.887before treatment reduced to 0.200±410 after treatment statistical analasis of data provedto be significant at P<0.001 (Table 33 & Graph 19).3. Effect on Karapada daha: Before treatment the mean score of Karapada daha was1.3±0.733 and after treatment it was 0.5±0.224 indicating that there was a significantimprovement. This result is highly significant at P<0.001 (Table 34 & Graph 20).4. Effect on Kara pada suptata: Improvement was seen in this symptom with areduction in the mean score from 0.90±0.852 to 0.150±0.366 which is statisticallysignificant at P<0.001 (Table 35 & Graph 21).5. Effect on Bahu ashee: There was no statistically significant change in thesymptomatology with the mean scores being 1.250±0.716 and 1.050±0.686 pre and posttreatment respectively (Table 36 & Graph 22).6. Effect on Trushna: The mean score of Trushna before treatment was 1.10±0.788treatment and this reduced to 0.050±0.224 following the treatment which indicates thatthe difference is highly significant statistically, ruling out the possibility of chance.(P<0.001) (Table 37 & Graph 23) 126
  • 146. Clinical study Results7. Effect of Ati sweda: The mean score for Sweda adhikya which was 1.150±0.745before treatment came down to 0.1±0.308 after the treatment. This difference is highlysignificant statistically. (P=<0.001) (Table 38 & Graph 24).8. Effect on Daurbalya: The mean score was 1.4±0.598 before treatment and 0.2±0.410after treatment. This is statistically highly significant at P<0.001 and rules out thepossibility of the change having occurred by chance (Table 39 & Graph 25).9. Effect on Sthoulya: The mean scores remained the same, thus indicating that adifference does not exist to obtain a descriptive statistical analysis of significance (table40 & Graph 26)10. Effect on FBS: The mean FBS score before treatment was 136.7±22.49 and aftertreatment 117.7±25.84 this is statistically highly significant at P<0.001 (Table 41 &Graph 27).11. Effect on PPBS: The mean scores of PPBS reduced from 228.15±49.62 to194.25±47.94 following the treatment. This result was found to be highly significant atP=<0.001 (table 42 & Graph 28).12. Effect on Urine sugar: The mean PPUS values showed a decrease from 0.5±0.513 to0.05±0.224. This change was significant statistically. (P<0.001) (Table 43 & Graph 29) 127
  • 147. Clinical Study Results RESULTS TABLETable 32: Effect on Prabhoota Mootrata Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P1.1550±0.686 0.750±0.786 0.800 0.616 0.138 5.582 <0.001Graph 18: Effect on Prabhoota Mootrata Effect on Prabuta mutrata 1.5 1.155 0.75 BT 1 Mean AT 0.5 0Table 33: Effect on Avila mutrata Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P1.050±0.887 0.200±0.410 0.850 0.745 0.167 5.101 <0.001Graph 19: Effect on Avila mutrata Effect on Avila Mutrata 1.5 1.05 BT 1 Mean AT 0.2 0.5 0 128
  • 148. Clinical Study ResultsTable 34: Effect on Karapada Daha Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P1.300±0.733 0.0500±0.224 1.250 0.716 0.160 7.804 <0.001Graph 20: Effect on Karapada Daha Effect on Karapada daha 1.3 1.5 BT 1 Mean 0.5 AT 0.5 0Table 35: Effect on Karapada Suptata Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P0.900±0.852 0.150±0.366 0.750 0.716 0.160 4.682 <0.001Graph 21: Effect on Karapada Suptata Effect on Karapada suptata 0.9 1 BT Mean 0.5 AT 0.15 0 129
  • 149. Clinical Study ResultsTable 36: Effect on Bahu Ashee Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P1.250±0.716 1.050±0.686 0.200 0.410 0.0918 2.179 = 0.42Graph 22: Effect on Bahu Ashee Effect on Bahu Ashee 1.25 1.3 1.2 BT 1.05 Mean 1.1 AT 1 0.9Table 37: Effect on Trushna Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P1.100±0.788 0.0500±0.224 1.050 0.759 0.170 6.185 <0.001Graph 23: Effect on Trushna Effect on Trushna 1.5 1.1 BT 1 Mean AT 0.5 0.05 0 130
  • 150. Clinical Study ResultsTable 38: Effect on Ati sweda Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P1.150±0.745 0.100±0.308 1.050 0.686 0.153 6.842 <0.001Graph 24: Effect on Ati sweda Effect on Atisweda 1.15 1.2 BT 1.1 AT Mean 1 1 0.9Table 39: Effect on Daurbalya Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P1.400±0.598 0.200±0.410 1.200 0.523 0.117 10.258 <0.001Graph 25: Effect on Daurbalya Effect on Dourbalya 1.4 1.5 BT 1 Mean AT 0.2 0.5 0 131
  • 151. Clinical Study ResultsTable 40. Effect on Sthoulya Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P0.750±0.716 0.750±0.716 0.000 0.000 0.000 0.000 =1.000Graph 26. Effect on Sthoulya Effect on sthoulya 1 0.75 0.75 BT Mean 0.5 AT 0Table 41: Effect on FBS Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P136.7±22.49 117.7±25.84 19.0 13.123 2.934 6.475 <0.001Graph 27: Effect on FBS Effect on FBS 136.7 140 130 117.7 BT Mean 120 AT 110 100 132
  • 152. Clinical Study ResultsTable 42: Effect on PPBS Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P228.15±49.62 194.25±47.94 33.900 19.963 4.464 7.594 <0.001Graph 28: Effect on PPBS Effect on PPBS 228.15 240 220 BT 194.25 Mean 200 AT 180 160Table 43: Effect on Urine Sugar Difference Mean Paired ‘t’ Test in Means BT AT S.D. S.E.M ‘t’ P0.500±0.513 0.0500±0.224 0.450 0.510 0.114 3.943 <0.001Graph 29: Effect on Urine Sugar Effect on Urine Sugar 0.5 0.6 BT 0.4 Mean AT 0.2 0.05 0 133
  • 153. Clinical study Discussion DISCUSSION Madhumeha is a widely evidential disease since ancient age till today andevidence is increasing day by day with lips and bounce with their complications andcomplexes. Diabetes mellitus is similar to Madhumeha which is a subtype of VatajaPrameha. Madhumeha is a disease in which the patient voids excessive quantity of urinehaving concordance with Madhu i.e. of Kashaya and Madhura taste, Ruksha texture andhoney like color. In Madhumeha, mainly the Vata and Kapha are predominant though thedisease is Tridoshakopanimittaja. The Vata may be provoked either directly by itsetiological factors or by the Avarana of its path by Kapha, Pitta or other Dushyas. So,Vagbhata has classified the Madhumeha into two categories i.e. DhatuapakarshanajanyaMadhumeha and Avarnajanya Madhumeha. Avaranajanya pathogenesis occurs due toetiological factors mainly concordant with Kapha and Pitta, but the vitiation of Vataoccurs due to Avarana. Dhatuapakarshanajanya pathology occurs due to depletion ofDhatus, because of the Vata vitiating etiological factors. Acharya Charaka has classifiedMadhumeha into Santarpanajanya and Apatarpanajanya. The ApatarpanajanyaMadhumeha can be correlated with Dhatuapakarshanajanya Madhumeha, while theSantarpanajanya Madhumeha correlates with Avaranajanya Madhuemeha. Therefore, thisdisease may be caused both by the under nutrition as well as by over nutrition. The firsttype of Madhumeha is considered to be Asadhya and no specific remedy is recommendedfor this. But, the later type has been told as Krichhra Sadhya and can be cured withextensive measurements. 134
  • 154. Clinical study Discussion The main pathophysiology behind Diabetes mellitus is the disturbed metabolismof the carbohydrates, fats and proteins due to either absolute or relative lack of Insulin.The Diabetes mellitus has been broadly classified as type 1 and type 2. The type 1Diabetes mellitus patients are usually asthenic in body constitution and suffer from it inthe early years of life, while the type 2 Diabetes mellitus patients are usually obese andsuffer from it in their 40’s. The type 2 Diabetes mellitus patients can be managed easilyby hypoglycemic drugs whereas in type 1 Diabetes mellitus patients besideshypoglycemic drugs, the Insulin therapy is obscure. So, the type 1 Diabetes mellitus isnearer to Dhatuapakarshanajanya Madhumeha while the type 2 Diabetes mellitusresembles to Avaranajanya Madhumeha. The detailed study of Madhumeha according to Ayurvedic classics and modernmedicine unveils the following facts. Madhumeha = madhusamam Diabetes Mellitus = honey urineBeeja, Beejabhaga & Beejabhaga avayava Genetic susceptibility in the 6th Chromosomeupatapa leading to Madhumeharambhaka dosha leading to IDDMdushti in Sahaja MadhumehaKulaja vikara Familial inheritance more in IDDMKaphamedokara ahara vihara sevana, Over eating and under activityAvyayama and Chinta tyagaKsheera, dadhi as Kaphakara ahara Bovine albuminVikara vighata abhava and Sahaja asatmya Auto immunitySthoulya upadrava Obesity leading to NIDDMAnashana Malnutrition in infancy predisposes to IDDM 135
  • 155. Clinical study DiscussionTwo kinds of madhumehis- Sthoola & Krusha Obese people are more predisposed to develophave been identified clearly the disease especially the NIDDM and the non-obese people also prone foe for DMPrabhoota Mootrata PolyuriaBahvashee PolyphagiaTrushna PolydipsiaAlasya LassitudeSthoulya (Margavarana janya) Rapid wt. gain (especially in NIDDM)Krusha (Sahaja) Rapid weight loss in IDDMMootra madhurya GlycosuriaTanu madhurya HyperglycaemiaKampa, Bhrama, Tamah ,Loulya upadravas Hypoglycemia: Sweating, nervousness, tremor, hunger, confusion, abnormal behaviour and loss of consciousnessBhrama,Tamah, Moorccha, Ketoacidosis & hyper-osmolarShoola,Chardi,Jwara Shwasa, Pipasa, Udavarta coma:Anorexia, vomiting, abdominal pain,Upadravas loss of consciousness, Kussmaul’s respiration. ComaSuptata Neuropathies: Numbness, paraesthesia, pain, abnormal gait.Arochaka, Avipaka, Amlika, Atisara,Shoola, Constipation, diarrhoea, dysphagia and otherUdavarta, Baddha pureeshata GI symptoms Though, the discovery of Insulin and other hypoglycemic drugs is a greatachievement of modern medical science but the hazardous side effects of hypoglycemicafter long term use are incurable and hence an ideal therapy is still obscure. “Diabetesmellitus” being a hereditary disease is spreading from generations to generation. The 136
  • 156. Clinical study Discussionchanging lifestyle, lack of exercise, fast food and stress are also major reasons for thenew patients and for the enhancement of the disease in old once. Unfortunately, thesecausative factors remain hidden and are ignored at management level. The Ayurvedicscientists are trying to find out the best herbal hypoglycemic drugs In the pathogenesis of the Avaranajanya Madhumeha, the Kapha and Pitta are themain Dosha, whereas the most important Dushyas are Meda and Kleda. In Madhumeha,the Dhatukshaya is also predominant. So, in its management such drugs have to beselected which are against Meda and Kleda as well as have the Rasayana effect. AsanadiKwatha is anubhoota yoga, which is been priscribing in S.D.M Ayurvedic Hospital,Udupi, Karnataka since 20 yrs. The most of the drugs of asanadi Kwatha are mentionedin Prameha adhyaya either in Charaka or Susrutha. This preparation conatians fourteendrugs. They are Asana, Saptarangi, Khadira, Sariva Manjiashta, Ushira, Chandana,Haritaki, Vibhitaki, Amalaki, Punarnava, Ashwaganda, Haridra, Gokshura these drugspossess hypoglycemic, Neuroprotective, Nephroprotective Medoghna,Mootrasangrahaniya, Rasayana, Deepana and Pachana properties. While deciding the inclusion criteria, the terms Sthoola & Krusha madhumehihave been used in a much broader sense than to mean only the abnormal states conveyedby them. In other words, the word Sthoola covers patients from normal to obese & theterm Krusha covers patients who were normal to under weight. The terms Madhumeha &Prameha have been used as synonyms throughout the study. Patients who attended theO.P & I.P section of S.D.M Ayurveda hospital were selected randomly, irrespective ofthe sexes, fulfilling all the criteria for inclusion & exclusion. Freshly diagnosed cases andcases that were not on allopathic medicines were taken for the study. The range of fasting 137
  • 157. Clinical study Discussion& postprandial blood sugar was fixed between 120 mg/dl -180 mg/dl & 160mg/dl to 300mg/dl respectively considering the safe limits of the disease. This was done to avoidputting the patient into the risk of developing complications as in the case of higher sugarvalues. Pre and post test design was planned and the patients were asked to take 40ml ofAsanadi Kwatha before food twice daily. Asanadi Kwatha is prepared from AsanadiKwatha churna and water in the proportion of 1:8( as most of the drugs are madyamadravya) i.e. 40 grams of Asanadi Kwatha churna and 320 ml of water it has to be boiledand reduced to ¼ i.e. 80 ml( 40 ml in two divided doses) FBS, PPBS and urine sugarwere conducted on a mandatory basis. Facilities for glycosylated haemoglobin test wereunavailable in the patients’ accessible area. The cost involved for performing glucosetolerance test along with serum glucose level was unaffordable for the patient, The Pratyatma lakshana of Madhumeha including Tanu madhuryata & Mutramadhuryata along with other most common symptoms were taken for assessment. Thisincluded the W.H.O. approved American Diabetic Association diagnostic criteria. Thesymptoms were graded and scored. Maximum number of patients belonged to the age group of 51-70 yrs. whichsupports the view that the prevalence of Type 2 DM is more in the middle to old age.There was an equal distribution of the disease in both the sexes, nothing specific can bederived from this. This may be due to the demographic facts. Hindus were 65%, whichagain indicative of demographic situation of this region. More number of patients wasfrom middle to upper middle class; this finding reflects the pattern of patients coming tothe hospital of this institute according to their socio-economic conditions and also theincreasing substantial sedentary habits among them. The incidence was also more in 138
  • 158. Clinical study Discussionpeople who were involved in professions, who did not involve much physical work likebusiness executives, shop owners, hotel cashiers & so on. Observation of addiction in thepresent study revealed that Maximum number of patients i.e. 45% were addicted toTea/Coffee followed by Beedi/Cigarette smoking 40%, 10% patients were addicted toalcohol and Tobacco chewing 5%. All these addictions decreased the natural immunityand also provoke the Vata to manifest the disease Madhumeha earlier and with severity.Majority of the patients i.e.50% were suffering from the disease for 1 – 3 years. Only20% of the patients confirmed the family history of Madhumeha which reflects the factthat a familial trait is associated with the disease, while the others, either were not awareof it or clearly ruled out any family history of Madhumeha. This gives a hint that, thedevelopment of Madhumeha is not totally familial. Majority of patients were of pittaKapha prakruti. None were of Pitta Vata & Kapha Pitta prakruti. Majority of the patientswere of Madhyama to Avara Sara, which indicates the involvement of Dhatus inMadhumeha. On treatment with Asanadi Kwatha, the following results were observed onthe subjective symptoms.1) Effect on Prabhoota mootrata: Mild to severe Prabhoota mootrata(both in terms ofquantity and frequency) was seen in 100% of patients, 69.2% relief was observed inPrabhuta Mutrata at statistically highly significant level (P<0.001), This relief in PrabhutaMutrata may be due to the Mutrasanghrahani action of Asana, Haridra and Saptarangi,and due to Kashaya Rasa of Asana & Saptarangi which exerts Stambhana action. It maybe possible that drug has acted upon Apana Vayu and corrected its vitiation. 139
  • 159. Clinical study Discussion2) Effect on Avila mootrata: In majority of patients Avila mutrata was observed, 80%improvement was seen in avila mutrata, this may be the combined effect of asanadiKwatha drugs.3) Effect on Trushna: Mild to severe Trushna was seen in 100% of the patients and mildto maximum improvement was seen in 90% of the patients indicating that AsanadiKwatha has good effect on the symptom Trushna. The relief in Trushna may be becausemost of the drugs are Kapha- Pitta Shamaka and also due to Trishnanigrahana action ofUshira and Chandana.4) Effect on Sthoulya: 15% patients were obese, 40% of patients were overweight fortheir age and height. The rest had normal weight. But reduction in weight was notobserved. It is however interesting to note that majority of patients were not obese.Almost 70% of the patients had an adipose abdomen, which corroborates the fact thatIndians have inherited condition called central adiposity (i.e. for a given body mass indexIndians have a higher amount of fat than other races). There have been strong evidencesimplicating this condition for the development of DM (Ramachandran – Diabeticresearch center, Chennai).5) Effect on Sweda adhikya: Mild to severe Sweda adhikya was seen in 75% of patientsand 90% of improvement was observed. Vitiation of Pitta Dosha causes Sweda-Atipravriti. Most of the ingredients of the Asanadi Kwatha are Kapha –Pitta Shamaka andSheeta Virya. Ushira having the action of Swedapanyana and Asana having KashayaRasa and Stambhana action might have checked the excessive sweating.6) Effect on Daurbalya: Mild to severe Dourbalya was seen in 100% of the patients andmoderate to maximum improvement was seen in 100% of patients. Rasayana & 140
  • 160. Clinical study Discussionantioxidant properties of the ingredients of Asanadi Kwatha prevent the Dhatu depletion.The Pramehagna properties of the ingredients of Asanadi Kwatha may facilitate entry ofglucose inside the cell for utilization, thus providing energy to the cells and the patientgets relief in Daurbalya.7) Effect on Kara pada daha: Mild to severe Kara pada daha was seen in 85% of thepatients & moderate to good improvement was seen in 95% of the patients. Relief in karapada daha may be due to most of the drugs are Pitta Kapha Shamaka and Sheeta Viryaand also Raktaprasadan Karma of Haridra, Manjishta and Dahaprashaman action ofUshira. Neuroprotective effect of Haridra, Ashwagandha, haritaki might have alsoprovided the relief in this manifestation.8) Effect of Karapada Suptata: 60% of the patients had mild to severe KarapadaSuptata & mild to maximum improvement was seen in 80% of them. RaktaprasadanaKarma of Haridra, Manjishta. and anti diabetic action of Saptarangi and Asana may haveprovided the relief in Kara-Pada Suptata. Neuroprotective effect of ashwaganda, HaritakiHaridra, may also have provided relief in this manifestation.9) Effect on Bahvashi: Mild to moderate Bahvashitva was seen in 80% of the patients16% improvement was observed. As most of the drugs are Pitta–Kapha Shamaka, thismay be the reason for the relief in Kshudha Adhika The following were the changes observed in the objective symptoms aftertreatment:1) Effect on Fasting Blood sugar (FBS): The mean FBS score before treatmentwas 136.7and after treatment 117.7This is statistically highly significant atP<0.001. 141
  • 161. Clinical study Discussion2) Effect on Post Prandial Blood Sugar (PPBS): The mean difference between before& after treatment is 33.9. Relief in PPBS was at statistically significant level (P<0.01). Effect on FBS & PPBS may be due to the Pramehagana action of variousingredients in Asanadi Kwatha like Asana, Saptarangi, Amalaki, Haridra, Khadira,Haritaki are the Mehagana drugs due to which both FBS & PPBS have reduced. Inmodern science, clinical & experimental studies depict that Asana, Saptarangi, Amalaki,Haridra, Kadira, Haritaki possess anti diabetic action. It was found that in borderlinecases, the sugar levels came to normal, but in cases with sugar levels near the upper limitof the range, it did not return to the normal limits. This may give a hint about a probablerequirement of an extension in the duration of treatment.3) Effect on Urine Sugar: The mean difference in the before treatment & after treatmentwas 0.45 this relief obtained could be due to the Mehagna property of the ingredients ofAsanadi Kwatha. It was observed that the symptoms that were mild returned back to normal afterone month of treatment but those that were moderate came down to mild & severesymptoms reduced to a moderate intensity. Moreover, the severity & number ofsymptoms seemed to be directly proportional to the increase in the serum glucose levelsbecause we found that patients with blood glucose levels at the upper limit of the rangeusually presented with moderate to severe symptoms than those at the lower limit of therange. Even the number of symptoms varied in the same manner.Most of the Asanadi Kwatha drugs have Tikta, kashaya rasa, laghu, rooksha guna andkatu vipaka. These are said to be kaphagna, Mehagna, Medogna andMootrasangrahaneeya. 142
  • 162. Clinical study Discussion Tikta, kashayarasa, laghu, rooksha guna produces rookshana effect andthey are having opposite qualities to that of kapha and Medas. Both Medas and Kaphabeing the main entity of the Samprapti, thus by breaking the Samprapti (correcting thevitiation of Medas and Kapha) treats the disease. Hence they act as Mehagna andkaphagna. When medas is reduced then the pressure on vapavahana is also diminished asit is the moolasthana of medovahasrothas. Bahudravata will be present in Madhumeha. Tikta, kashayarasa present inthis yoga produces shoshana effect. Bahudravata will be reduced by the absorption ofexcessive fluid from the body cells. When bahudravata reaching basthi reduces thenprabhoothamootrata, pratyatmalakshana of Madhumeha also reduces. Pipasa which isdependent on prabhoothamootrata also subsides. Asanadi kashaya reduces medasthereby Sthoulya and as it is mootrasangrahaneeya, absorbs bahudrava and hence reducespolyuria, and polydipsia and thereby checks the pathogenesis of Madhumeha. In summary, it can be said that the present study shows Significant remission inSigns & symptoms of illness Madhumeha vis–a-vis DM corroborated with definitereduction in blood sugar levels. Though there is significant reduction the normal valuesof sugar were not achieved by the period of one month and therefore it is imperative thatdiet and exercise will help in management of the disease. 143
  • 163. EFFECT OF TREATMENT Table No 58: Effect on Kandu Kandu (mean score) Difference % Paired ‘t’ Test in Means BT (±SD) AT (±SD) S.D. S.E.M ‘t’ P 1.450 0.000 1.450 100 1.099 0.246 5.900 P<0.001 (± 1.099) (± 0.000) On Kandu (mild to moderate) drastic improvement was seen by the effect ofPTGG and CHCD, i.e. before the treatment the mean score was 1.45 and reduced to 0after the treatment and this change that occurred with the treatment, is statisticallysignificant (P<0.001). Further details with standard deviation, standard error of Mean, ‘t’value, P values are given above in the table. Table No 59: Effect on Erythema Erythema Difference % Paired ‘t’ Test (mean score) in Means BT (±SD) AT (±SD) S.D. S.E.M ‘t’ P 3.000 0.750 2.250 75 0.851 0.190 11.828 P<0.001 (± 0.562) (± 0.786) Statistically it was observed that the mean score in erythema before the treatmentwas 3.00 which reduced to 0.75 after the treatment. This remission of the symptom afterthe treatment is statistically significant (P=<0.001). Particulars of statistics are givenabove. Fig No 36 Effect on Kandu and Erythema 3 3 2.5 2 1.45 1.5 BT 1 0.75 AT 0.5 0 0 Kandu Erythema
  • 164. Table No 60: Effect on Scaling: Scaling (mean Difference % Paired ‘t’ Test score) in Means BT (±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.550 0.250 2.300 90.19 0.923 0.206 11.139 P<0.001 (± 0.887) (± 0.444) Statistical analysis revealed that the mean score of Scaling was 2.550 before thetreatment was reduced to 0.250 after the treatment and this change that occurred with thetreatment is statistically significant (P = <0.001). Further details with standard deviation,standard error of mean, ‘t’ value, and P values are given above. Table No 61: Effect on Shyava ,Raktakrishna varna Shyava Varna Difference % Paired ‘t’ Test (mean score) in Means BT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.900 1.250 1.650 56.89 0.933 0.209 7.906 P<0.001 (± 0.641) (± 0.851) Statistical analysis revealed that the mean score of Shyava,Rakta Krishnavarna was 2.900 before the treatment was reduced to 1.250 after the treatment and thischange that occurred with the treatment is statistically significant (P = <0.001). Furtherdetails with standarddeviation, standard error of mean, ‘t’ value, and P values are givenabove. Fig No. 37 Effect on Scaling and Shyava ,Raktakrishna varna 3 2.5 2 1.5 BT AT 1 0.5 0 Scaling Shyavata
  • 165. Table No 62: Effect on Kinakhara sparsha Kinakharasparsha Difference % Paired ‘t’ Test (mean score) in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.100 0.500 1.600 76.19 0.598 0.134 11.961 P<0.001(± 0.553) (± 0.688) Statistical analysis revealed that the mean score of Kinakhara sparsha was 2.100before the treatment was reduced to 0.500 after the treatment and this change thatoccurred with the treatment is statistically significant (P = <0.001). Further details withstandard deviation, standard error of mean, ‘t’ value, and P values are given above. Table No 63: Effect on Rookshata: Rookshata Difference % Paired ‘t’ Test (mean score) in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.150 0.350 1.800 83.72 0.768 0.172 10.485 P<0.001(± 0.671) (± 0.587)Statistical analysis revealed that the mean score of Rookshata was 2.150 before thetreatment was reduced to 0.350 after the treatment and this change that occurred with thetreatment is statistically significant (P = <0.001). Further details with standard deviation,standard error of mean, ‘t’ value, and P values are given above Fig No. 38 Effect on Kinakhara sparsha and Rookshata 2.5 2.1 2.15 2 1.5 BT 1 AT 0.5 0.35 0.5 0 Kinakhar Rooksha
  • 166. Table No 64: Effect on Vritta Vritta (mean score) Difference % Paired ‘t’ Test in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.950 1.100 1.850 62.71 1.268 0.284 6.525 P<0.001(± 0.999) (± 1.071) Statistical analysis revealed that the mean score of Vritta was 2.950 before thetreatment was reduced to 1.110 after the treatment and this change that occurred with thetreatment is statistically significant (P = <0.001). Further details with standard deviation,standard error of mean, ‘t’ value, and P values are given above. Table No 65: Effect on GhanaGhana (mean score) Difference & Paired ‘t’ Test in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 2.100 1.000 1.100 52.38 1.071 0.240 4.593 P<0.001(± 0.968) (± 1.124) Statistical analysis revealed that the mean score of Ghana was 2.110 before thetreatment was reduced to 1.000 after the treatment and this change that occurred with thetreatment is statistically significant (P = <0.001). Further details with standard deviation,standard error of mean, ‘t’ value, and P values are given above. Fig No 39 Effect on Vritta and Ghana 2.95 3 2.5 2.1 2 1.5 BT 1.1 1 AT 1 0.5 0 Vritta Ghana
  • 167. Table No 66: Effect on Nakhadushti Nakhadushti Difference % Paired ‘t’ Test (mean score) in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 0.450 0.450 0.000 0 0.000 0.000 0.000 P=1.000(± 1.146) (± 1.146) Statistical analysis revealed that the mean score of Scaling was 0.450 before thetreatment was remained same as 0.450 after the treatment and this change that occurredwith the treatment is statistically not significant (P =1.000). Further details with standarddeviation, standard error of mean, ‘t’ value, and P values are given above. Table No 67: Changes in PASI scoring PASI Difference % Paired ‘t’ Test (mean score) in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 15.740 4.070 11.670 74.14 9.024 2.018 5.783 P<0.001(±12.471) (± 5.857) Statistical analysis revealed that the mean score of PASI was 15.740 before thetreatment was reduced to 4.070 after the treatment and this change that occurred with thetreatment is statistically significant (P = <0.001). Further details with standard deviation,standard error of mean, ‘t’ value, and P values are given above. Fig No 40. Effect on Nakhadushti PASI scoring 15.74 16 14 12 10 8 BT 6 4.07 AT 4 2 0.45 0.45 0 N.Dushti PASI
  • 168. Table No 68: Effect on Auspitz sign Auspitz Difference % Paired ‘t’ Test (mean score) in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 0.850 0.150 0.700 85.35 0.470 0.105 6.658 P<0.001(± 0.366) (± 0.366) Statistical analysis revealed that the mean score of Auspitz sign was 0.850 beforethe treatment was reduced to 0.150 after the treatment and this change that occurred withthe treatment is statistically significant (P = <0.001). Further details with standarddeviation, standard error of mean, ‘t’ value, and P values are given above. Table No 69: Effect on Candlegreece sign Candlegreece sign Difference % Paired ‘t’ Test (mean score) in MeansBT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 0.950 0.250 0.700 73.68 0.470 0.105 6.658 P<0.001(± 0.224) (± 0.444) Statistical analysis revealed that the mean score of Candlegreace sign was 0.950before the treatment was reduced to 0.250 after the treatment and this change thatoccurred with the treatment is statistically significant (P = <0.001). Further details withstandard deviation, standard error of mean, ‘t’ value, and P values are given above. Fig No. 41 Effect on Auspitz sign and Candlegreece sign 1 0.8 0.6 BT 0.4 AT 0.2 0 Auspitz C.Greece
  • 169. Table No70: Effect on Koebners phenomena: Koebners Difference % Paired ‘t’ Test phenomena in Means (mean score)BT(±SD) AT(±SD) S.D. S.E.M ‘t’ P 0.200 0.200 0.000 0 0.000 0.000 0.000 P=1.000(± 0.410) (± 0.410) Statistical analysis revealed that the mean score of Scaling was 0.200 before thetreatment was remained same as 0.200 after the treatment and this change that occurredwith the treatment is statistically not significant (P =1.000). Further details with standarddeviation, standard error of mean, ‘t’ value, and P values are given above. Fig No 42 Effect on Koebners phenomena 0.2 0.2 0.2 0.15 0.1 BT AT 0.05 0 Koe.Phen
  • 170. Summary SUMMARY The frame of the dissertation work entitled "A Clinical Study on theAsanadi qwatha in management of Madhumeha” is designed in following Aims &objectives 1) To do a comprehensive literary study on Madhumeha 2) To evaluate the effect of Asanadi kwatha in Sthoola & Krusha Madhumehis. 3) To evaluate the effect of Asanadi kwatha in type 2 diabetes mellitus patients The whole topic is elaborated in four parts and is named as Review of literature. Methodology, Discussion and Conclusion. Review of literature contains Prologue, Historical review, conceptual study, Drugreview.In prologue, gravity of the problem and previous works on this study has been mentioned.Conceptual Study:Historical glimpses with regards to disease Madhumeha (Diabetes mellitus) traces thevarious developments right from the Vedic period up to the modern era.The disease Madhumeha has been dealt from both the Ayurvedic point of view as well asmodern point of view. Its Nirukti & paribasha, Nidana, Purvarupa, Rupa, Samprapti,Sadhya-Asadhyadta, Upadrava, Arishta lakshana, Chikitsa and Pathya-Apathya havebeen described in an elaborative manner. The disease review from the modern point ofview deals with definition, aetiology, prediabetic state, clinical features, pathogenesis,complications, treatment and life style management of Diabetes mellitus. 146
  • 171. SummaryDrug study: In the drug study individual drugs of Asanadi qwatha have been described indetail with latest possible research information. The Asanadi qwatha contains fourteenherbs viz. Asana, Saptarangi, Khadira, Sariva, Manjishta, Ushira, Chandana, Harithaki,Vibhitaki, Amalaki, Punarnava, Ashwagandha, Haridra. and Gokshura.Methodology:The second part comprises of Aims & objectives, Material and methods which includesinclusion criteria, exclusion criteria, diagnostic criteria, assessment criteria, laboratoryinvestigations, There after observations and results of the therapy has been discussed.Materials and Method: 25 patients of Madhumeha were registered in this study out of which total 20patients completed treatment. Asanadi qwatha was given in the dose of 40 ml twice daily before meals withwater for 30 days with out altering their routine dietary and physical activities.Observations: The maximum no. of patients i.e. 50% were from the age group of 51 to 70 years,maximum no. of patients were urban inhabitants (65%), Max. were sedentary i.e. 40%,Maximum number of patients i.e. 80% of this series were non-vegetarian, 80 % patientswere taking Madhura Rasa dominant diet, 45% were addicted to Tea/Coffee. Maximum number of patients i.e. 80% confirmed that they were not having anyfamily history of Madhumeha The maximum number of the patients i.e. 50 % were suffering from the diseasefor last 1 – 3 years, Maximum no. of patients i.e. 45% were having Pittaja-Kapha prakriti. 147
  • 172. Summary The maximum number of patients were normal weight i.e; 45 % and 15% wereobese. Vyayama Shakti was found Avara in 65% patients, The maximum number of patients i.e.; 50% were found to have PravaraAbhyavaharana Shakti and Maximum i.e.; 55% patients were having Krura Koshtha,majority i.e. 50 % of the patients were having Tikshnagni, 60% patients were havingnormal systolic blood pressure, 55% patients were having normal diastolic bloodpressure. The prominent Nidanas reported were Guru Ahara (70%), Madhura Ahara(80%), Snigdha Ahara (65%), Katu-Tikta Ahara Sevana was found in 35% patients.Avyayama was found in 75% patients, while Chinta was found in 45% patients. DravaAhara (50%), Diwaswapna (80%), Asya Sukha (75%). The following were the changes observed in the subjective symptoms aftertreatment:1) Effect on Prabhoota mootrata: Mild to severe Prabhoota mootrata(both in terms ofquantity and frequency) was seen in 100% of patients, 69.2% relief was observed inPrabhuta Mutrata at statistically highly significant level (P<0.001),2) Effect on Avila mootrata: In majority of patients Avila mutrata was observed, 80%improvement was seen in avila mutrata.3) Effect on Trushna: Mild to severe Trushna was seen in 100% of the patients and mildto maximum improvement was seen in 90% of the patients.4) Effect on Sthoulya: 15% patients were obese, 40% of patients were overweight fortheir age and height. The rest had normal weight. But reduction in weight was notobserved. 148
  • 173. Summary5) Effect on Sweda adhikya: Mild to severe Sweda adhikya was seen in 75% of patientsand 90% of improvement was observed.6) Effect on Daurbalya: Mild to severe Dourbalya was seen in 100% of the patients andmoderate to maximum improvement was seen in 100% of patients.7) Effect on Kara pada daha: Mild to severe Kara pada daha was seen in 85% of thepatients & moderate to good improvement was seen in 95% of the patients.8) Effect of Karapada Suptata: 60% of the patients had mild to severe Karapada Suptata& mild to maximum improvement was seen in 80% of them.9) Effect on Bahvashi: Mild to moderate Bahvashitva was seen in 80% of the patients16% improvement was observed. The following were the changes observed in the objective symptoms aftertreatment:1) Effect on Fasting Blood sugar (FBS): The mean FBS score before treatmentwas 136.7and after treatment 117.7. This is statistically highly significant atP<0.001.2) Effect on Post Prandial Blood Sugar (PPBS): The mean difference between before &after treatment is 33.9. Relief in PPBS was at statistically significant level (P<0.01).3) Effect on Urine Sugar: The mean difference in the before treatment & after treatmentwas 0.45. 149
  • 174. Summary Discussion This section deals with the discussion based on the clinical study. Criticaldiscussion with probable reasoning and lastly overall effect of therapy have beenpresentedConclusions The last section deals with the Summary and Conclusions drawn from the presentstudy. 150
  • 175. DEPARTMENT OF KAYA CHIKITSA S. D. M. COLLEGE OF AYURVEDA, UDUPI. CASE PROFORMA FOR CLINICAL STUDY ON MADHUMEHAI. ATURA VIVARA 1. Atura Nama : 10. Antah Kramanka : 2. Linga : M / F 11.Bahi Kramanka : 3. Vaya : ___ years. 12. Shayyagara Kramanka 4. Vaivahika Vruttanta : M / UM / W / D 13. Shayya Kramanka : 5. Vrutti : 14.Pravesha Dinanka : 6. Jati : H / M / C / J / Si 15.Nirgamana Dinanka : 7. Saksharata : UE / PS / MS / HS / GR / PG 16.Vilasa : 8. Samajika Sthithi : VP / P / LM / M / UM / R 17.Phone : 9. Dinanka : 18.E-mail :II. VEDANA SAMUCHRAYAM A. PRADHANA VEDANA : 1) Mootra Sambandhi : *Frequency __times / day, __times / night. *Color : ________since __days. *Density : Milky White / Buffy / Turbid / Clear since ____ days. * Amount (approx)_________ ml/24 hours since ____ days. * Discomfort during urination __________ since ____ days. * Urge for micturition after drinking water Yes / No. 2) PIPASA SAMBANDHI - has observed increased feeling of thirst Yes Since___days / No 3) AHARA ABHYAVAHARANA SAMBHANDHI- has observed unusual increase of appetite. Yes Since __Days / No
  • 176. 4) SWEDA SAMBHANDHI - has observed unusual increase of sweat & body odour. Yes Since ___Days / No 5) ANYAB) ANUBANDHA VEDANA :III. VEDANA VRUTTANTAIV. POORVA VYADHI CHIKITSA VRUTTANTAV. KOUTUMBIKA VRUTTANTA Relative Dead / Alive Health status Treatment historyVI. VYAKTHIGATA VRUTTANTA : 1. AHARA SAMBANDHI VRUTTANTA : Veg / MixedAHARA : frequency of intake / day ________(SARVAGRAHA)PARIGRAHA (Approximate amount of intake per meal) Staple : Amount / day in gram /calRice / Wheat / Ragi / Bread productsBengal gram (toor dal) / Black gram (urad dal) / Green gram (moong dal) / Horse gram /Chanaka / Others Vegetables : Amount / day in grams / calGreen leafy / Stem / Roots tuber / Rhizome / Others. Fruits : Amount /day / week in grams / calBanana / Grape / Apple / Chikku / Pineapple / Mango / Others
  • 177. Milk & Dairy products : Amount /day / week in grams / calMilk/Curds/Butter/Ghee/Butter milk/Others Sugar & its products : Amount /day / week in grams / calSugar/Jaggery/Chocolate Desserts : Amount /day / week in grams /calMilk / Cream preparations / Ghee butter preparations / Dalda / Vanaspathi preparationCurd preparation / Ice cream / fruit salads / Pastries / wafers / cakes Deep fried food stuffs : Amount / day / week in grams / calVada / Bonda / Pakoda / Bajji / Other fried snacks Oils : Amount /day / week in grams / calSunflower/Coconut/Ground nut /Dalda/Vanaspathi/Ghee/Mustard/Others Meat : Amount /day / week / months in grams / calChicken/Mutton/Pork/Beef/Sea food/Egg/Others Beverages : Amount /day / week in grams / calTea/Coffee/Alcohol2. VIHARA SAMBANDHI VRUTTANTASleep : ___Hours / day : ___ Hours / night : Disturbed : Due toExercise: Type No exercise Hours _______ per day _______ hours / weekStress: Type Relieving factors Aggravating factors Days/year of exposure No stressSamshodhana: Undergone Yes / NoType of profession: Sedentary / Involves physical strain involves mental strain / Both. Since ________ Years .Relaxation (Apart from day / night sleep) : Prayer / Meditation / Others.Recreation / Entertainment : Television / Indoor games / Outdoor gamesSexual intercourse: __________ times / week1. Mala : ________ times daily regular / irregular
  • 178. 2. Mootra : ________ times daily3. Madakari Dravya Abhyasa : Smoking ___ / day : since __years Alcohol __ ml / day : since __ years Tobacco chewing : since __ years Tobacco snuff : since __ year4. Anya Abhyasa :VII. RAJO SAMBANDHI VRUTTANTA : 1. Menstruating / attained menopause at ________ years of age. 2. Menstrual cycle : 3. History of : Udavartini/Asrugdara/ Shwethapradar / Anya YonigataVikara 4. P ____ G _____ L ____ D ____ 5. History of infertility : primary / secondaryVIII MANASIKA VRUTTANTA:IX. VITAL SIGNS II III IV I VISIT VISIT VISIT VISIT1. Pulse (Nadi) / Min2. BP ___ mmHg o3. Temperature F4. Heart rate / Min5. Respiratory rate / Min
  • 179. X. GENERAL PHYSICAL EXAMINATION Built and Nourishment : __Wt __ Ht Pallor / Edema / Nail changes / Cyanosis / Icterus / Lymphadenopathy / NeckXI. SYSTEMIC EXAMINATION RESPIRATORY SYSTEM : GASTRO INTESTINAL SYSTEM : CARDIOVASCULAR SYSTEM : GENITOURINARY SYSTEM : CENTRAL NERVOUS SYSTEM : LOCOMOTOR SYSTEM :Examination of the limbs : Pulses / Ulcer ( if any)XII SROTO PAREEKSHA : • Pranavaha Srotas : • Udakavaha Srotas : • Annavaha Srotas : • Rasavaha Srotas : • Raktavaha Srotas : • Mamsavaha Srotas : • Medavaha Srotas : • Astivaha Srotas : • Majjavaha Srotas: • Shukravaha Srotas: • Mootravaha Srotas : • Pureeshavaha Srotas: • Swedavaha Srotas :
  • 180. XIII. ROOPA SANKALANAA. ROOPA (SAMANYA)1. Sweda adhikya2. Anga Gandha3. Anga Shaithilya4. Anga Sada5. Hridayopadeha6. Netropadeha7. Jihwopadeha8. Sravanopadeha9. Taluni malotpatti10. Danteshu malotpatti11. Ghanangata12. Keshativruddhi13. Keshajatellabhava14. Nakhativruddhi15. Sheetapriyatwam16. Gala shosha17. Talu shosha18. Asya madhurya19. Karadaha20. Padadaha21. Mootrapipilikabhisarana22. Shuklamootrata23. Snigdha gatrata24. Picchila gatrata25. Guru gatrata26. Pipasa27. Shwasa dourgandhya
  • 181. 28. Tandra29. Kara suptata30. Pada suptata31. Anga suptata32. Alasya33. Mukha shosha34. Kaya chidresha upadeha35. Sarvakala nidra36. Pipilika shareerabhesaranaB. VISHESHA ROOPA1. Prabhoota mootrala2. Avila mootrata3. Sthoulya4. Bahu ashee5. Snighdhangata6. Shayyasanaswapnasheela (activity)7. Krushatra8. Alpashee9. Rookshata10. Paribramanasheela11. Mutra madhurya (urine sugar)12. Mutra kashaya varna13. Mutra pandu varna14. Tanu madhurya (FBS PPBS)
  • 182. C. UPADRAVA1. Trushna2. Daha3. Atisara4. Dourbalya5. Arochaka6. Avipaka7. Alagi vidradi adipootimamsapidaka8. Udavarta9. Kampa10. Hridgraha11. Shoola12. Nidranasha13. Shosha14. Kasa15. Sthambha16. Badha purishatraD. COMPLICATIONS1. Retinopathy2. Nephropathy3. Neuropathy
  • 183. 4. Atherosclerosis5. Peripheral ischemia6. Diabetic hand7. Diabetic foot8. Cerebrovascular accidents9. Ischemic heart disease10. Gangrene11. Carbuncles12. Skin changesXiV. INVESTIGATION :A. BLOOD I II III IV1) FBS mg/dl2) PPBS mg/dl3) RBS mg/dl4) Urine Sugar
  • 184. B. ROUTINE I Visit II Visit III Visit IV VisitHAEMATOLOGYTotal WBC Count(cells/cumm)LymphocytesMonocytesNeutrophilsEosionophilsBasophilsHb%ESR (in mm/I hour)E. OTHER INVESTIGATIONSXV. SAMPRAPTI GHATAKA DOSHA : DUSHYA : SROTAS : SROTODUSTI LAKSHANA : AGNI : AMA : UDBHAVA STHANA : SANCHARA STHANA : ADHISHTANA : VYAKTA STHANA : ROGA MARGA :
  • 185. XVI. UPASHAYA ANUPASHAYA :XVII. VYADHI :XVIII. PRAKARA :XIX. SADYASADYATA :XX. CHIKITSA :STHOOLA KRUSHAXXI. FOLLOW UP ASSESSMENT CRITERIA (FORTNIGHTLY CHECK UP) Subsequent I Visit II Visit III Visit IV Visit V Visit VI Visit Visits1. Prabhoola Mootrata2. Avila Mootrala3. Thrushna4. Sthoulya5. Sweda adhikya6. Dourbalya7. Karapada daha8. Karapada suptata9. Tingling sensation10. Bahu ashee11. FBS12. PPBS
  • 186. 13. GHb (if done)14. GTT (if done)15. Urine sugar VIKRITI : HETU : ROGI BALA : LINGA : DESHA : ROGA BALA : PRAKRUTI : KALA :CHIKITSA : ASANADI KWATHA 40 ml BD.
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