EVALUATION OF THE EFFICACY OF BHUMYAMALAKYADI CHURNA IN MADHUMEHA (WITH SPECIAL REFERENCE TO ITS HYPOGLYCEMIC EFFECT) Thesis submitted to the Rajiv Gandhi University of Health Sciences Karnataka,Bangalore In partial fulfillment of regulations for the Award of the degree of DOCTOR OF MEDICINE (AYURVEDA) By SHASHIDHAR. T. HOMBAL. Guide Dr. Ch. Ranga Rao. M.D. (Ayu) Professor and Head of the Department Post Graduate and Research Centre D.G.M.Ay.Medical College, Gadag. Co-Guide Dr. Siva Rama Prasad Ketamakka. M.D. (Ayu) Reader Post Graduate and Research Centre D.G.M.Ay.Medical College, Gadag. POST GRADUATE AND RESEARCH CENTRE DEPARTMENT OF KAYACHIKITSA D.G.M.AY.MEDICAL COLLEGE GADAG.
EVALUATION OF THE EFFICACY OF BHUMYAMALAKYADI CHURNA IN MADHUMEHA ,SHASHIDHAR. T. HOMBAL , Post Graduate Studies & Research Center, D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG
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EVALUATION OF THE EFFICACY OF BHUMYAMALAKYADI CHURNA IN
MADHUMEHA
(WITH SPECIAL REFERENCE TO ITS HYPOGLYCEMIC EFFECT)
Thesis submitted to the Rajiv Gandhi University of Health Sciences Karnataka,Bangalore
In partial fulfillment of regulations for the Award of the degree of
DOCTOR OF MEDICINE (AYURVEDA)
By
SHASHIDHAR. T. HOMBAL.
Guide Dr. Ch. Ranga Rao. M . D . (Ay u )
Professor and Head of the Department Post Graduate and Research Centre D.G.M.Ay.Medical College, Gadag.
Co-Guide
Dr. Siva Rama Prasad Ketamakka. M.D. (Ayu) Reader
Post Graduate and Research Centre D.G.M.Ay.Medical College, Gadag.
POST GRADUATE AND RESEARCH CENTRE DEPARTMENT OF KAYACHIKITSA
D.G.M.AY.MEDICAL COLLEGE GADAG.
Ayurmitra
TAyComprehended
LIST OF ILLUSTRATIONS
Sl. No. Figure Name Page No. 1. Photograph of Haritaki 56 2. Photograph of Bibhitaki 58 3. Photograph of Amalaki 60 4. Photograph of Pippali 62 5. Photograph of Guggulu 64 6. Photograph of Madhu 66 7. Photograph of Gomutra 68
List of Master Charts
Sl No Master Charts Page No
1. Demographic data 79
2. Data related to Personal history 80
3. Data related to Complaints 81
4. Data related to Associated Complaints 82
5. Data related to Upadravas 83
6 A. Data related to Objective Parameters 84
6 B. Data related to Objective Parameters 85
7 A. Data related to Lab Investigations 86
7 B. Data related to Lab Investigations 87
List of Figures
Sl No Figures Page No
1. Showing Age and Sex ratio 89
2. Showing the Religion incidence 90
3. Showing the Occupation incidence 91
4. Showing the Economical status incidence 92
5. Showing the Diet incidence 93
6. Showing the Family history incidence 94
7. Showing the Chronicity 95
8 Showing the body weight of Group A 103
9. Showing the body weight of Group B 103 10. Circumference of Udara of Group A 104 11. Circumference of Udara of Group B 104 12. Circumference of Spik of Group A 105 13. Circumference of Spik of Group B 105 14. Circumference of Sthana of Group A 106 15. Circumference of Sthana of Group B 106 16. Serum Cholesterol of Group A 107
17. Serum Cholesterol of Group B 107 18. Serum Triglyceride of Group A 108
19. Serum Triglyceride of Group B 108 20. Serum HDL Cholesterol of Group A 109 21. Serum HDL Cholesterol of Group B 109 22. Serum LDL Cholesterol of Group A 110 23. Serum HDL Cholesterol of Group B 110 24. Serum VLDL Cholesterol of Group A 111 25. Serum VLDL Cholesterol of Group B 111 26. Random Blood Sugar of Group A 112 27. Random Blood Sugar of Group B 112 28. Showing the Result 114
4) CHIKITSA 47 5) DRUG REVIEW 54 6) MATERIAL AND METHODS 71 7) OBSERVATION, ANALYSIS AND INTERPRETATION 79
8) CONCLUSION 115 9) SUMMERY 118
BIBLIOGRAPHY APPENDIX
Acknowledgement
ACKNOWLEDGEMENT
I am highly indebted to my guide, Dr Ch. Ranga Rao, H.O.D.
Department of Post Graduate and Research centre, sri D.G.M.Ayurvedic
Medical Col lege, Gadag for his valuable suggestions and guidance in
completing this work successful ly.
I am heart i ly thankful to Dr V.V.S.Shastr i . Under whose guidance
my work was started and he was the teacher who inspired me to take the
combinat ion of the drug mentioned in this thesis.
I am ever grateful to my Co-guide Dr. Siva Ram Prasad Ketamakka
who was a helping hand throughout the work and supported me in
completing the work in st ipulated t ime.
I am thankful to our Principal Dr G.B.Pati l for his support in
completing this work successful ly.
I am very much thankful to Mr. Nandakumar for his valuable help in
stat ist ical calculations.
I am thankful to Dr A.K.Panda and al l other staff of DGM col lege for
their help.
Acknowledgement
I acknowledge to our col lage l ibrar ian Mr V.M.Mundanamani and
his assistant Mr Sureban for support ing me by providing lot of books for
the study.
I am thankful to Mr Gir iachar Off icer National Information Centre
(NIC) Gadag, for giving me information about the work going on in
di f ferent parts of the world regarding this subject.
My personal thanks to Mr.N.N.Bhat and Mr C.S.Bhat who helped
me in understanding the Sanskri t versions.
I am thankful to Dr.(Mrs) M.D.Gojanur for support ing me by
referring the cases for tr ial.
I am thankful to my col leagues and fr iends who supported me in
cl inical tr ials and made the tr ial successful.
I am thankful to al l the pat ients who agreed to undergo the
treatment with the tr ial drug.
I am highly indebted to my beloved parents, who framed a proper
path for my carr ier.
Acknowledgement
I express my heartfel t grat i tude to al l my family members for their
constant help, love and care rendered during my study.
I am thankful to al l my teachers, from primary education to post
graduate education for helping me in bui lding up my carrier.
This l ist is incomplete without remembering my small sunny Kiran
(18 months) whose smile inspired and kept me cheerful throughout my
work.
I wish to thank al l the persons who have helped me directly and
indirect ly with apologies for my inabi l i ty to identi fy them individual ly.
Acknowledgement
ACKNOWLEDGEMENT
I am highly indebted to my guide, Dr Ch. Ranga Rao, H.O.D.
Department of Post Graduate and Research centre, sri D.G.M.Ayurvedic
Medical Col lege, Gadag for his valuable suggestions and guidance in
completing this work successful ly.
I am heart i ly thankful to Dr V.V.S.Shastr i . Under whose guidance
my work was started and he was the teacher who inspired me to take the
combinat ion of the drug mentioned in this thesis.
I am ever grateful to my Co-guide Dr. Siva Ram Prasad Ketamakka
who was a helping hand throughout the work and supported me in
completing the work in st ipulated t ime.
I am thankful to our Principal Dr G.B.Pati l for his support in
completing this work successful ly.
I am very much thankful to Mr. Nandakumar for his valuable help in
stat ist ical calculations.
I am thankful to Dr A.K.Panda and al l other staff of DGM col lege for
their help.
Acknowledgement
I acknowledge to our col lage l ibrar ian Mr V.M.Mundanamani and
his assistant Mr Sureban for support ing me by providing lot of books for
the study.
I am thankful to Mr Gir iachar Off icer National Information Centre
(NIC) Gadag, for giving me information about the work going on in
di f ferent parts of the world regarding this subject.
My personal thanks to Mr.N.N.Bhat and Mr C.S.Bhat who helped
me in understanding the Sanskri t versions.
I am thankful to Dr.(Mrs) M.D.Gojanur for support ing me by
referring the cases for tr ial.
I am thankful to my col leagues and fr iends who supported me in
cl inical tr ials and made the tr ial successful.
I am thankful to al l the pat ients who agreed to undergo the
treatment with the tr ial drug.
I am highly indebted to my beloved parents, who framed a proper
path for my carr ier.
Acknowledgement
I express my heartfel t grat i tude to al l my family members for their
constant help, love and care rendered during my study.
I am thankful to al l my teachers, from primary education to post
graduate education for helping me in bui lding up my carrier.
This l ist is incomplete without remembering my small sunny Kiran
(18 months) whose smile inspired and kept me cheerful throughout my
work.
I wish to thank al l the persons who have helped me directly and
indirect ly with apologies for my inabi l i ty to identi fy them individual ly.
Introduction 1
Madhumeha is emerging as the chronic non-communicable disease
of concern in developing countr ies. With changing environment,
urbanisat ion and al tered l i fe-style giving more comforts and sedentary l i fe
to human, simultaneously offer ing metabol ic diseases l ike Madhumeha.
Madhumeha is a disease in which certain pathological changes are
noticed in ur ine, the most important being the presence of sugar. Since
this disease is connected with the urinary system with the presence of
sugar in the urine, the comparison of Madhumeha with Diabetes Mell i tus
is just i f iable.
Madhumeha is also one of the identi f ied major cause of morbidi ty
and mortal i ty in India1. In further, Indians have high ethnic susceptibi l i ty
for developing Madhumeha at a younger age group. The disease usual ly
occurs after 30 years of age, seen more in male than in female.
Being a slow onset and often relat ively asymptomatic disease,
remains undiagnosed at onset, or even i f diagnosed is often ignored by
persons aff l icted with i t . In addit ion lack of awareness amongst health
professionals and inadequate health care faci l i t ies compound the problem
of Madhumeha related complications in our country2.
Introduction 2
The alarming rise in non – communicable diseases l ike Madhumeha
warrants immediate attent ion of the experts to develop and propose,
formulate, establ ish, not only effective treatment schedules, but also to
plan preventive measures against Madhumeha and control the morbidi ty
rate due to this disease. Ayurveda proposes a comfortable remedy as
pal l iat ive therapy.
ITHIHASA
There is precious information given by our Acharyas about al l the
aspects of the disease, which reveal the pathological aspects of disease
and make them easy to understand. They had a thorough knowledge of
the entire disease that can be observed in their l i terature. We can
observe the classical references which indicate the disease as one of the
dreadful and chronic. Our ancestors have tr ied to know about the
disease from various angles, which made them to think in many aspects
of the disease. By observat ion alone they have classif ied the disease
elaborately. Thus to understand the disease we have to know the subject
already exist ing since the days of Vedas which give valuable information
about the disease.
VEDIC PERIOD
Vedas are the oldest l i terature of civi l ization. Ayurveda is the
Upanga of Atharvan Veda. In Vedas we f ind two words “Asrava” and
Introduction 3
“Prameha”. In Atharvana Veda Asrava vyadhis are mentioned in which
Nasasrava, At imootra and Atisara are included3. The term Asrava i f
formed from “A – srava” means to f low.
In Atharvana Veda 6 / 44 / 3 “Visanaka” drug is indicated in vata
vyadhi. Kesava commenting on this, explained “Vatikruta nasani” as “
Vatikruta asravasya nasani”, means i t is indicated in Asrava vyadhis. In
the Manthra 2-3-1-3 of Atharvana Veda, the drugs emerged from valmika
are indicated in At isara, Atimootra and Nadivranam4.
This clearly indicates the prevalence of this disease with i ts
remedy in the Vedic period.
SAMHITA PERIOD
After Vedic period facts about Madhumeha were further explored by
Atreya which are recorded in “ Charaka Samhita” a complete treat ise of
medical sciences of i ts era. He explains various factors pertaining to
et iology, pathogenesis, complications and methods of treatment in detai l
in his treat ise. I t is a point of histor ical importance that the book
mentions the loss of sweet substance from urine5.
Charaka also mentioned in sutra sthana that the Madhumeha
occurs due to avri ta of Vayu6, and explains the mythological origin of
Introduction 4
Madhumeha in Nidana sthana7. During the destruction of Daksha’s as
sacri f ice, Gulma f i rst manifested in human being who f led in al l direct ions
due to the agitat ions in their body. Because of f leeing, swimming,
running, f ly ing, jumping etc. Pramehas and Kustas manifested themselves
in addit ion to the intake of Ghee.
Bhela samhita which is contemporary to Charaka samhita describes
the two types of Madhumeha i .e. prakruta prabhava (congenital) and
Swakruta (acquired)Prabhava8.
The most notable contribution of Sushruta was to devote a
separate chapter for the management of Madhumeha and he has tr ied
some specif ic preparations of minerals and vegitat ions. Further he has
also described in a separate chapter for the management of Carbuncles
which are the Upadravas of Madhumeha9.
After Sushruta, Vagbhata made great contribut ion to Indian
medicine. He simpl i f ied the exist ing knowledge and gave some new
preparat ions and ideas in the text. He classif ied two types of Madhumeha
on the basis of pathogenesis are Dhatukshayaja and Avaranaja10.
Artha shastra of kout i lya (321 – 296 BC) mentions a method to
induce Prameha in Human deal ing with the sense to injure the enemy.
Introduction 5
The spot obtained from burning chancl ion (krukalaka) and house l izard
(Gruha goul ika) together with the intestines of mott led frog (chitra bheka)
and honey, i f administered causes Prameha. This evidently points the
existence of Diabetogenic technique in the ancient t imes11.
MEDIEVAL PERIOD
This period of history of Indian medicine is known as a period of
commentators. Hence most of the books of this period are of col lections
and thoughts of previous authors, commentaries of previous books.
Madhavakara (9t h century A.D.) in his book Madhava nidana
compiled the thoughts of his earl ier authors without adding any thing new
to the knowledge on Madhumeha.
Gayadasa (11t h Century A.D.) commentator of Sushruta Samhita
elucidated that avi lata of urine in Prameha was due to the presence of
some components of dooshyas i .e. meda, mamsa etc12 .
Chakrapani, the commentator of Charaka samhita and the author of
Chakradatta, in the same period contr ibuted nothing signif icant with
reference to etiology of Prameha but recommended medicines and
regimen prescribed by Charaka and Sushruta and some of his own.
Introduction 6
Dalhana, another commentator of Sushruta samhita (12t h century)
contributed a myth that females do not suffer from Madhumeha13.
Sharangadara ( 13t h century AD) prescribed some new recipes for
the management of Prameha but did not contr ibute any thing in the f ield
of et iopathogenesis.
Bhavamishra (16t h century AD) contributed to the history of
Prameha by adding some new herbal and metal l ic preparat ions for the
management of Prameha14.
After Bhavamisra the development of Ayurveda is not so optimist ic
and had been stagnated. The concepts of ancient India regarding
Madhumeha are quite al ike with modern concepts. Descript ions of
Charaka, Sushruta show that even in that ancient t ime, Indian scholars
were famil iar with etiology, pathogenesis, symptomology and
complicat ions of Prameha, out standing being the knowledge of genetic
role in the etiopathogenesis. The regimen prescribed by them are useful
even in present era also, and these texts and their concepts do not
remain mearly as the histor ical mi le stones but have become the hope
of the Madhumeha cure at present sinerio.
Introduction 7
HISTORICAL MILESTONES.15
- Atharvana Veda is the oldest l i terature, which explains Madhumeha.
- In 2500 BC Eabers Papyrus ( Egypt ) wrote the f i rst cl inical
descript ion as “the disease without pain and melts the body” was
documented.
- In 600 BC Charaka (India) cl inical ly described Madhumeha and noted
role of heredity and Sweetness in ur ine.
- In 400 BC Sushruta (India) described same as that of Charaka.
- In 30 BC – 38 AD Celsus (Greece) gave some cl inical descript ion.
- In 1s t AD Aretaus (Greece) introduced the name as diabetes meaning
“to run through a pipe” .
- In 2nd AD Claudius Galenus proved that by consuming the drinks
which weakens the kidney wi l l al low the l iquids without change.
- In the same century Tchang Tchong king proved this as the disease of
thrust.
Introduction 8
- In 600 AD Aetius (Amida) treated this disease by using sedatives.
- In 980 – 1037 AD Avicenna ( Arab ) explained about Diabetic
Gangrene and put forward the question as “ is there any relat ion
between pancreas”
- In 1727 Brunner.J.C. ( Swiss ) removed the pancreas from the dogs
and found that they developed thirst and polyurea.
- In 1770 Thomas wi l l is ( England ) proved the di f ference between
Diabetes Mallets and Diabetes Insipidus.
- In 1775 Matheu Dobson Evaporated the specimen of ur ine of a
Diabetic patient and discovered a residue which was almost glucose.
- In 1782 Thomas Cawley recorded the disease.
- In 1788 Cawley (Engl ish) described pathology of pancreas.
- In 1815 M. Chevreul found out the presence of glucose in the urine.
Introduction 9
- In 1839 Bernard Naunyn studied the relat ion between the metabol ic
disturbance and pancreas.
- In 1841 Trommer found the test for urine glucose.
- In 1848 Claude Bernard proposed that the production of sugar in the
l iver is the reason for the r ise in the blood glucose Laval. He injured
the base of the fourth ventr ic le and proved the increase of blood sugar
level, he also proved when the blood sugar level is raised the sugar
starts f lowing out through urine. Even after the lowering of the blood
glucose level the urine contains glucose was the major discovery by
Claude Bernard.
- In 1845 Boucardet establ ished the relat ion between the Diabetes and
Pancreas.
- In 1850 Fehl ing found the test for testing the urine sugar.
- In 1867 Paul Langerhans (Germany) found islets of langerhans.
- In 1874 kusmal found the symptoms caused by increase in acitone in
the body.
Introduction 10
- In 1874 Oacar Minkowski found the acidosis.
- In 1886 Joshaf wan maring and Oscar Minkowski proved the
induct ion of diabetes by removing the Pancreas.
- In 1870 Clande Bernard ( France ) Noted sugar storage in l iver as
glucogon and elevated blood sugar in diabetes.
- In 1901 E.L.O.Pie proved the increase and decrease in the blood
glucose level is due to langerhans.
- In 1907 M.L Lane di f ferent iated and named the langerhans as two
types “alpha and beta“.
- In 1921 J.J.R.Macleod, Frederick . G . Banting and Charles.H. Best
(Toronto )discovered Insul in
- In 1926 H.C.Hagedorn mixed protimine to insul in and made i t to defuse
s lowly so that i t can act for longer t ime.
- In 1944 Von Noorden ( Vienna ) Bel ieved that l iver play a role in
diabetes.
Introduction 11
- In 1952 Sanger found the structure of the insul in.
- In 1954 A. Shef found Carbutamide was working as a hypoglycemic
agent. This was the f i rst oral hypoglycemic agent, but as i t had many
side effects i t was drown back from the market and a new drug similar
in the function of Carbutamide was introduced as Tobutamide which has
less side effects.
- In 1970 On words Merwin Gl iedman and other transplanted pancreas
culture of Is lets of cel ls of pancreas transplant of beta cel ls.
Even in 1999 also the research is going on throughout the world.
St i l l we are fai l ing to put ful l point to these milestones and newer aspects
of the disease are emerging out day by day.
Some of the latest research going throughout the country and abroad is given
below16,17.
- Toxicological Evaluat ion of Fenugreek seeds in Diabetic patients.
By Sharma R.D. at PG Dept, SN Medical col lege, Agra. –1996
- Consti tut ional study of pat ients of Diabetes Mell i tus vis-Avis
Madhumeha by R H Singh at Dept of Kayachiki tsa, B.H.U. 1996
Introduction 12
- Prognosis of Prameha on the Basis of Insul in level.
By Upadhyay at Dept of KC, I.M.S, B.H.U, Varnasi. 1996
- Diabetic foot ulcers treated the Ayurvedic way
By Ojha J K. at Dept of DG, B.H.U, Varnasi. – 1997
- Scope and use of Indigenous Herbal drugs in Madhumeha an Indian
Scenario. By Mukherjee.S K at C.D.R.I, Lucknow.- 1997
- Potential antidiabetic agents form plant sources. By R K Goyal at Dept
of Pharmacology, L M Col lege of Pharmacy, Ahmedabad.- 1997
-
- Evaluat ion of hypoglycemic act ivity of Tradit ional Herbal preparat ion
By Negam S A at Department of Pharmacology, NRC, Egypt. 1997.
- Ant i diabet ic property of neem seed By Kannan J at Pharmacy Dept,
Faculty of tech and Engg, MS Universi ty of Boroda. Baroda 1997
- Hypoglycemic effect of Trigonel la foenum Leaf in Diabetic By A. Barry
at Dept of pathology and forensic Medicine, Universi ty of Basrah 1997.
Introduction 13
References
1 API Text book of Medicine pp 205
2 Diagnoses of Diabetes pp 2
3 Ayurveda I thisa pp 26
4 Ayurveda I thisa pp 29
5 Charaka Nidana 4 / 37
6 Charaka Sutra 17 / 78.
7 Charaka Nidana 8 / 11
8 Bhela Samhita Nidana sthana 6 / 1 – 4.
9 Sushruta Chiki tsa 12 / 16
10 Astanga .Hridaya.Nidana 10 / 8
11 Ardha Sastra of Kouti lya 16 / 179 / 1.
12 Su NI Naya Chandrika Commentory.6 / 6.
13 Nibandha sangraha on Su Ni 6 / 33
14 Bhava prakasha Madyama kanda 38 / 45 15 Sihimootra roga by A. Narayanappa.pp 4 16 Al l ied Ayurvedic Medical Research Abstracts (AAMRA) 17 Researches in Ayurveda 1997
Shareera 13
Charaka explained that the persons who take excess and heavy
food or food with sour and salty taste, new r ice, fresh wine and enjoy
long sleep wi l l increase, the kapha, pi t ta, meda and mamsa and obstructs
the Vata together with the ojus come down to the vast i and causes
Madhumeha1. By this i t can be seen that the vast i is involved in the
product ion of Madhumeha. In Madhumeha, Prabhoota mootrata is the
main lakshana. I t is a symptom of mootravaha srotodusti also2. Hence in
Madhumeha mootravaha srotodust i is present.
Charaka mentioned that Prameha occur whenever the Medas
(srotas) is vi t iated3. vr ikka and vapa are the moolas of Medovaha
Srotas4. So the involvement of vr ikkas is present in Madhumeha.
Thrishna is an important lakshana. The cause for tr ishna is Udakavaha
Srotodusti5. Talu and kloma are the moolas for Udakavaha srotas6.
Hence the involvement of Talu and Kloma are present in the product ion of
Madhumeha. Liver plays an important role in dhatuparinama. In
Madhumeha dhatuparinama alters because of the involvement of most of
the dhatus present in the pathogenesis. Hence the l iver is responsible in
the production of Madhumeha.
Thus i t can be said that the organs responsible for the product ion
of Madhumeha are -
Shareera 14
1. Taalu
2. Kloma
3. Vrikka
4. Vasti
5. Yakri t
But in ayurveda the knowledge of rachana and kriya of Madhumeha
are st i l l in controversy, but with the help of modern science the
Kriyatmaka vivechana can be discussed.
TALU
The classical texts in Ayurveda have given the brief descript ion
about Talu. I t is located above the kanta and becomes the base of the
siras as i t is evident from the del iberations in Bhela samhita. I t is the
moola for the Udakavaha srotas7. Charaka mentioned Talushosha and
pipasa wi l l exist i f Udakavaha Srotas is vi t iated8. Sushruta mentioned
nine Talugatha vyadhis9 . Charaka and Kashyapa stated that the union of
two bones forms Talu10.
KLOMA
Ayurveda acharyas stated that Kloma is the moola for Udakavaha
Srotas11. Al l acharyas mentioned this as one among the Kostangas12.
Shareera 15
Though there are many schools of thoughts regarding the anatomical
identi f ication, In Sushruta samhita i t is said that kloma is explained with
Yakri t which is located in the r ight side of the body13. Dalhana whi le
commenting on this said that i t is in the r ight side of body which is laying
down below the Yakri t and i t is also cal led as Ti lakam. Vagbhata says
that Kloma is located along with Yakri t in the r ight side of the body. I ts
combinat ion according to Sharangadhara samhita in Pit ta which is
agniroopa14. He has mentioned Agnashaya as i ts synonym. Adhamalla
whi le commenting on this says that i ts formation is with the sonitha ki t ta.
I t is in the r ight side and in contact with the l iver. He has also given
Ti lam as a synonym to Kloma15.
Charaka says that Talumoola and Kloma are the seats of
Udakavaha srotas. I f these srotases are vi t iated the pathological
changes i .e. shosha of above organs and thirst develops16. Chakrapani
whi le commenting on Kloma said that i t is a Pipasa sthana (thirst centre).
Sushruta also said as above and on injury to these srotases the
immediate death occurs besides polydipsia.
Based on the above descript ions i t is clear that Kloma in one
among the Kostangas and located adjacent to the Yakri t . The nearest
organs to the l iver are Gal lbladder and Pancreas. I t is also clear that
Shareera 16
only Pancreactomy causes the polydipsia and death so i t can be
considered as Kloma.
VRIKKAS
Vrikkas are two in number and are si tuated in Kosta. Al l acharyas
included vr ikkas in kostangas. In Dalhana commentary on Sushruta the
vr ikkas are described as two f leshy bodies, each si tuated on ei ther side
of spine and their shape as being l ike rounded bodies17. These are said
to be composed of the essence of the Rakta and Medas18. Sharangadara
whi le describing their function says that vr ikkas are said to be the
nourishers of the abdominal fat19. Adamalla whi le commenting on the
above states that vr ikkas are two rounded bodies in the abdomen which
are derived form the essence of the blood and fat and they originate form
fat. They are stated to be concerned with the nutr i t ion of the abdominal
fat. Ayruvedacharyas Charak, Dalhana, Chakrapani says vrikkas are two
in number and they are si tuated below the chest20.
VASTI
Embryological ly, Vasti is stated to be maternal contribut ion. I t is
stated to be derived form the essence of Rakta and kapha supported by
Pit ta in to which Vayu also enters21. Vast i has been included under
kostangas and Ashayas by al l acharyas. I t is stated to be one in
Shareera 17
number22. The term Vasti , Mutravasti , Vastipudaka, Mutrashaya and
Mutradhara seem to have been used as synonyms in Ayurvedic texts23.
Charaka whi le describing the locat ion of Vasti has stated that vasti
is si tuated in between the Sthoolaguda, Sevani, Sukravaha naadies and
Motravaha naadies24. According to Sushruta, Vast i is near to Nabhi, Kat i ,
Guda, Vankshana and Shepha. He further stated that vasti , Pourusha,
Vrushana and Guda are al l interrelated and si tuated in the pelvic cavity25.
According to Bhavamishra and Sharangadara, Vasti is located below the
Pakwashaya. Vagbhata says that i t is located inside the kat i26. Sushruta
states that i t is s ituated near the Garbhashaya in females27.
Regarding the shape and structure of the Vast i , Sushruta has
stated that i ts shape looks l ike that of “Alabu” and ful l of Siras and
Sanyus al l around. I t is stated to be Tanu twak i .e. a thin volved organ or
i ts coverings are thin and membranous. I t has one exit and l ies with i ts
mouth downwards28. Vagbhata has described i ts shape as Dhanur Vakra
i .e. bent l ike bow having one opening downwards and composed of l i t t le
muscles and blood. Adamalla described i ts shape as “Charmaka
Latwakara” that is l ike bag of leather. The Acharyas described i t to be
the storehouse of Mootra and seat of “Prana” being one of the important
marmas. Charaka says that i t is reservoir of mootra where al l the
Ambhuvaha Srotases ends. He also explained vasti as the moola of
Shareera 18
Mootravaha srotas. Sushruta stated that Mootraghata, Prameha, Sukra
doshas, Ashmari develops from Vasti only29.
YAKRIT
Since the Vedic period, the traces of gross anatomical knowledge
of Yakri t are avai lable. Sayana the commentator of Vedas whi le
commenting on the word Yakan coined in atharvana veda described that
Yakan is si tuated near the heart. The ward Yakan in his view means
Yakri t . Yakri t is described as one of the Matruja angas due to i ts
softness30 and i t is included in Kostangas. Yakri t in i ts embryonic stage
is formed by the shonitha. Yakri t is si tuated on the r ight side, below the
Hridaya31 and i t is the moola for the Raktavaha srotas32. Sushruta
mentioned Raktadharakala is present in Yakri t33.
SHAREERA KRIYA
Agni plays an important role in manifestation of Madhumeha hence
concept of Agni carr ies importance in the study of Madhumeha. Agni or
Jataragni is the main cause for every parinamas, or changes in the body.
Dahana (burning) and Paka (Chemical act ion) are the chief actions of
agni. I t spl i ts the Vi jateeya dravyas into sajateeya dravyas for easy
absorpt ion. The ingested food after reaching Amashaya enters the
digest ion by Antaragni. (Pachaka pit ta) in the presence of samana vayu
Shareera 19
and Kledaka kapha which effects the digest ion. The Ahara parinamakara
bhavas are Ushma, Vayu, Kleda, Sneha, and kala which are essential for
normal ahara pachana. The digestion and other metabol ism in the body
can be done only in presence of Agni.
The synonyms of Agni are kayagni, antaragni, kostagni,
audaryagni. There is no Agni other than Pitta, as i ts actions perform in
the l iving body is Paka or pachana. Acharyas mentioned 13 types of
agnis in the body. They are one Jataragni, f ive bhootagnis and seven
dhathwagnis. Samana vayu, which is located nearer to Jataragni moves
al l over the kosta, col lects the ingested food. Then separates prasada
and ki t ta bhagas of Ahara into Ahara rasa and mootra, pureesha
respectively.
According to the Ayurvedic physiology Bhutagnipaka fol lows
Jataragnipaka and i t completes the process of internal digestion, i t is
only after the complet ion of Bhootagnipaka the formation of ahara rasa is
possible. Dhatwagnipaka does not start t i l l the Bhootagnis completes i ts
process of digestion and supply the Sajaat iya nutrients to the
Dhatwagnis. But i t can be said that the si te of action of Bhootagnis starts
from the intestines t i l l the cel l membrane, the l iver being in between the
Bhutagnipaka that wi l l be predominant in i t . In the event of the fai lure of
the funct ion of Bhootagnis, the Dhatwagni wi l l not be in a posit ion to bui ld
Shareera 20
the respective dhatus. That is how the def icient function of Bhootagnis is
to be understood.
Agni assumes names of Vishamagni, Teekshnagni, Mandagni, and
Samagni according to doshic inf luence on i t .
Charaka says mandagni by i ts qual i t ies causes ajeerna and mala
sanchaya, thereby i t leads to several diseases. Mandagni vi t iates kapha,
kapha in turn vi t iates the other dhatus part icularly medo dhatu, and this
leads to Prameha. Hence the role of agni is to be considerable in the
study of Madhumeha.
Ayurveda has mentioned about the formation of Mootra and i ts
excret ion. Mootra has been described as the Drava Bhaga of the Kit ta
and i t is produced in Amapakvashaya, The l iquid port ion is said to
separated form the sol id fraction in the pakvashaya by the pureeshadhara
kala under the inf luence of Samana vayu, brought in to vasti and from
there i t is excreted by the Apanavata. Mootra is said to be an out come
of the digest ion of ingested food, and the seat of i ts production is
pakvashaya. Mootra is stated to be a mala derived form the food
ingested in four-fold manner. The l iquid port ion of ki t ta bhaga after
absorpt ion circulates in the body and i t is f inal ly carr ied to vrikkas by two
mutravaha dhamanis which divide in to innumerable branches forming the
mutravaha srotamsi through which i t oozes and there i t is named Mutra.
Shareera 21
From vrikkas, two Gavinis carry i t to vasti . Even though Vrikkas have
been mentioned in Ayurveda their relat ion with the formation of mootra
has not been clearly described. A deep study of Ayurveda classics
enl ightens to certain extent about mootropatt i . I f Vrikka, Gavini and
Medhra are considered as one system of srotas for the purpose of the
product ion and excretion of ur ine, I t remains stored in vast i t i l l is
excreted during mutra pravrutt i . I f so, there can be no di fference between
the views of Ayurveda and modern medicine.
MODERN ASPECT
Diabetes mell i tus is a chronic disease. I t results due to disturbance
in carbohydrate metabol ism and deficiency of Insul in34 secreted by the
Beta cel ls of Is lets of langerhans of pancreas, but hormones of pi tui tary
and adrenal glands are also int imately related to the development of
Diabetes State. Liver plays an important role in the metabol ism for
carbohydrate. I t stores glucose in the form of glycogen under the
inf luence of Insul in. Any alterat ion in this function leads to diabetes35.
So the involvement of organs in diabetes mell i tus are
- pi tui tary gland
- Pancreas.
- Adrenal gland
- Liver.
Shareera 22
PITUTARY GLAND36
This is a exceedingly important endocrine gland with a wide range
of functions including the control of the other endocrine glands and of
body growth.
This gland measures 1.5 cm in the coronal plane, 1 cm in the
sagital plane and 0.75 cm in vert ical form. I t l ies within the sel la Tarsica
of the sphenoid bone and posterio superior to the sphenoid air sinuses
below the optic chiasma. I t is f lattened ovoid lying in the hypophyseal
fossa (sel la Tarasica) and connected to the inferior surface of the
hypothalamic part of the brain by the infundibulum. Structural ly the gland
can be divided into two main parts
a) Anterior lobe which is composed of Adeno hypophyseas t issue.
b) Posterior lobe which is Neurohypophuyseas.
Posterior lobe of the hypophysis is the expanded inferior end of the
infundibulum and is developed from the brain. The anterior lobe is much
larger than the posterior lobe and consists of three parts, which part ly
surround that lobe and the infundibulum. The distal part forms most of
the anterior lobe. I t is separated form the posterior lobe by the thin sheet
of glandular t issues ( intermediate part) appl ied to the posterior lobe. The
infudibular part is a narrow upward projection of the distal part. The
Shareera 23
anterior lobe develops from the ectoderm and has only vascular
connection with the brain.
Anterior lobe is the master gland of endocrine system, because i t
produces proteotrophic hormones which effects the other ductless glands.
In these secretions two hormones are having direct action on
carbohydrate metabol ism. If any disturbance occurs i t leads to
Hyperglycemia or Hypoglycemia.
The hormones secreted are Growth hormone or somatotrophic
hormone (GH of STH ) and Adreno Cort ico Trophic Hormone (ACTH).
The pitui tary effect of STH on carbohydrate metabol ism is to st imulate i ts
storage. Administrat ion of growth hormone in animal or in man produces
hyperglycemia and glycosuria. So the growth hormone is diabetogenic
effect especial ly in man. The hormone is however increases the
glycogen content of cardiac muscle. Administrat ion of ACTH produces
simi lar effects as induced by growth hormone. Both STH and ACTH
increase gluconeogenesis and diminish the rate of oxidat ion of glucose.
Thus the anterior pi tui tary has a diabetogenic role.
GH (growth hormone) is also known as somatotropin, i ts pr incipal
function is to act on the skeleton and skeletal muscles, in part icular to
Shareera 24
increase their rate of growth and maintain their size once growth is
attained. GH causes cel ls to grow and mult iply by direct ly increasing the
rate at which amino acids enter cel ls and are bui l t up into proteins. GH is
considered to be a hormone of protein anabol ism since i t increases the
rate of protein synthesis. GH also promotes fat catabol ism that is i t
causes cel ls to switch from burning carbohydrates to burning fats for
energy released. At the same t ime GH accelerates the rate at which
glycogen stored in the l iver is converted into glucose and released in the
blood. Since the cel ls loosing fats for energy however they do not
consume as much glucose, the result is the increase in the blood sugar
level. A condit ion cal led hyperglycemia. This process is cal led
diabetogenic effect because it masks the elevated blood glucose level of
diabetes mell i tus. GH seems to produce many of i ts effects by convert ing
other factors in to growth promoting substance cal led soerto medians and
insul in l ike growth factors (IGF).
Other hormones can indirectly affect insul in production however for
instance GH raises blood glucose level and the r ise in glucose level
tr iggers insul in secret ion. ACTH by st imulat ing the secret ion of
glucocort icoids brings about hyperglycemia and also directly st imulates
the release of insul in GHIF (romatostatin) inhibi ts the secret ion of insul in.
One stimulus that inhibi ts GH secret ion is hyperglycemia high blood
sugar level. An abnormally high blood sugar level st imulates the
Shareera 25
hypothalamus to secrete the regulat ing factor GHIF (somatisat ion) GHIF
inhibi ts the release of GHAF and thus the secretion of GH. As a result
blood sugar level decreases.
PANCREAS37
The pancreas is a compound alveolar gland. I t has got both
endocrine and exocrine funct ions. I t l ies against the posterior abdominal
wal l behind peri toneum. The adult pancreas consists of a Head, Neck,
Body and Tai l . The whole organ is about 15 cm long with the r ight margin
of the head in contact with the descending part of the duodenum and the
tai l is in contact with the spleen. The disease diabetes mell i tus is
considered only to i ts endocrine secretion that is Insul in, so i t is more
important to go through i ts endocrine part.
ISLETS OF LANGERHANS
The islets of Langerhans are composed of various components that
are organized to form micro-organs. The mass of is lets within a pancreas
is dynamic and changes both with growth and development and with
functional chal lenges. As we learn more about the regulat ion of
di f ferent iat ion of is let cel l types, we also may learn how to enhance the
growth of is let cel ls, part icularly the beta cel ls.
Shareera 26
Is lets function both singly and in concert. Recent work has
revealed grater diversi ty in is lets than that previously recognized. There
is funct ional heterogeneity between islets and beta cel ls within the same
islet. Numerous peptides other than the four main is let hormones
( insul in, glucagon, somatostat in, and pancreat ic polypeptide) have been
immuno-local ized in is lets.
The islets of Langerhans are clusters of endocrine t issue scattered
throughout the exocrine pancreas. In the adult mammal, the is lets are 1
to 2% of the pancreat ic mass and thus comprise around 1gm of t issue in
the adult human. Islets are a complex mixture of cel ls and function both
separately as micro-organs and in concert as the endocrine pancreas.
Although the direct secret ion of insul in and glucagon form islets into the
portal vein has obvious advantages with respect to inf luence on hepatic
function. The islet mass is dynamic, adjusting to meet the changing
needs of the individual, whose size and level of activ i ty vary at di f ferent
stages of l i fe. When the islet mass cannot adjust to meet the demand,
diabetes results.
The pancreas of the adult human contains about 200 units, or 8mg,
of insul in. The size of an islet can range from only a few cel ls and less
than 40 micrometer in diameter to about 5000 cel ls and 400 micrometer
in diameter.
Shareera 27
GROWTH OF ISLET
The growth capacity of the beta cel l depends on the st imulus and
the abi l i ty of the cel l to recognize the st imulus as wel l as on the number
of beta cel ls that can enter the cel l cycle and undergo mitosis. There is
an increased incidence of polyploid beta cel ls in the diabetic human.
Although there may be numerous st imul i for beta-cel l growth, three major
st imul i are known. Glucose has been shown to st imulate modest growth
of ei ther neonatal or adult pancreat ic beta-cel ls in culture. Pregnancy
has been shown to cause both increased repl icat ion and mass of beta-
cel ls. As a paral lel f inding, in vi tro studies have shown that prolact in,
placental lactogen and growth hormone can st imulate repl icat ion of beta-
cel ls. Diabetes results only i f increased cel l loss or functional demands
cannot be met.
COMPONENTS OF THE ISLETS OF LANGERHANS
There are three major endocrine cel l types in is lets : the insul in
producing beta-cel l , the glucagon producing alpha-cel l , the somatostat in
producing delta-cel l .
Alpha-cell
The alpha cel ls are usual ly smaller and more columnar than the
beta cel ls and wel l granulated with granules 200 to 250 nm in diameter.
The granules are electron dense with narrow halo of less-dense material
Shareera 28
and a t ight ly f i t t ing granule-l imit ing membrane. There is l i t t le species of
variat ion.
Beta-cell
The beta cel ls are polyhedral, being trancated pyramids, and are
usual ly wel l granulated with secretary granules 250 to 350 nm in
diameter.
Delta-cell
The delta-cel ls are usual ly smaller than either alpha or beta cel ls,
are wel l granulated, and are often dendri t ic in shape. Within a delta cel l
the electron density of granules varies great ly. Each granule, 200 to 250
nm in diameter, contains material of homogenous moderate density that
f i l ls the granule-l imit ing membrane.
Table showing cel ls and their relat ive hormones
Cel l type Size of secretary granule (nm) % of cel ls Hormone
Beta 250 – 350 60 – 80 Insul in
Alfa 200 – 250 15 – 20 Glucagon
delta 200 - 250 5 – 10 somatostat in
MICROVASCULATURE
The islets are highly vascularized and has a direct arter iolar blood
supply. The fenestrae render these capi l laries highly permeable. The
Shareera 29
blood f low to the islets has been found to be disproport ionately large (10
to 20% of the pancreatic blood f low) for the 1 – 2% of pancreatic volume
. Factors regulat ing islet blood f low may effect is let hormone secretion.
High concentrations of glucose have been shown to enhance pancreat ic
blood f low and to preferent ial ly increase islet blood f low.
NERVES
The pancreas is innervated by sympathetic f ibers from the cel iac
gangl ion and by parasympathetic f ibers form the vagus nerve. These
parasympathetic f ibers synapse in small gangl ia dispersed in the
pancreas. They may act as pacemakers for the osci l lat ions in hormone
levels that occur without extr insic nervous connections, as in the isolated
perfused canine pancreas. Within the pancreas, nerve f ibers terminate in
perivascular, periacinar, and perinsular areas. Within the is lets the
nerves fol low the blood vessels and terminate within the pericapi l lary
space, within the capi l lary basement membrane, or closely apposed to
the endocrine cel ls38
Functions of these hormones :
INSULIN:
The insul in is hypoglycemic, ant i diabetic factor and the protein
bound hormone that regulates the blood glucose. I t also increases the
Shareera 30
oxidat ion of glucose to CO2 in the t issues and depresses
gluconeogenesis i .e. formation of glucose from the sources other than
carbohydrates.
Insul in increases combustion of sugar in the t issue and also helps
in the treatment of glucose in the cel ls. I t increases synthesis of
glycogen from sugar and lactate both in the l iver and muscle. This is
cal led the directive effect of insul in. Insul in promotes the uptake of
glucose inside the cel ls and the intercel lular phosphorylat ion of glucose
to glucose–6–phosphate. Glucose–6–phosphate i tsel f also appears to be
a specif ic activator of glycogen synthesis.
Insulin effect on protein metabolism:
I t prevents gluconeogenesis Glucose is normally formed from
proteins and l ipids in the l iver. In diabetes this process is enhanced.
High blood sugar level in diabetes is due to over product ion of glucose.
In the starving diabetes dextrose ni trogen ratio is fair ly constant. This
shows that both sugar and ni trogen are coming form the same source i .e.
proteins. When insul in is given both sugar and nitrogen excretion fai ls,
showing that formation of new glucose from proteins has been interfered.
Shareera 31
Insulin effect on fat metabolism:
I t prevents formation of ketone bodies (anti ketogenic). In advance
diabetes, excess ketone bodies are formed in l iver, due to incomplete
combustion of fatty acids. After the administrat ion of Insul in more sugars
burn and l iver glycogen increases displacing the l ipids. Hence l ipid
combustion is discouraged and ketosis disappears.
Insul in decreases the cholesteremia and l ipademia. I t also prevents
accumulation of excess l ipid in the l iver and breakdown of l ipid in
Adipose t issue.
GLUCOGON :-
The Alpha cel ls of the islets of Langerhans secrete Glucogon. I t is
a polypeptide hormone with 29 aminoacids having molecular weight of
3,485. This polypeptide has been completely synthesized. Glucogon
causes glycogenolysis in the l iver and antagonist to l iver by depriving the
action of Insul in.
The blood sugar level chief ly controls the secretary activi ty of
Alpha and Beta cel ls. Hyperglycemia st imulates the release of Insul in
where as, hypoglycemia wi l l release the glycogen. There is no good
evidence that a tropic hormone secreted by the pitui tary, directly
inf luences the secretary act ivi ty of the pancreatic is lets, through
secret ions derived form other endocrine glands for example, the adrenal
Shareera 32
gland have some effects. I f the is lets are completely removed or
extensively damaged, the lack of or reduced Insul in formation results in
hyperglycemia and the condit ion of diabetes mell i tus (Madhumeha).
Relat ively normal carbohydrates metabol ism can then be restored by
supplementat ion of insul in.
I t is necessary to point out however that though a def iciency of
insul in production and release may result in Diabetes, not al l cases of
Diabetes are due to a deficiency in Insul in product ion. Even pi tui tary,
Liver and Adrenals are also involved in this process. Cl inical syndromes
involving abnormal carbohydrate metabol ism and abnormal blood sugar
levels may result f rom either deficiency or excess product ion of Insul in
and Glycogen. The latter when injected result in an increase in blood
sugar. Excess production of insul in as in cases of Islet tumors results in
hypoglycemic and attains neurological changes, excess product ion of
Gastrin, acidi ty and peptic ulceration.
ADRENAL (SUPRA RENAL) GLANDS
The adrenal glands are si tuated on the upper poles of the kidneys.
Each gland weighs about 4 gm.
Microscopic structure - A dist inct connect ive t issue capsule surrounds
the parenchyma of the gland. Beneath the capsule the cortex is arranged
in 3 layers. They are -
Shareera 33
Zona Glomerulosa.
Zona Fasculata
Zona Reticularis
Zona Glomerulosa : - The outer layer which varies in thickness form
almost total absence to clusters of a dozen or more smal l cel ls is known
as Zona Glomerulosa. Zona Glomerulosa secretes mainly aldosterone
that is concerned with the salt and water balance and acts on the distal
convoluted tubule and col lecting ducts of the kidney. I t also secrets a
small amount of glucocort icoids and sex hormones.
Zona Fasculata : - inside the f i rst layer the cel ls are larger and form
more or less paral lel radial columns. They commonly contain fat droplets
which give them a spongy appearance. This region is known as a Zona
Fasculata. This layer secretes predominantly Glucocort icoide.
Zona Reticularis . : - Centre of the gland the regular arrangement of cel ls
of the Zona fasciculata is replaced by one of anastomosing cel l cords
forming the Zona Reticular is, which secretes sex hormones and a small
amount of Glucocort icoids but no Aldosterone.
The adrenal Medul la is chief ly composed of chromaff in cel ls
(phaeochromocytes) which ei ther secrete Adrenal ine or Nor- adrenal ine.
Shareera 34
LIVER :-
The l iver is the largest gland in the body. The greater part of the
Liver l ies under the covering of the r ibs and coastal cart i lage. The l iver
is a dark brown, highly vascular and soft organ that is commonly ruptured
or torn in abdominal injur ies. I t is approximately one f i f teenth of the body
weight in adult.
The l iver is determined by the surrounding organs i t retains the
shape of a blunt edge i t has two surfaces. Diaphragmatic surface
divisible into Superior, Anterio, posterior and right parts according to the
direct ion in which i f faces and visceral (posterior) surface faces
posterior ly and Inferiorly. Liver is divided into four lobes Right,
Quadrate, Caudate and Left lobes.
Functions of l iver in carbohydrate metabol ism are:-
1. Storage of Glycogen.
2. Conversion of Galactose and fructose into glucose.
3. Gluconeogenesis
4. Formation of many important chemical compounds from the
intermediate products of Carbohydrate Metabol ism.
Shareera 35
Liver is especial ly important for maintaining a normal blood glucose
concentration. For instance storage of glycogen al lows the l iver to
remove excess glucose from blood, store i t and then return i t in to the
blood when the blood glucose concentrat ion begins to fal l too low. This
is cal led the glucose buffer function of the l iver. As an example,
immediately after a meal containing large amounts of carbohydrates the
blood glucose concentrat ion raises about three t imes as much in the
person with a non functional l iver as in a person with a normal l iver.
Gluconeogenesis in the l iver is also concerned with maintaining a
normal blood glucose concentration for glucose neogenesis occurs to a
signif icant extent only when the glucose concentration begins to fal l
below normal. In such case large amounts of amino acids are converted
into glucose, there by helping to maintain a relat ively normal blood
glucose concentrat ion.
Shareera 36
SHAREERA
References
1 Charaka Nidana 4 / 4
2 Charaka Vimana 5 / 7
3 Ibid 5 / 7
4 Ibid 5 / 7
5 Ibid 5 / 7
6 Ibid 5 / 7
7 Sushruta Shareera 9 / 15
8 Charaka Vimana 5 / 7
9 Sushruta Nidana 16 / 42
10 Ibid 16 /45
11 Charaka Vimana 5 / 8
12 Charaka Shareera 7 /15
13 Sushruta Shareera 4 / 23
14 Sharangadara Poorva khanda 5 / 63
15 Adamalla on Sharngadhara 5 / 83
16 Charaka Vimana 5 / 8
17 Sushruta Nidana 7 / 18
18 Sushruta Shareera 4 / 30
19 Sharangadhara poorva khanda 5 / 40
20 Charaka Shareera 7 / 7
Shareera 37
21 Sushruta Shreera 4 / 26
22 Ibid 4 / 47
23 Charaka Shareera 9 / 4
24 Ibid 9 / 4
25 Sushruta Nidana 3 / 17,29
26 Astanga Hridaya Shareera 4 / 10
27 Sushruta Chikitsa 7 / 33
28 Sushruta Nidana 3 / 18
29 Ibid 3 /15
30 Sushruta Nidana 3 / 15
31 Dalhana on Su Sh 4 /23
32 Charaka Vimana 5 / 7
33 Sushruta Shareera 4 / 10
34 API Text of Medicine by Sanani pp 205
35 Ibid pp 204
36 Principles of Anatomy and Physiology by Gregfard Tortara
37 Joslin’s diabetes Mellitus. pp15
38 Ibid pp 216
Nidana 36
HETU
I t is bel ieved that Prameha is a hereditary disease and many
factors play an important in the product ion of the disease as a cl inical
enti ty. They are age, sex, diet, body weight, Infect ion, pregnancy, etc.
Emotional stress and trauma have also been considered as etiological
factors of Prameha. Charaka considers Madhumeha as one out of the four
veri t ies of vataja Pramehas1. He has also stated that al l factors that
increase Kapha are the causative factors of the Pramehas2. The general
et iological factors of Prameha as stated by Charaka are3 – “Addict ion to
the pleasures of lounging and sleeping, excessive use of curds, meat
juice of domestic, aquatic and wet land animals, mi lk or diary products,
newly harvested grains and drinks and products of jaggery".
The et iological factors as stated by Sushruta are simi lar to Charaka
and capable of vi t iat ing mainly the Kapha dosha. Sushruta states that al l
variet ies of Prameha, i f not properly treated and attended to at the onset,
may ult imately develop into Madhumeha4. Based on the etiology,
Sushruta has classif ied Prameha into two variet ies as sahaja and
apathya nimittaja. Apathya nimit taja is subdivided into two as Ahara
nimit taja and vihara nimit taja.
Nidana 37
1. Sahaja or Genetic origin.
Charaka4 and Susrata5 have evaluated that beeja dosha is also a
cause for Prameha. Further Sushruta has included Madhumeha in the
Adibala pravri t taja category of disease.
The term beeja has been considered as a sukra and shonitha5,
which correlates with the sperm and ovum of modern concepts. Beejas
are vi t iated with dosha (Vata especial ly responsible for division of cel ls
makes certain abnormali t ies in chromosomal galaxy of sperm or ovum)
are responsible for genesis of Prameha, In gross the organs which are
responsible for producing Prameha are ambuvaha srotas, mamsa, kleda,
kloma, mootravaha srotas. They are deformed since bir th and susceptible
to get Prameha, aggravated by nimit ta karana. This may be because of
the selective discriminative of these organs to develop Prameha. As a
result of defective beeja when Prameha is developed, then the person is
cal led as a Jatha Pramehi pat ient. Jata Pramehi6 has been considered as
a Kulaja vikara7. Few diseases included under this category are Kusta,
Arsha, Meha, Kshaya etc. Kulaja vikaras means the diseases, which are
carr ied from the former generat ion to the successive generat ion, and they
are of the defects in the genetic code.
Nidana 38
2. Apatya nimittaja
Apathya is the main cause for the disease. Apathya includes both
ahara and vihara. Al l acharyas have stressed the indulgence of
unwholesome food and vihara in the production of Prameha. Ahara and
vihara that increases kapha, medas and mootra lead to the genesis of
Prameha.
Charaka explains the Nidana8 as Amla, Lavana, Madhura Rasa and
Guru, Snigdha guna dravyas, Curd, Milk, Mamsa rasa of aquatic animals,
Fresh cereals. Guda and Guda vikara.aharas and Sitt ing idle, Excessive
sleep, Disl ike for walking, act ivi t ies and to take bath are the viharas for
Madhumeha.
Sushruta explains the Nidana9 as Madhura Rasa, Medhya, Snigdha,
Sheeta guna dravyas. Nava anna, Wine, Meat of animals l iv ing in marshy
lands and Guda as aaharaj hetus. Laziness, Day sleep, inactiveness as
viharaja hetus of Madhumeha.
Vagbhata explains the Nidana10 as Madhura, Amla, Lavana Rasa,
Guru, Snigdha, Sheeta, Picchi la Guna dravyas, Nava anna, Madhya,
Anupa Mamsa, Ikshu rasa, Guda and Guda vikara, Dadhi, Paya as ahara
Nidana 39
and Sit t ing for long t ime, Sexual intercourse, Sleeping excessively as
viharaja Nidana for Madhumeha.
Charaka has explained the vishista nidanas, of Prameha according
to their doshas, they are as fol low.
Kaphaja prameha nidana11.
Aharaja.
The frequent and excessive use of newly harvested rice
This plant is common and quite wi ld in the jungles in India, I t is
cult ivated throughout India, chiefly in the Tamil nadu, Bengal and
Maharastra Presidencies. And also widely cult ivated in tropical
countries.
Part used -
Leaves.
Brief description44 -
Eranda is eka varshika or bahuvarshayu gulma or vr ikshaka
which grows up to 17feet. Leaves are green 30 – 60 cm in diameter
with 5 – 10 projections. leaf stem wil l be 4 – 12 inch long and tublar.
Flowers are unisexual, male f lowers are above and the females are
Drug Review 82
below in the plant. Frui t is thorny and 1 – 3 cms in diameter. Seeds
are oval, shiny, mult icolored and hard, which yields oi l .
Pharmacological properties45 –
Guna – Snigdha, Tikshna, Sukshma.
Rasa – kashaya, Madhura.
Vipaka –. Madhura.
Veerya – Ushna.
Doshaghnata – Kapha vata shamak.
Chemical composition46 –
Fixed oi l 45 to 52 %, Ricinine, proteins 20 pc., starch, mucilage,
and ash 10pc.,
Actions concerned to disease –
Leaves are useful in “vata” and “kapha” diseases, used in l iver
troubles47, especial ly enlarged Liver and Mutravishodaka48,
Drug Review 83
REFERENCE
1 The Indian Materia medica pp 596 2 Indian Medicinal Plants pp 1625 3 Bhava prakasha Guduchadi verga pp 443 4 Indian Medicinal Plants pp 1627 5 Indian Medicinal Plants pp 1625 6 Indian Medicinal Plants pp 1625 7 Bhava prakasha pp 444 8 by Tonosaki K at Central Reseach Laborator ies, Aj inomoto Co., Inc.
Kawasaki, Japan. In 1996 9 by Ota M at Central Research Laboratories Aj inomoto Co , Inc,
Kawasaki, Japan in 1995 10 The Indian Materia medica pp 598 11 The Indian Materia medica pp 598 12 The Indian Materia medica pp 598 13 Sushruta Sutrasthana 38 / 13, 74 14 by Tanaka K at Division of veterinary pharmacology, Nippon veterinary and
animal science university, Tokyo. Japan. In 1997 15 by Nakajyo S at Division of veterinary pharmacology, Nippon veterinary and
animal science university, Tokyo. Japan. In 1996 16 by Imoto T at Department of physiology, Faculty of Medicine, Tottor i
University, Yonago, Japan. In 1995 17 The Indian Materica Medica pp 469 18 Indian Medicinal Plants pp 1361 19 Bhava Prakasha, Gudchadi varga – pp 429 20 Indian Medicinal Plants pp 1363 21 Indian Medicinal Plants pp 1361 22 Indian Medicinal Plants pp 1361 23 Bhava Prakasha, Gudchadi varga – pp 430 24 The Indian Materica Medica pp 469 25 Indian Medicinal Plants pp 1361 26 The Indian Materica Medica pp 469 27 Indian Medicinal Plants pp 2223
Drug Review 84
28 The Indian Materica Medica pp 949 29 Bhava Prakasha, Gudchadi varga – pp 460 30 Indian Medicinal Plants pp 2223 31 Indian Medicinal Plants pp 2223 32 Indian Medicinal Plants pp 2223 33 Bhava Prakasha, Gudchadi varga – pp 460 34 Indian Medicinal Plants pp 2223 35 Indian Medicinal Plants pp 2223 36 The Indian Materica Medica pp 949 37 Bhava Prakasha, Gudchadi varga – pp 460 38 Raja Niguntu pp 263 39 Bhava Prakasha, Gudchadi varga – pp 299 40 The Indian Materica Medica pp1065 41 Indian Medicinal Plants pp 2275 42 The Indian Materica Medica pp1065 43 The Indian Materica Medica pp1065 44 The Indian Materica Medica pp1065 45 Bhava Prakasha, Gudchadi varga – pp 299 46 The Indian Materica Medica pp1065 47 Indian Medicinal Plants pp 2275 48 Bhava Prakasha, Gudchadi varga – pp 299
Chikitsa 69
The term Chiki tsa is derived form the root “KIT ROGAPANAYANE”1.
According to Amaarkosha Chikitsa is Ruk Pratikr iya. Chikitsa is the
process by which the doshas and dhatus are brought into normalcy.
Madhumeha is a chronic relapsing disease and may also develop as a
hereditary disease. Madhumeha patients are divided in two variet ies.
1. Sthula and 2. Krisa
Sthula patients are capable of withstanding the shodhana karma and
the krisa patients are incapable of withstanding i t . Therefore a sthula
patient has to be treated with the sodhana chiki tsa and drisha with
pal iat ive treatment.
For every Shodhana chiki tsa the pat ient should undergo poorva
karma. But the Madhumeha patient is prohibi ted from undergoing sweda
karma 3. In sthula patient after complet ion of sneha karma the doshas
should be el iminated by urdhava and adhosodhana as Vamana and
Virechana respect ively.
After the completion of the Sodhana karma the pat ient has to be
subjected for samsarjana krama. Even though the madhumeha is
santarpana janya roga, the pat ient should not be subjected to Apatarpana
kriya, because i t may result in to Gulma, Kshaya, Mehana shoola, vasti
Chikitsa 70
shoola and Mootra graha. The Brimhana chiki tsa should be carried out
considering the strength of the jataragni of the individual pat ient4. A krisa
or emaciated, and Durbala or weak pat ient who is not capable of
withstanding the shodhana karma requires Bhrimhana chiki tsa5.
Even though the vataja Pramehas are stated to be incurable the duty
of physician is to treat the pat ient and prevent the future complicat ions.
Therefore vataja Prameha should be treated.
SHAMSAMANA CHIKITSA
Shamana chiki tsa is indicated for a Prameha patient who is not
el igible for shodhana chiki tsa, and also the patient who has completed the
shodana karma.
Many variet ies of decoctions, choornas and lehyas have been
described for the treatment of the twenty variet ies of Pramehas by al l
Ayurvedic authori t ies. Vyayam, udvarthana, snana, jala sechana and the
lepas with Twak, Ela, Agar and chandana are useful in Prameha patient6.
Avoiding the causative factors (Nidana) is also a treatment7. In our
tr ial we have used only shamana therapy, which has yield a very
signif icant result.
Chikitsa 71
The pat ient of prameha who is not f i t for evacuation should be
subjected to pacif icatory management for al leviat ion of the disease such
as mantha (churned drink), extracts, l inctus made of barley powder and
l ight edibles. He should eat rough food art ic les such as boi led barley,
barley cakes, f lour of parched grains and apupa with palatable meat -
soup of wi ld birds part icularly gal l inaceous and peckers. He should take
old shal i r ice with soup of mudga etc. and bit ter vegetables added with oi l
of dant i and ingudi or l inseed and mustard. In cereals, he should use
shashtika and wi ld r ice. The diet of the patient of prameha should consist
mainly of barley. One suffering form kaphaja prameha should eat various
preparat ions of barley added with honey. Barley grain dipped in decoction
of tr iphala for the whole night make a saturat ing food taken with honey.
The patient may also take them regularly mixed with vinegar for al leviat ion
of Prameha. He should use f lour of parched grains, bolus, parched grains
and other various edibles made of barley impregnated with deccoctions of
durgs prescribed in kaphaja prameha. Various preparat ions of barley
mixed with the meat of ass, horse, bul l , swan and spotted deer should be
prescribed. The seeds of bamboo and wheat may also be used in forms
simi lar to those of barley8.
Chikitsa 72
REFERENCE
1 Shabda Sthoma Mahanidhi
3 Charaka Sutra 14 / 16
4 Charaka Chikitsa 6 / 16,17
5 Ibid 6 / 15
6 Ibid 6 / 48
7 Ibid 6 / 51
8 Ibid 6 / 18 – 24.
Materials & Methods 83
MATERIAL AND METHODS
Materials -
a. Materials for literary search.
Literary search is done from classical Ayurvedic texts, Modern
texts, Medlar search and updated through journals.
b. Materials for clinical study.
Bhumyamalakyadi churna, composed of
Madhunashini
Eranda
Bhumyamalaki
Bhringaraj
is taken for the cl inical tr ial .
Collection of Drugs: -
Al l the drugs were personally col lected from Kapat hi l ls, and were
conf irmed their identi ty by the Botanist.
Method of Preparation: -
Panchangas of above said drugs were cleaned thoroughly by
running water to take out physical impuri t ies and dried in the shade. The
dried herbs were powdered separately in the pulval iser to get a f ine
powder.
Materials & Methods 84
Again the wet drugs are col lected, to extract swarasa, which is
ut i l ised for giving bhavana to the corresponding herb powders to increase
their potency. These powders are mixed in proport ions and f i l led in
500mg capsules for easy palatabi l i ty for the patient.
CLINICAL TRIAL
Methods :
Selection of Sample
Pat ients suffer ing from Madhumeha are selected from the
Post Graduate And Research Centre OPD/IPD of D.G.M. Ayurvedic
Col lege Hospital and medical camp organised exclusively for
Madhumeha patients at Post Graduate And Research Centre of
D.G.M. Ayurvedic col lege Hospital , Gadag.
Inclusive criteria -
- Pat ients between the age of 25 to 65 years
- Irrespective of sex
- Less than 5 years chronici ty.
Exclusive criteria -
- Pat ients having known organic lesions.
- Insul in dependent
Materials & Methods 85
Laboratory Investigations
The selected pat ients were subjected to fol lowing laboratory
investigat ions
Fast ing blood sugar
Post partal blood sugar
Urine sugar
Serum cholesterol
Diagnostic Criteria
Diagnosis was made on the basis of subject ive parameters
mentioned in the classics and object ive ( lab invest igations) parameters.
Table showing the normal values of objective parameters.
Lab investigat ions Normal values
Fasting blood sugar 80 –120 mg%
Post partal blood sugar 110 – 140 mg%
Serum Cholesterol 120 – 250 mg%
Urine sugar Ni l
Materials & Methods 86
Lab investigation methods
1. Blood Glucose
Blood glucose is determined by using Gluzyme Glucose reagent
set.
Procedure – blood is col lected in a ster i l ized container. Serum is
separated form the cel ls at the earl iest possible t ime (within 30 min), then
the blood is mixed with the reagent (working solution) and heated at
37°C. for 15 min. and then observed in colorimeter under 520 nm.
pipett ing scheme
Blank Standard Test
Working enzyme reagent (ml) 3.0 3.0 3.0
Dist i l led water (ml) 0.025 - -
Standard (ml) - 0.025 -
Sample (ml) - - 0.025
Calculation
Glucose in mg/dl = Absorbance of sample X 100 Absorbance of standard
and the result is recorded in the case sheet.
2. Urine sugar
Urine is col lected in a test tube and mixed with 5ml of Benedicts
solution and heated t i l l i t boi ls, i t is al lowed to cool to room temperature
and then the colour change is noted.
Materials & Methods 87
3. Serum Cholesterol
Modif ied Al lain’s method Cholesterol ki t is used for measuring the
cholesterol level. blood is col lected in a ster i l ized container. Serum is
separated form the cel ls and mixed with the working reagent and by
using the colorimeter (green f i l ter) the cholesterol was estimated.
pipett ing scheme
Blank Standard Test
Working enzyme reagent (ml) 1.0 1.0 1.0
Dist i l led water (ml) 0.01 - -
Cholesterol Standard (ml) - 0.01 -
Sample (ml) - - 0.01
Calculation -
Total Cholesterol in mg% = A of (T) x 200 A of (S)
Study design -
Prospective cl inical trai l .
Sample size -
30 patients are subjected for the study. They are grouped as
A) Hyperglycemic and Hypol ipidimic
B) Hyperglycemic and Hyperl ipidimic
Materials & Methods 88
In each group 15 patients are included on the bases of lab
investigat ions.
Posology - 3gms / 24 hours in divided dose
Duration of treatment -
Durat ion of the study was 30 days from the day of ini t iat ion of
“Bhumyamalakyadi Churna”.
Follow up –
Al l the patients were asked to report every Partnight fol lowup.
Diet -
Pat ients were asked to take regular bl ind diet as far as possible.
-
Criteria for assessment of treatment –
Results of the treatment were assessed on the bases of di f ferences
between the base l ine data and assessment data. The lab investigat ion
variables were subjected for stat ist ical analysis by applying student ‘ t ’
test and paired ‘ t ’ test.
Observation, Analysis & Interpretation 89
Thirty patients are selected for the cl inical study and grouped into
group A and B each of f i f teen. The data col lected is as fol lows –
Demographic data
Master chart - 1
Sl No
OPD No
Date of Initiation
Name A Yrs
S Rl
O E S
Dt F H
F O
Gr Result
1 4477 06/07/99 TRR 58 M 1 2 2 M P 1 B Relieved 2 7510 24/08/99 SRT 43 M 1 1 3 M M 2 A Palliative 3 11186 27/10/99 PNY 50 M 1 1 1 V N 2 B Relieved 4 11187 27/10/99 GHK 62 M 1 1 2 V N 2 A Palliative 5 11188 27/10/99 HBG 40 M 1 1 3 V P 2 B Palliative 6 11189 27/10/99 MBL 42 M 1 1 3 V M 2 A Relieved 7 11191 27/10/99 IPM 48 M 1 1 2 V P 2 B Not responded 8 11192 27/10/99 VMV 59 M 1 2 2 V P 2 A Relieved 9 11193 27/10/99 MBK 64 M 1 1 2 V P 2 A Relieved 10 11194 27/10/99 MKJ 48 M 1 1 2 V P 1 B Not responded 11 11198 27/10/99 NTB 40 F 1 1 4 M N 1 B Relieved 12 11199 27/10/99 CNS 62 M 1 1 4 V P 2 A Relieved 13 11201 27/10/99 SSB 39 M 1 2 3 M M 1 B Not responded 14 11202 27/10/99 CBG 52 M 1 1 4 M N 2 A Palliative 15 11330 27/10/99 RPA 56 M 1 3 1 V N 1 A Palliative 16 11346 27/10/99 AAB 38 F 2 2 3 M P 1 B Relieved 17 11397 28/10/99 CSP 57 M 1 2 4 V P 2 B Palliative 18 11456 28/10/99 ASN 49 F 1 1 3 V P 1 B Relieved 19 11627 01/11/99 PHW 58 F 1 1 3 M N 2 B Not responded 20 11686 02/11/99 BSM 54 M 1 2 4 M P 2 A Palliative 21 11689 02/11/99 GTH 60 F 1 1 4 V N 2 B Palliative 22 11709 03/11/99 NKB 45 M 1 1 3 M P 1 A Palliative 23 11820 04/11/99 SFN 50 M 1 1 4 M P 2 A Relieved 24 11891 04/11/99 TVR 47 M 1 1 3 M M 1 B Relieved 25 11895 07/11/99 PSB 39 F 1 1 4 V M 2 A Palliative 26 11919 08/11/99 MSA 43 F 1 1 3 V P 2 B Relieved 27 12044 11/11/99 AKJ 36 M 1 1 4 V P 2 A Not responded 28 12335 11/11/99 MNR 48 M 1 1 4 M M 2 A Relieved 29 12357 16/11/99 SSM 39 M 1 1 4 V M 2 B Relieved 30 12633 21/11/99 MSB 61 M 1 1 4 V P 2 A Relieved
AY – Age in Yea rs, S – Sex (M – Male, F – Female), Rl - Religion (1- Hindu, 2 - Muslim, 3 - others), O - Occupation (1 - Sedentary, 2 - Active, 3 - Labor), ES - Economical status (1= 0-1Lack,2=1-2 L,3=2-3 L,4=3 L & above), Dt - Diet (v - vegetarian, M - mixed) FH – Family history (P- Paternal, M – Maternal,N – nil), FO – Fresh / Old (1 - Fresh, 2 – Old ) Gr – Group ( A – Hyperglycemic & Hypolipidimic, B - Hyperglycemic & Hyperlipidimic),
Publ ished by Lange Medical publ icat ions, Maruzen.
The Ayurveda Encyclopedia
by Swami Sada shiva Tirtha. 1s t edit ion 1998
Publ ished by Indian books centre, Delhi. Your Guide to Health
Bibliography
By Cl i f ford R. Anderson. 10t h edit ion 1999
Publ ished by G.S.Robert Cl ive, Pune.
Yogaratnakara with Vaidyaprabha hindi commentary
By Dr Indradev Tripathi 1s t edit ion 1998
Publ ished by krishnadas Academy, Varanasi.
Nidana Chiki tsa Hastamalaka
By Ranaji t Roy Desai. 1s t edit ion 1978
Publ ished by Baidyanath Ayurveda bhavan, Nagapur.
Cl inical Methods in Ayurveda
By K.R. Srikantamurthy. 2n d edit ion 1996
Publ ished by Chaukhambha Oriental ia, Varanasi.
From Fat to Fi t
By Dr D.R.Gala. 1s t edit ion 1998
Publ ished by Navneet Publ icat ions Ltd, Gujarat.
Schafer’s essentials of Histology
By Schafers 16t h edit ion 1954
Publ ished by Orient longmans l td.
CASE SHEET FOR “MADHUMEHA”
POST GRADUATE AND RESEARCH CENTERE,(KAYACHIKITSA) SHRI. D.G.M.AYURVEDIC MEDICAL COLLEGE, GADAG.
Guide : Dr.V.V.S.Sastri, Dr Shashidhar.T.Hombal. D.Ay.M.(BHU) M.D. Scholar Co-guide : Dr. Shivarama Prasad Kethamakka. M.A.(Astro),M.D.(Ay) 1. Name of the Patient Sl.No. 2. Father’s/Husband’s Name OPD No 3. Age - Years IPD No 4. Sex - M F Bed No 5. Religion Hindu Muslim Christian Sikh Date of Schedule initiation Date of Schedule completion 6. Occupation - Sedentary Active Labour 7. Economical status Poor Middle class Higher middle class Higher class 8.Diet - Veg Mixed 9. Address Pin 10. Selection Included Group A Hyperglycemic & Hypolipidimic
Excluded B Hyperglycemic & Hyperlipidimic 11. Result Relived Palliative Not responded Discontinued
12. Chief complaints with duration.
Duration No
Complaints < 1 Yr 1Yr 2 Yrs 3 Yrs 4Yrs 5Yrs
After Treatment
1 Prabhoota mootrata 2 Avila mootrata 3 Ashaktata 4 Shareera bhara hani 5 Jangaha mamsa graha 6 Mootra madhuryata 13. History of present illness : Disease was detected
As accidental In regular check up By suspicion
14. Family history 15. Personal History.
a. Ahara
Madhura Sheeta Snigdha
Guda Dugdha Nava anna Dahi
Gramya Guda vikriti Audaka Dugdha vikriti
Mamsa
Anupa b. Vihara
Avyayama Diwaswapna Swapnasukham
c. Manishika- Chinta. Yes No
16. Samanaya Pareeksha.
a. Pulse b. Blood pressure c. Temprature d. Height e. Respitation f. Weight
Patient. Brother Sister
Brother Father Mother
Grandfather Grandmother
Sister Sister Brother
Grandfather Grandmother
17. Poorvaroopa.
Lakshanas B A Lakshanas B A Dantadeenam Malatvam Trishna Pada daha Maldhikyata in bahya chidra Pani daha Swedadhikya Deha chikkanata Sheeta iccha Shareera durgandha Swasa Mukha madhurta Mutra madhurata Talu kloma shosha Mutra shuklata Kesh jatilata Tandra Nakha vriddhi Nidra Alasya Shitalangata
18. Roopa.
Lakshanas Before treatment After treatment Prabhoota mootrata Avila mootrata Madhura mootrata
19. Sroto Pareeksha
A – Udakavaha B - Mootravaha
Lakshanas B A Lakshanas B A Jihwa shosha Alpalpa mootrata Talu shosha Mootara rodha Osta shosha Adhika mootra Kloma shosha Sashoola mootra Prawridha pipasa Basti stabdhata C - Mamsavaha
D - Medovaha
Lakshanas B A Lakshanas B A Arbuda Sweda Arsha Snighanagata Mamsa shosha Sthulashophata Shira granthi
A Before 209.80 56.549 14.600 15.18 6.726 P< 0.001 Highly significant
After 107.66 16.162 4.1730
Fasting blood sugar
B Before 219.20 80.109 20.684 21.16 4.964 P< 0.001 Highly significant
After 114.13 17.381 4.4879
Post partalblood sugar
A Before 321.87 95.517 24.662 25.12 6.938 P< 0.001 Highly significant
After 147.53 18.638 4.8125
Post partalblood sugar
B Before 308.27 103.52 26.730 27.87 5.664 P< 0.001 Highly significant
After 150.40 30.572 7.8938
Serum Cholesterol
A Before 177.53 29.130 7.5200 10.47 0.3752 P > 0.05 Notsignificant
After 173.60 28.250 7.2900
Serum Cholesterol
B Before 328.00 39.740 10.260 14.64 0.3141 P > 0.05 Not significant
After 323.40 40.740 10.450
Urine sugar
A Before 1.2 0.4900 0.1272 0.141 7.326 P< 001 Highly significant
After 0.16 0.2400 0.0629
Urine sugar
B Before 1.36 0.5400 0.1419 0.156 7.419 P< 001 Highly significant
After 0.2 0.2500 0.0654
RESULTS
Group A Relived
Group A palliative Group A Not
responded
Group B Relived
Group B palliative
Group B Not responded
CONCLUSION
The trial drug, “Bhumymalakyadi churna” had a very good effect on all the patients, not only by regulating their blood glucose levels but also by relieving them from the signs and symptoms.