Scientific Basis for Ayurvedic Therapies -13

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

1. Trikatu — Piper nigrum, Piper longum, and Zingiber officinale with meals60

2. Triphala — Powder of the fruits of Terminalia chibula, Terminlia berberica, and Emblica

officinale61

3. Common widely used Indian guggulu (Commiphora wightii) preparations in an

initial large dose and as subsequent maintenance doses offer 10 to 20% deductions

in body weight62

In the near future, other single plants and formulations can be investigated by fast-track

reverse pharmacology — experiential, exploratory, and experimental research by global

collaborative herbal research efforts.

Acknowledgments

The authors acknowledge the substantial help of Chhaya Godse for her assistance in

literature search. Sapna Shetty and Anupama Bhaskaran are also thanked for their tireless

efforts for typing and retyping the manuscript.

We are indebted to Dr. Lakshmi Chandra Mishra, the editor of this book, for his valuable

suggestions on the first and second drafts. We also thank Dr. R. Venkataraman, the president

of Bharatiya Vidya Bhavan, for the facilities and inspiration for the review.

TABLE 9.7

Medicinal Plants in Ayurveda for Obesity

Name Parts Dosage per Day

Anupan

(With)

Unique

Activity

Major

Formulation Ref.

Commiphora wighti

(guggulu)

Gum 2–4 g three times/

day

Hot water Rejuvinative Medoharguggulu

47, 48

Terminalia chelula

(haritaki)

Fruits 1–2 g two times/

day

Honey Memory

enhancer

Triphala 49, 50

Tereminalia belerica

(bibhitaka)

Fruits 0.75–1.5 g two

times/day

Warm water Sedative Triphala 51

Emblica officinalis

(amalaki)

Fruits 3–6 g three times/

day

Cow’s milk Antiaging Chyavanprash 52

Picrorrhiza kurroa

(kutki)

Roots 0.5–1 g two times/

day

Honey Hydrocholeretic Arogyawardhini 53

Curcuma longa

(haridra)

Rhizome 2–4 g three times/

day

Warm water Hypolipidemic Churna 54

Plantago ovata

(isabgol)

Husk 5–10 g one time/

day

Cow’s milk Antithirst Sat-Isabgol 55

Note: For correspondence with Dr. Ashok D.B. Vaidya, e-mail to bhaspa@bom5.vsnl.net.in

© 2004 by CRC Press LLC

Obesity (Medoroga) in Ayurveda 163

References

1. Munshi, V.D. (translator), Ashtang Hridaya, Sastum Sahityavardhak Mudranalaya, Ahmedabad,

India, 1952, p. 135.

2. Nehru, J.L., Discovery of India, J.N. Memorial Fund, Eds., Oxford University Press, New York,

1989.

3. Svoboda, R.E., Prakriti – Your Ayurvedic Constitution, 1st ed., Motilal Banarasidas, New Delhi,

1989–1999.

4. Dossey, L., Meaning and Medicine, 1st ed., Bantam Books, New York, 1991, p. 66.

5. Shashtri, P.K. (translator), Charak Sanhita, 2nd ed., Chaukhambha Sanskrit Sansthan, Varanasi,

India, 1983, p. 279.

6. Bhagwat, B.K.. Triphala-guggul in Sthoulya in Ayurveda Research Papers III, Kulkarni, P.H., Ed.,

Ayurved Rasashala, Pune, India, 1995, p. 215

7. Vaidya, A.B., Vaidya, R.A., and Nagral, S.I., Ayurveda and a different kind of evidence: from

Lord Macaulay to Lord Walton (1835 to 2001 AD), J. Assn. Physicians India, 49, 534, 2001.

8. Vaidya, A.B., We can still learn from Indian medicine, CIBA-GEIGY J., 4, 17, 1979.

9. Bhatt, A.D. et al., Conceptual and methodologic challenges of assessing the short-term efficacy

of Guggulu (Commiphora mukul) in obesity: data emergent from a naturalistic trial, J. Postgrad.

Med., 41, 5–7, 1995.

10. Vaidya, R.A. et al., Clinical endocrine and metabolic studies in the kindred of familial partial

lipodystrophy — a syndrome of insulin resistance, J. Assn. Physicians India, 50, 773, 2002.

11. Satyavati, G.V., Dwarakanath, C., and Tripathi, S.N., Experimental studies on the hypocholesterolemic

effect of Commiphora mukul (Guggulu), Indian J. Med. Res., 57, 1950, 1969.

12. Munshi,V.D. (translator), Ashtang Hriday, Sastum Sahityavardhak Mudranalaya, Ahamdabad,

India, 1952, p. 101.

13. Munshi, V.D. (translator), Ashtang Hriday, Sastum Sahityavardhak Mudranalaya, Ahmedabad,

India, 1952, p. 111.

14. Shastri, P.K. (translator), Charak Sanhita, Part II, 2nd ed., Chaukhambha Sanskrit Sanathan,

Varansi, India, 1983, p. 380.

15. Acharya, J.T. (translator), Sushrut Sanhita of Sushrut, Nirnay Sagar Press, Mumbai, India, 1915,

p. 65.

16. Shastri, P.K. (translator), Charak Sanhita, Part I, 2nd ed., Chaukhambha Sanskrit Sanathan,

Varansi, India, 1983, p. 593.

17. Shastri, P.K. (translator), Charak Sanhita, Part I, 2nd ed., Chaukhambha Sanskrit Sanathan,

Varansi, India, 1983, p. 595.

18. Shastri, P.K. (translator), Charak Sanhita, Part I, 2nd ed., Chaukhambha Sanskrit Sanathan,

Varanasi, India, 1983, p. 281.

19. Shastri, S. (translator), Madhav Nidanam Madhukosh Vyakhya, Part I, Chaukhambha Sansrit

Sansthan, Varanasi, India, 1985, p. 28.

20. Foster, W.R. and Burton, B.T., Health implications of obesity, Ann. Intern. Med., 103, 1024, 1985.

21. Petrelli, J.M., Calle, E.E., Rodrigues, C., et al., Body mass index, height and post menopausal

breast cancer mortality in a prospective cohort of US women, Cancer Causes Control, 13, 325,

2002.

22. Munshi, V.D., Ashtang Hriday: Sastum Sahityavardhak Mudranalaya, Ahmedabad, India, 1952,

p. 132.

23. Mishra, B.S., Bhavprakash of Shree Bhavmishra, Part II, Chaukhambha Sanskrit Sansthan, Varanasi,

India, 1988, p. 406.

24. Parekh, R., Sharangadhar Sanhita, Sastum Sahityavardhak Mudranalaya, Ahmedabad, India,

1955, p. 126.

25. Grunstein, R.R. and Widcox, I., Sleep-disordered breathing and obesity, Clin. Endocrinol. Metab.

Baillier’s, 8, 601, 1994.

26. Gislason, T. et al., Prevalence of sleep apnoea syndrome, J. Clin. Epidemiol., 41, 571, 1988.

27. Daugero, K.D., A new perspective on glucocorticoid feedback: relation to stress, carbohydrate

feeding and feeding behaviour, J. Neuroendocrinol., 13, 1088, 2001.

28. Acharya, J.T., Sushrut Sanhita of Sushrut, Nirnay Sagar Press, Bombay, 1915, p. 98.

29. Shastri, P.K. (translator), Charak Sanhita, Part I, 2nd ed., Chaukhambha Sanskrit Sanathan,

Varansi, India, 1983, p. 430.

30. Shastri, S., Madhav Nidan-Madhukosh Vyukhya, Part I, 15th ed., Chaukhambha Sanskrit

Sansthan, Varanasi, India, 1985, p. 63.

31. Larsson, B. et al., Abdominal adipose distribution, obesity and risk of cardiovascular disease

and death: 13 year follow up of participants in the study of men born in 1913, Br. Med. J., 288,

1401, 1984.

32. Shringi, M.S., Vaidya, R.A., Vaidya, A.B., et al., Unpublished data, 2002.

33. Bray, G.A., Coherent, preventive and management strategies for obesity, in The Origins and

Consequences of Obesity, Chadwick, D.J. and Cardea, G., Eds., John Wiley & Sons, London, 1996,

p. 228.

34. Swoboda, R.E. (translator), Prakriti: Your Ayurvedic Constitution, 1st ed., Motilal Banarasidas,

New Delhi, 1994, p. 132.

35. Shastri, P.K. (translator), Charak Sanhita, Part II, 2nd ed., Chaukhabha Sanskrit Sansthan,

Varanasi, India, 1983, p. 189.

36. Ranade, S. and Paranjape, G.R. (translator), Ashtang Sangraha-Sutrasthan, 2nd ed., Anmol

Prakashan, Pune, India, 1982, p. 307.

37. Kasture, H.S. (translator), Ayurvediya Panchakarma Vidnyan, 3rd ed., Shri Baidyanath Ayurved

Bhavan Pvt. Ltd., Kolkata, India, 1985, p. 247.

38. Swoboda, R.E. (translator), Prakriti: Your Ayurvedic Constitution, 1st ed., Motilal Banarasidas,

New Delhi, 1994, p. 108.

39. Parikh, R.J. (translator), Sharangadhara Sanhita, 1st ed., Sastum Sahityavardhak, Mudranalaya,

Ahmedabad, India, 1955, p. 232.

40. Ranade, S. and Paranjape, G.R., Ashtang Sangraha-Sutrasthan, 2nd ed., Anmol Prakashan, Pune,

India, 1982, p. 317.

41. Nityanand, S. and Kapoor, N.K., Hypocholesterolemic effect commiphora mukul resin (guggul),

Ind. J. Exp. Biol., 9, 376, 1971.

42. Paranjpe, P., Patki, P., and Patwardhan, P., Ayurvedic treatment of obesity: a randomised

double blind, placebo-controlled clinical trial, J. Ethnopharmacol., 29, 1–11, 1990.

43. Ranade, S. and Paranjape, G.R., Asthangsangraha Sutrasthan, 2nd ed., Anmol Prakashan Pune,

India, 1979, chap. 3.

44. Shastri, G.M. (translator), Charak Sanhita, Part I, 1st ed., Sastum Sahitya Vardhak, Karyalaya,

Ahmadabad, India, 1959, p. 543.

45. Dwivedi, V., Saidhantic vivaran, in Aushadhi Vidnyan Shastra, 1st ed., Baidyanath Ayurved

Bhavan Pvt. Ltd., Kolkata, India, 1970, p. 161.

46. Shastri, G.M., Medoroga nidan, in Yogratnakar, Sastum Sahitya Vardhak, Karyalaya, Ahmadabad,

India, 1971, p. 758.

47. Satyavati, G.V. et al., Experimental studies on the hypocholesterolemic effect of Commiphora

mukul (guggul), Ind. J. Med. Res., 57, 1950, 1969.

48. Sairam, T.B., Home Remedies, Vol. 2, Penguin Books, New Delhi, 1999, p. 132.

49. Munshi, V.D., Ashtangahridaya, 1st ed., Sanstum Satityavardhak, Mudranalaya, Ahmedabad,

India, 1952, p. 134.

50. Bhavan’s Swami Prakashananda Ayurveda Research Centre (SPARC), Selected Medicinal Plants

of India, CHEMEXCIL, 1992, chap. 98.

51. Sairam, T.B., Home Remedies, Vol. 2, Penguin Books, New Delhi, 1999.

52. Shastri, P.K., Charak Sanhita, 2nd ed., Chaukhambha Sanskrit Santhan, Varanasi, India, 1983,

p. 11.

53. Vaidya, A.B. et al., A double-blind clinical trial of Arogyawardhini — an Ayurvedic drug —

in acute viral hepatitis, Ind. J. Med. Res., 72, 588, 1980.

54. Godkar, P.B., Narayanan, P., and Bhide, S.V., Hypocholesterolemic effect of turmeric extract

on swiss mice, Ind. J. Pharmacol., 28, 177, 1996.

© 2004 by CRC Press LLC

Obesity (Medoroga) in Ayurveda 165

55. Bhavan’s Swami Prakashananda Ayurveda Research Centre (SPARC), Selected Medicinal Plants

of India, CHEMEXIL, 1992, p. 249.

56. Ranade, S. and Pranajpe, G., Ashtangasangraha: Sutrastana, 2nd ed., 1979, p. 280.

57. Svoboda, R.E., Routine in Prakruti your Ayurvedic constitution, 1st ed., 1994, pp. 18, 108.

58. Ranade, S., Natural healing through Ayurveda, Motilal Banarasidas, 1st ed., 1994, 66.

59. Kasture, H.S., Ayurvediya Panchakarma: Vidnyana, 3rd ed., Vaidyanath Ayurved Bhavan, Nagpur,

India, 1985, p. 245.

60. Ranade, S. and Pranajpe, G., Ashtangasangraha: Sutrastana, 2nd ed., 1979, p. 283.

61. Bhavan’s Swami Prakashananda Ayurveda Research Centre (SPARC), Selected Medicinal Plants,

CHEMEXCIL, 1992, p. 103.

62. Satyavati, G.V., Guggulipid: a promising hypolipidaemic agent from gum guggul (Commiphora

wightii). Economic and medicinal plant research, Plants Traditional Med., 5, 47, 1991.

Rheumatoid Arthritis, Osteoarthritis, and Gout

Lakshmi Chandra Mishra

10.1 Introduction

There are three basic types of musculoskeletal joint diseases described in Ayurveda,

namely,

amavata, sandhivata,

and

vatarakta

, that are characterized by pain and swelling of

the joints. In modern medicine, the diseases closely resembling

amavata

,

sandhigat vata

,

and

vata rakta

are rheumatoid arthritis (RA), osteoarthritis (OA), and gouty arthritis,

respectively. RA is described first followed by brief descriptions of OA, gout, and other

vataja

musculoskeletal diseases.

10.2 Rheumatoid Arthritis

Amavata

(RA) is described in Ayurveda as a constitutional disorder with clinical manifestations

of joint swelling, pain, and stiffness in the ankle, knee, hip joints, wrist, elbow, and

shoulder. The incidence of RA ranges from 0.3 to 1.5% in most populations of the world

and the rate is two to three times higher in females than in males. The peak incidence of

onset of RA is in persons 30 to 60 years old, but no age is immune. The severity of RA

may range from mild oligoarticular illness of a brief duration and very little or no joint

damage to polyarthritis with marked functional impairment.

RA is commonly treated with nonsteroidal anti-inflammatory drugs (NSAIDs). These

drugs do not modify disease progression.

1

They have a tendency to cause adverse gastrointestinal

effects that may range from mild dyspepsia and heartburn to ulceration of

the stomach and duodenum, and many produce fatal consequences.

2,3

Despite the popularity

of NSAIDs, their use to treat OA has been controversial.

4

In one survey, 27% of the

patients suffering from arthritis in the U.S. had used complementary alternative medicine

therapies (CAM).

5

In a recent survey in India, 43% had used CAM therapies.

6

Diseasemodifying

therapies, such as methotrexate, leflunomide, sulfasalazine, gold salts, penicillamine,

azathropine, cyclophosphamide, and chlorambucil, are used to modify the course

of the disease but have serious toxic effects. These toxic effects include aplastic anemia

(potentially life threatening), liver toxicity, gastrointestinal toxicity, leukopenia, and skin

rashes.

The mechanism of action of NSAIDs is believed to be via inhibition of cyclooxygenase

(COX) enzyme that is now known to exist in two separate isoforms. The COX-1 isoform

is responsible for maintaining prostaglandin synthesis in the gastric mucosa, platelets,

and kidney and its inhibition results in toxic effects in the organs. The COX-2 isoform

is responsible for prostaglandin production in inflamed tissues, including RA synovium,

and its inhibition results in beneficial effect in the effected tissues. Recently developed

NSAIDs seem to offer some selective inhibition of COX-2 isoform resulting in less

toxicity.

7

Corticosteroids are given to patients who are not responsive to NSAIDs, but

corticosteroids may produce serious side effects, particularly after prolonged use. Dozens

of therapies for RA have been used in Ayurvedic medicine for thousands of years.

No serious side effect has been reported even after prolonged use of these therapies.

For these reasons, interest in Ayurvedic management of RA is steadily growing around

the world.

10.2.1 Pathogensis and Etiology (

Samprapti

and

Vyadhi Haitu

)

Pathogenesis of RA in Ayurveda is considered to be due to the formation of

ama

(metabolic

toxic waste materials) in the intestine caused by poor digestive power.

Ama

physically

resembles

kapha,

thus it tends to deposit in

kapha

locations, primarily the joints. When

ama

is vitiated (function impaired) by

vata

,

amavata

disease is produced.

The etiological factors in the pathogenesis of

amavata

are incompatible diet, poor digestion,

and sedentary habits.

8

Poor digestion due to weak digestive power leads to the

formation of

ama

in the intestine and is absorbed and distributed to all parts of the body.

When

ama

is vitiated by the other three

dosas,

all types of diseases develop in the body.

An attempt has been made to determine if a relationship exists between the incidence

of RA and other factors such as body constitution, lifestyle, and dietary habits of arthritis

patients.

8

Patients positive for RA factor

were of

vata-pittaja

body constitution. They had

poor digestive power, a tendency to eat an incompatible diet, a high level of erythrocyte

sedimentation rate (ESR), and low hemoglobin levels. This group has more patients with

sedentary habits than the patients with negative RA factor. Patients with a negative RA

factor were found to be of

vata-kaphaja

constitution. They had better digestive power,

eating habits, a more active lifestyle, lower levels of ESR, and higher levels of hemoglobin

than did the RA factor positive patients. The authors suggested that Ayurvedic pathology

of RA based on body constitution seems to be of two types:

vata-pittaja

(RA positive) and

vata-kaphaja

(RA negative). They also concluded that RA-negative patients may have a

better prognosis than do RA-positive patients. This is because immunity may be better

developed by

rasayanas

in the RA-negative patients.

It is currently believed in conventional medicine that genetic susceptibility, primary exogenous

arthritogen, autoimmune reactions in joint components, and mediators of the joint

damage are the factors involved in pathogenesis of RA.

9

RA is believed to be an autoimmune

disease. It is likely that

ama

contains some arthritogenic autoantigens that trigger the autoimmune

reaction in a susceptible host, causing the development of RA. Although rheumatoid

factors are found in 80% of the RA patients, these factors are not known to cause the disease.

1

Rheumatoid factors are also found to occur in other diseases that are characterized by chronic

antigenic stimulation. These include bacterial endocarditis, tuberculosis, syphilis,

kala-azar

,

viral infections, intravenous drug abuse, and liver cirrhosis.

10.2.2 Clinical Description (

Rog

Vivaran)

In Ayurvedic texts, the description of signs and symptoms of RA (

amavata

) includes pain

(scorpionlike bite) and inflammation of one or more joints, particularly the hand, foot,

thigh, sacrum, knees, and metatarsophalangeal (MTP). Joints develop swelling, tenderness,

and reddish or bluish discoloration.

The characteristic feature of RA in conventional medicine is the persistent inflammation

in the synovial membranes, usually of peripheral joints. Patients show loss of appetite,

indigestion, constipation, occasionally low fever, malaise, fatigue, pain in different parts

of the body, feeling of heaviness in the body, sleeplessness, and stiffness in the chest area.

The seven criteria formulated by American Rheumatology Association

10

and the American

College of Rheumatology

1

to classify RA are summarized as follows:

1. Morning stiffness in and around the joints for an hour or more, continuous for 4

weeks or more; swelling of soft tissue of three or more joints, continuous for 4

weeks or more

2. Swelling of soft tissue of three or more joints

3. Swelling of soft tissue of hand joints (proximal interphalangeal [PIP], metacarpophalangeal

or [MCP], or wrist)

4. Symmetrical swelling of soft tissue

5. Subcutaneous nodules

6. Serum rheumatoid factor

7. Erosions or periarticular osteopenia in hand or wrist joints seen on radiograph

Criteria 1 to 4 must continue for 4 weeks or more, and criteria 2 to 5 must be observed

by a physician.

The prominent clinical features of RA include swelling of the PIP; MCP in the hands;

loss of motion in the wrists; pain in the thumb; synovial proliferation and effusion in the

knees; painful deformities of the toes in the feet; and ankle or tarsal collapse, resulting in

painful valgus deformities.

10.2.3 Clinical Examination and Diagnosis (

Nidan

)

The standard eight-point diagnosis of Ayurveda is used to diagnose RA and determine

for the classical signs of arthritis as discussed above. There is no specific laboratory

diagnostic test for RA. Although only 80% of the patients are found to be positive for RA

factor, the standard eight-point diagnosis is still one of the tests often used by physicians

for diagnosis.

10.2.4 Clinical Course and Prognosis (

Sadhyata

)

RA is often considered a benign disease, but it may cause considerable disability, crippling,

and death. Patients sometimes recover spontaneously and achieve complete remission. In

most cases, the disease becomes chronic, resulting in functional deterioration of the joints

and disability.

10.2.5 Strategy for Prevention

As previously mentioned, the major causative factors in the pathogenesis of RA are weak

digestive power, leading to accumulation of

ama

, and a sedentary lifestyle. The strategy

to prevent RA needs to include herbal formulas that improve digestion and clean the

intestine from

ama

and a healthy active lifestyle as discussed in Ayurveda under daily

which dosas are vitiated as discussed in Chapter 2. Additionally, patients are examined

routine. One must eat easily digestible food according to the body constitution and make

sure that bowel movement is regular. Regular exercise is very important to prevent RA

and arthritis.

10.2.6 Therapy (

Chikitsa

)

The basic strategy of treating RA is to reduce the accumulated

ama

in the body and balance

vata

, encourage proper exercise, maintain a normal healthy lifestyle, and provide adequate

rest. First, the food intake is reduced to a bare minimum, giving only boiled rice and well

cooked

mung dal

(lentil) soup for 1 to 2 months to help clean the body of

ama

.

This diet

is believed to increase metabolism and elimination of disease-producing

ama

. Herbs or

herbal formulas (e.g.,

Panchkola

, 2 g/day; equal parts of

Piper longum

root and fruits,

Piper

chava

,

Plumbago zeylanica,

and

Zinziber officinale

powders)

are given during this period to

clean the body, improve the digestion, and reduce the inflammation (

Commiphora mukulcontaining

formulas) and pain.

11

Suitable herbal formulas are determined based on body constitution, disturbed

dosa

,

and other disease conditions. For example,

Gokksharadi

guggul

is recommended for patients

who also suffer from kidney disorders,

Pushkarmoola guggul

is suggested for patients with

heart problems, and

Kanchnar guggul

is recommended for patients with lymphadenopathy.

11

Some of the commercially available commonly used herbs and formulas are prediet

consisting of easily digestible light food, is given ghee

(dehydrated butter), and may

be asked to use a medicated sesame-oil enema to remove fat soluble toxic materials from

the gastrointestinal tract. The patient is asked to do easy exercises and yoga. Body massage

with oil, and hot fomentation may also be added to the treatment. Classic Panchakarma

TABLE 10.1

Common Anti-Inflammatory Herbs Used in

Ayurvedic Formulas

Sanskrit and Botanical Names

Ashwagandha

(

Withania sosmnifera

)

Bhallataka (Semecarpus anacardium)

Bhutala (Circuligo orchioides)

Chitraka (Plumbago zeylanica)

Eranda (Ricinus communis)

Goraksa (Vitex negundo)

Guggulu (Commiphora mukul)

Haritika (Terminalia chebula)

Harsinger (Nyctanthes arbor tristis)

Karanja (Pongamia glabra)

Kirayat (Andrographis paniculata)

Kupilu (Strychnos nux-vomica)

Madhuka (Basia latifolia)

Madhuyasti (Glycyrrhiza glabra)

Punarnava (Boerrhavia diffusa)

Rasna (Inula racemosa)

Rasona (Allium sativum)

Sunthi (Zinziber officinalis)

Vatsanabha (Aconimtum chasmenthum)

Vidanga (Embelia ribes)

Yavasaka (Alhagi pseudalhagi)

sented in Table 10.1 through Table 10.3. The patient is slowly brought back to a normal

encouraging results.12

Clinical trials based on the above basic strategy of treatment using a variety of Ayurvedic

herbal formulas are summarized below.

10.2.6.1 Zingiber officinale–Tinospora cordifolia Decoction, Vatagajanankusa Rasa,

and Maharasnadi Kwath

Z. officinalis–T. cordifolia decoction was given (50 ml three times/day) to 40 RA patients

(group B) and Yograj guggul (1 g/day), Vatagajanankusa rasa (250 mg three times/day), and

Maharasnadi kwath (50 ml three times/day) were administered to 37 arthritis patients

(group A) for 6 to 8 weeks. There were a total of 48 males and 29 females. The diagnosis

was confirmed based on 1959 American Rheumatism Association (ARA) criteria. All

patients received a limited vegetarian diet without fish or chicken. Both treatments were

TABLE 10.2

Formulas from Ayurvedic Formulary (AF) of India for Arthritis Treatment (1978)

Name Dose

AF

Section Name Dose

AF

Section

Kanchnar guggul 3 g 5:1 Rasa parpati 250 mg 16:3

Goksharidi guggul 3 g 5:3 Anand Bhaijarava rasa 250 mg 20:3

Trayodashang guggul 3 g 5:4 Mahalakshmi vilas rasa 250 mg 20:27

Yograj guggul 3 g 5:7 Sarvanabhupati rasa 250 mg 20:51

Vyousadi guggul 3 g 5:9 Rasnadi kvath curpa 48 g 4:27

Vatari guggul 3 g 5:10 Rasnadi kvath curpa maha 48 g 4:28

Simhanad guggul 3 g 5:12 Das-mula-haritiki 12 g 3:14

Ajamodadi curpa 6 g 7:1 Amrta ghrit 12 g 6:1

Nimbadi curpa 3 g 7:20 Brhat saindhavadya taila massage 8:40

Pancasma curpa 3 g 7:22 Kotamuckkadi taila massage 8:10

Vaisvanara curpa 3 g 7:30 Jiraka-modka 3 g 3:12

TABLE 10.3

Miscellaneous Ayurvedic Formulas for the Treatment of RA

Name Reference Name Reference

Brhat vata cintamani BRa Maha rasnadi kvath SSf

Chandrprabha vati SYSb Sunthi guduci kvath 13d

Copper bhasma RSc Puskarmoola guggul Shukla 1996

Gudici kvatha 20d Suvarna samirapannag rasa BRa

Gold bhasma SYSb Rasnadi guggul YRg

Mrtyunjaya rasa BRa Trailokya cintamani BRa

Maha Narayan taila CDe Vatari guggul BRa

Vatgajankush rasa BRa

aBR = Bhesajya Ratnavali.

bSYS = Sidha Yog Sangraha.

cRS = Rasayan Sar.

d

eCD = Chakardatta.

fSS = Sarangdhar Samhita.

gYR = Yog Ratnakar.

therapy described in Chapter 5 was evaluated in RA patients and was found to give

effective in reducing pain and swelling, and the decoction treatment was found to be

relatively more effective than the Yograj guggul combination.13

10.2.6.2 Dasmularista, Pippalyasava, and Vettumaran Gutika

Dasmularista, Pippalyasava, and Vettumaran Gutika were examined in 83 arthritis patients

(1959 ARA criteria). Forty-three percent of the patients were unable to walk, and remaining

cases showed varying degree of functional impairment of the joints. Measurements of

swollen elbow, wrist, ankle, and knee joints were taken before and after treatment. An

average of 90 days of treatment was found to be the minimum to obtain satisfactory

improvements. Time taken for disappearance of RA ranged from 20 to 30 days. The results

suggested that the combination of the above three formulas was effective in the acute

stage of RA.14

10.2.6.3 Rasonadi Kvatha15

Rasonadi Kvatha was evaluated in 50 RA patients. The diagnosis was confirmed based on

ARA 1959 criteria.16 Kvatha is a decoction of equal parts of Z. officinalis, Allium sativum,

and Vitex negundo. A dose of 25 ml of the decoction representing 25 g of each ingredient

was given three times/day for 6 weeks. During the acute inflammatory stage of the disease,

patients were treated with external application of poultice and Baluka hot sand fomentation.

The participants’ diet consisted of rice, bread, lentil soup, cream of wheat, and milk

during the 6-week trial period. Pippalyadi churna or Visatundika vati was also administered

during the acute phase to relieve pain. The results were assessed based on the degree of

pain, swelling, tenderness, and restriction of affected joints. The change in functional

capacity was measured by functional tests. Authors observed significant improvement in

all the parameters. Most of the patients showed complete relief from pain.16

10.2.6.4 Withania somnifera, Boswellia serrata, Curcuma longa, and a Zinc

Complex (Articulin-F)

A herbomineral formulation containing roots of W. somnifera, the stem of B. serrata, rhizomes

of C. longa, and a zinc complex (Articulin-F) was evaluated in a randomized, doubleblind,

placebo-controlled, crossover study in 42 patients with OA. Clinical efficacy was

evaluated every fortnight on the basis of severity of pain, morning stiffness, Ritchie,

articular index, joint score, disability score, and grip strength. Other parameters like

erythrocyte sedimentation rate and radiological examination were carried out on a

monthly basis. Treatment with the herbomineral formulation produced a significant drop

in the severity of pain (p < 0.001) and disability score (p < 0.05). Radiological assessment

did not show any significant changes and no serious adverse effect was observed.17

10.2.6.5 Ginger (Zingiber officinale)

Ginger has been reported to be beneficial in seven arthritic patients.18 In one study, ginger

was given to 56 patients (28 with RA, 18 with OA, and 10 with muscular discomfort).

More than 75% of the patients experienced varying degrees of relief from pain and

swelling. All the patients with muscular discomfort experienced relief from pain. None

of the patients reported adverse effects during the treatment period from 3 months to 2.5

years. The authors suggested that at least one of the mechanisms by which ginger shows

its ameliorative effects could be related to inhibition of prostaglandin and leukotriene

biosynthesis (dual inhibitor of eicosanoid biosynthesis).19

10.2.6.6 Tinospora cordifolia, Balsamodendrom mukul, and Alpinia officinarum

Tinospora cordifolia, Balsamodendrom mukul, and Alpinia officinarum were evaluated in 40 RA

patients selected based on 1959 ARA criteria.20 Forty patients (ages 10 to 65) were selected

for the study on the basis of pain, swelling of multiple joints, and elevation of erythroicyte

sedimentation rate. All patients were treated for the first 10 days as follows:

Day 1 — Fasting

Days 2–6 — Panchkola (2 g/day) to improve digestion and clean ama for days 2 to 6

Day 7 —Ricinus communis oil (30 ml) at 6 A.M. with hot water

Days 8–10 — Panchkola powder (2 g/day) with hot water

On day 11, the patients were separated randomly into 2 groups of 20 each. The first group

was given 60 ml of T. cordifolia decoction, 1 ml of oil extract (sneha) of T. cordifolia, and 2

g of B. mukul three times/day. The second group received the same regimen except B.

mukul was replaced by 2 g of A. officinarum.

The decoction consisted of one part of leaves and stem of the herb, boiled in four parts

of water until one part of the water was left. The oil extract fortified three times consisted

of 1 part herbal paste, 4 parts of sesame seed oil, and 16 parts of the decoction, boiled 6

to 8 h/day for 3 days to reduce the volume to one fourth of the total amount. It was

filtered and the procedure was repeated three times.

A light diet was given in the first stage of 10 days and a normal hospital diet was given

for rest of the treatment period. Criteria for assessment and classification of results followed

were those adopted by American Medical Association (AMA). The authors stated

that the improvement in signs and symptoms were highly encouraging and statistically

significant at 0.1% level.

10.2.6.7 Fasting

Because ama is considered a major causal factor for RA, elimination of ama by fasting was

studied in RA patients (1959 ARA criteria). The patients were subjected to total fasting

for 2 days and partial fasting for the next 43 days. Notable clinical remission of signs and

symptoms were observed, including a decrease in rheumatoid factor (RF) titer and chemically

reactive proteins (CRP), which may be attributed to a decrease in ama.21

10.2.6.8 Elimination of Ama by a Purgative (Gandharva hasta kashaya)

The effect of eliminating ama by purgatives was evaluated in 60 arthritic patients.

Gandharva hastadi kvath (50 ml), a purgative, was given three to four times/day for 21

days. The ingredients of the decoction were equal parts of Gandharva hasta (Ricinus communis),

Karavya (Pongamia glabra), Chitraka (Plumbago zeylanica), Shunti (Zinziber officinalis),

Haritaka (Terminalia chebula), Punarnava (Boerrhavia diffusa), Yavasaka (Alhagi pseudalhagi),

and Bhutala (Circuligo orchioides). Of 60 patients, 46 were cured (complete disappearance

of disease symptoms) and 14 showed significant relief in symptoms. Three patients had

a relapse over a period of 1 year after observation. The study further confirms the hypothesis

that the origin of arthritis is the formation of ama in the intestine.22

10.2.6.9 Vatari Guggul (Bhasajya Ratnavali) and Maharasnadi Kvatha

A dose of 1 g of Vatari guggul was given three times/day and Maharasnadi kvatha

(Sarangdhar samhita) was given 20 ml three times/day in 24 RA patients. Vatari guggul

consisted of castor oil, sulfur, guggul (Commiphora mukul), haritiki (Terminalia chebula),

amalki (Phyllanthus emblica), and vibhitiki (Terminalia belerica). The major ingredient of

Maharasnadi kvath was rasna (Inula recemosa). The results indicate a significant improvement

in pain (p < 0.001) and a decrease in ESR levels (p < 0.001) in subjective and

objective parameters (p < 0.001).23

10.2.6.10 Ashwagandha (Withania somnifera)

Ashwagandha (Withania somnifera) has been shown to have antiarthritic activity in animal

models of RA.24–28 In a recent clinical trial, 3 g of the drug was given three times/day with

milk to 77 RA patients. The improvement in signs and symptoms of RA was good in

22.7%, moderate in 53.4%, and poor in 22.07%; there was no response in 2.59% of the

patients.29

10.2.6.11 Purified Guggul and Guduchyadi Kvath

Purified guggul and Guduchyadi kvath were given to 34 RA patients for 6 weeks. Authors

observed marked improvement in signs and symptoms in 27 patients, moderate improvement

in 4 patients, and no improvement in 3 patients.

10.2.7 Scientific Basis for the Use of Ayurvedic Herbs in Arthritis

Ayurvedic herbs have been investigated in animal models of arthritis for anti-inflammatory

effect in the same way as synthetic drugs have been for the past 30 years. The three

most common animal models currently used to investigate anti-inflammatory effect of

drugs are (1) adjuvant-induced, (2) streptococcal cell-wall induced, and (3) collageninduced

models.30 Agents currently in clinical use or trials that are active in these models

include corticosteroids, methotrexate, nonsteroidal anti-inflammatory drugs, cyclosporin

A, leflunomide, interleukin-1 receptor antagonist, and soluble tumor necrosis factor receptors.

Animal models of OA include mouse and guinea pig spontaneous OA, meniscotomy

and ligament transection in guinea pigs, meniscotomy in rabbits, and meniscotomy and

cruciate transection in dogs. None of these models have a proven track record of predictability

in human disease presentation because none of the agents have been proven to

provide anything other than symptomatic relief.31

The studies to assess anti-inflammatory activity and analgesic activity are evaluated,

and the results supporting the use of Ayurvedic therapies in arthritis are summarized

below.

10.2.7.1 Anti-Inflammatory Activity

10.2.7.1.1 Vanda roxburghii

Vanda roxburghii has been shown to have anti-inflammatory activity in albino rats.32

10.2.7.1.2 Gum-Guggul from Commiphora mukul

Anti-inflammatory activity of guggul has been reported by several investigators.33–35 In

another study, phenylbutazone, ibuprofen, and fraction "A" of gum-guggul from Commiphora

mukkul were administered orally at a daily dose of 100, 100, and 500 mg/kg, respectively,

for a period of 5 months. All three drugs decreased the thickness of joint swelling

during the course of the drug treatment.36

The anti-inflammatory effect of extracts of guggul resins of four species of the Burseraceae

plant family, Boswellia dalzielli, Boswellia carteri (gum olibanum), Commiphora mukul, and

Commiphora incisa, were screened in arthritis models in rat. The aqueous extracts of the

resins of B. dalzielli, C. incisa, and C. mukul significantly inhibited both the maximal edema

response and the total edema response during 6 h of carrageenan-induced rat paw edema.

The octanordammarane triterpenes, mansumbinone and mansumbinoic acid, were isolated

from the resin of C. incisa. Prophylactical administration of mansumbinone proved

to be more than 20 times less potent than indomethacin and prednisolone in inhibiting

carrageenan-induced rat paw edema. The acid was able to reverse an established carrageenan-

induced inflammatory response when administered 2 h after induction. Daily

administration of mansumbinoic acid at 1.5 ¥ 10–4 mol kg-1 dose level significantly reduced

joint swelling in adjuvant-induced arthritic rats.37

New triterpenes, Myrrhanol A and Myrrhanone A, isolated from guggul-gum resins (C.

mukul), were found to have a potent anti-inflammatory effect on adjuvant-induced air-pouch

granuloma of mice. The study indicated that the anti-inflammatory effect of Myrrhanol A

was greater than that produced by hydrocortisone and the 50% extract of the crude resin.

Authors suggested that Myrrhanol A may be a potent anti-inflammatory agent.38

10.2.7.1.3 Harsinger (Nyctanthes arbor tristis)

The water-soluble portion of the alcoholic extract of the leaves of Nyctanthes arbor tristis

(NAT) was screened for the presence of anti-inflammatory activity. NAT inhibited acute

inflammatory edema produced by different phlogistic agents, such as carrageenin, formalin,

histamine, 5-hydroxytryptamine, turpentine oil, and hyaluronidase, in the hindpaw

of rats. It also inhibited the inflammation in adjuvant-induced arthritic models. In subacute

models, NAT was found to check granulation tissue formation significantly in the granuloma

pouch and cotton-pellet test. Acute and chronic phases of formaldehyde-induced

arthritis were significantly inhibited. Anti-inflammatory activity in leaves of NAT supports

its use in various inflammatory conditions by the followers of the Ayurvedic system of

medicine.39

10.2.7.1.4 Semecarpus anacardium nut

A chloroform extract of Semecarpus anacardium nut was found to significantly reduce acute

inflammation and was also active against the secondary lesions of adjuvant-induced

arthritis in rats.40

A milk extract of S. anacardium nut was found to have anti-inflammatory effect in

adjuvant-induced arthritis in rats at the dose level of 150 mg/kg.41 The mechanistic studies

indicated that the diseased state of adjuvant arthritis may be associated with augmented

lipid peroxidation; the studies also concluded that the administration of the drug may

exert its antiarthritic effect by retarding lipid peroxidation and causing a modulation in

a cellular antioxidant (AO) defense system.42

10.2.7.1.5 Crataeva nurvala

The effect of triterpenes from stem bark was studied for its effect on lipid peroxidation in

adjuvant induced arthritis in rats. Lupeol, a pentacyclic triterpene of C. nurvala stem bark,

and its ester, lupeol linoleate, were synthesized and tested for anti-inflammatory activity

in complete Freund's adjuvant-induced arthritic rats. The arthritic rats showed a significant

increase in lipid peroxide level in plasma; a decrease of lipid peroxide in the liver; an

increase in the AO enzymes, SOD, GPX, and catalase in both the liver and hemolysate;

and a decrease in blood glutathione. Lupeol and lupeol linoleate at 50 mg kg-1 body weight

daily for 8 days, from 11 to 18 days after the adjuvant injection brought back the alterations

to normal levels. The effect of lupeol linoleate was found to be better in this respect when

compared with lupeol.43

10.2.7.1.6 Hemidesmus indicus (HI)

The anti-inflammatory activity of the pure compound (2-hydroxy-4-methoxy benzoic acid)

isolated and purified from anantamul root extract was investigated. 2-OH-4-MeO benzoic

acid effectively neutralized inflammation induced by Vipera russelli venom in male albino

mice and reduced cotton-pellet–induced granuloma in rats. The compound produced a

significant fall in body temperature in yeast-induced pyrexia in rats but did not change

the normothermic body temperature. The compound effectively neutralized vipervenom–

induced changes in serum phosphatase and transaminase activity in male albino

rats. It also neutralized free radical formation as estimated by thiobaraturic acid reactive

substances (TBARS) and SOD activities.44

10.2.7.1.7 Andrographis paniculata

Andrographolide, a diterpenoid lactone isolated from Andrographis paniculata (anti-inflammatory

herb), was investigated for the ability to prevent phorbol-12-myristate-13-acetate

(PMA)–induced reactive oxygen species (ROS) production, as well as N-formyl-methionylleucyl-

phenylalanine (fMLP)–induced adhesion by rat neutrophils. The study showed that

PMA (100 ng/ml) induced rapid accumulation of H2O2 and O2 in neutrophils within 30

min. Andrographolide (0.1 to 10 mM) pretreatment (10 min, 37ºC) significantly reduced

the accumulation of these two oxygen-radical metabolites. Administration of andrographolide

also significantly prevented fMLP-induced neutrophils adhesion. These data suggest

that the mechanism of anti-inflammatory action of andrographolide may be via

preventing ROS production and neutrophils adhesion.45

10.2.7.1.8 Aglaia roxburghiana (AG)

Alcoholic extracts of aerial portions and fruits of AR and the triterpines, roxburghiadiol

A and B, were studied in carrageenin-induced rat-paw edema, cotton-pellet granuloma,

and mast-cell degranulation induced by compound 48/48. The extract and the triterpines

were found to be effective anti-inflammatory agents in this study.46

10.2.7.2 Analgesic Activity

There are few data available on the analgesic activity of antiarthritic herbs. A p-quinone,

embeline, derived from Embelia ribes was investigated for analgesic activity. The potassium

salt of embeline was found to be effective by oral, i.m., and i.c. routes of administration

and the results compared well with morphine. Although potassium embelate acts centrally

to produce analgesia, its effect is not antagonized by naloxone indicating a different central

site of action. It has no abstinence syndrome as observed with morphine and no demonstrable

anti-inflammatory action. The anlagesic effect of the alkaloid provides a scientific

basis for its use in arthritis. In addition, lack of any adverse effects, high therapeutic index,

and absence of abstinence syndrome provide basis for long-term safety of embelate as an

analgesic.47

10.2.7.3 Mechanism of Action

One of the mechanisms of anti-inflammatory activity of Ayurvedic herbs may the AO

property. Andrographolide isolated from leaves of Andrographis paniculata has been shown

to inhibit nitric oxide generation in endotoxin-stimulated macrophages.48

The AO activity of two polyherbal formulations, Maharasnadhi quatha (MRQ) and Weldehi

choornaya (WC), used by Ayurvedic medical practitioners in Srilanka for the treatment of

RA patients, was assessed on SOD, GPX and catalase, lipid peroxidation (as estimated by

TBARS generation), concentrations of serum iron, hemoglobin (Hb), and the total ironbinding

capacity (TIBC). The overall results of the study demonstrated that MRQ has

greater AO potential than WC.49

In another study,50 the mechanism of suppression of inducible nitric oxide synthase

(iNOS) and (COX-2) by ergolide, a sesquiterpene lactone from Inula Britannica, was investigated.

Ergolide markedly attenuated the iNOS activity in a cell-free extract of LPS/IFNgamma-

stimulated RAW 264.7 macrophages and markedly decreased the production of

prostaglandin E(2) (PGE(2)) in cell-free extract of the macrophages in a concentrationdependent

manner, without alteration of the catalytic activity of COX-2. Ergolide

decreased the level of iNOS and COX-2 protein, and iNOS RNA caused by stimulation

of LPS/IFN-gamma in a concentration-dependent manner and inhibited nuclear factorkappaB

(NF-kappaB) activation, a transcription factor necessary for iNOS and COX-2

expression in response to LPS/IFN-gamma. This effect was accompanied by the parallel

reduction of nuclear translocation of the subunit p65 of NF-kappaB as well as IkappaBalpha

degradation. These effects were completely blocked by treatment with cysteine. This

finding suggests that the inhibitory effect of ergolide may be mediated by alkylation of

NF-kappaB or an upstream molecule of NF-kappaB. Ergolide also directly inhibited the

DNA-binding activity of active NF-kappaB in LPS/IFN-gamma-pretreated RAW 264.7

macrophages. The authors suggested that the overall effect of ergolide is the suppression

of the expression of iNOS and COX-2, which play important roles in the inflammatorysignaling

pathway.

10.3 Osteoarthritis (Sandhigat Vata)

10.3.1 Introduction

Sandhigat Vata (Krostuka-sirsa) is primarily a disease of vitiated vata settling into bone and

bone marrow without any involvement of ama. The disease is characterized by acute pain,

stiffness of the joints, impairment of the function of the joints, loss of muscle strength, and

sleeplessness. This disorder resembles OA, which is also characterized by acute pain,

involvement of diarthroidial joints, and functional limitations. Sedentary lifestyle as a

causative factor of amavata is scientifically valid.51 Current experiments in rabbits have

shown that short repetitive immobilization induces OA. Even a 4-day immobilization

period had a cumulative effect in producing OA.52

10.3.2 Clinical Description

OA starts out with pain in one joint but subsequently spreads to other joints. The joints

commonly involved are the big toe, fingers, hip, knees, and both lumbar and cervical

spine. Ankles are generally spared except in the secondary form of OA. These joints in

the advanced stage of the disease exhibit deformity. Patients do not show the presence of

the RA factor.

 

Om Tat Sat

                                                        

(Continued...) 

(My humble salutations to H H Maharshi ji,  Brahmasri Sreeman Lakshmi Chandra Mishra ji and other eminent medical scholars and doctors   for the collection)