Scientific Basis for Ayurvedic Therapies -27

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

In a clinical trial (n = 55), Eclipta alba showed marked symptomatic relief in NUD and

peptic ulcer patients. Total response in NUD was excellent in 62.9%, good in 17.1%, poor

TABLE 22.3

Antiulcerogenic Activity of Some Medicinal Plants

Drugs

(Common/Ayurvedic Name) Experimental Models Mechanism of Action Ref.

Abies pindrow Royle, Fam.

 Pinaceae

(Talisapatra)

Petroleum ether (PE), acetone (AE),

chloroform (CE), and ethanolic (EE)

extracts of leaves

CRS- induced GU in rats Antistress activity 74

Benincasa hispida, Fam. Cucurbitaceae

(Petha or Golkaddu)

Fresh juice, supernatant and residue

fraction of centrifuged juice, PE and

EE

Aspirin (ASP) + restraint,

swimming stress,

indomethacin plus

histamine- and serotonininduced

ulcers in rats and

mice

— 75

Camellia sinensis, Fam.

Ternstroemiaceae (green tea)

Hot water extract

Cold + restraint–stressinduced

ulcers in rats

— 76

Centella asiatica, Fam. Umbelliferae

(Brahma-manduki)

Fresh juice of whole plant

CRS-, EtOH-, ASP-, and PLinduced

GU in rats

No effect on acidpepsin

secretion,

increase in mucin

secretion and life span

of mucosal cells

77

Convolvulus pluricaulis, Fam.

Convolvulaceae (Shankupuspi)

Fresh juice of whole plant

CRS-, EtOH-, ASP-, and PLinduced

GU in rats

No effect on acidpepsin

secretion,

increase in mucin

secretion and life span

of mucosal cells

78

Emblica officinalis Gaertn. Fam.

Euphorbiaceae

(Amla) Fresh juice of fruit plup

CRS-, EtOH-, ASP-, and PLinduced

GU in rats and

acetic-acid–induced

healing

model

Decreased the acid and

pepsin secretion and

increased mucus

secretion

79

Garcinia cambogia, Fam. Guttiferae

(Kukum)

Fruit extract

Indomethacin Decrease in acid-pepsin

secretion and

promotion

of mucosal defensive

80

Honey Ethanol-induced increased

vascular permeability

changes in the rat stomach

Free-radical scavenger 81

Pongamia pinnata, Leguminosae

(Karanj or Karanja)

PE, AE, CE, and EE extracts of seeds

PE, AE, CE, and EE extracts of roots

RS-induced GU in mice

RS- and PL- induced GU in

rats

—

Decrease in acid pepsin

82, 83

Satavari Mandur PL- and CRS-induced GU

in rats

No effect on acidpepsin

secretion and

promotes mucosal

defensive factors by

enhancing mucin

secretion and life span

of mucosal cells

84

Shilajit

per se effect

PL-, IS-, and ASP-induced

GU in rats and CYS- and

HIST-induced DU in rats

and GP, respectively

Tendency to decrease

acid-pepsin secretion

and significant increase

in mucin secretion

in 5.7%, and 14.3% patients dropped out of the study. Radiological assessment confirmed

the symptomatic improvement. Of 25 DU cases, 48% were under excellent response, 24%

were under good response, and 16% showed poor response; 12% did not show any

response to the treatment. The was drug given in the form of powder (30 g) in three

divided doses/day for 1 month in NUD cases and for 3 months in DU cases. The drug

also showed significant reduction in free HCL and total acidity in both the groups (NUD

and UD).73

Various other herbal drugs have been reported to have antiulcerogenic activity. These

and the entities involved in the activity have been isolated. These are summarized in

22.10 Summary

Ayurveda has a clear description of etiology, pathology, and treatment for gastroduodenal

ulcers. Scientific evidence was also found in the literature in support of use of the following

Ayurvedic herbs: Abies pindrow, Benincasa hispida, Camellia sinensis, Centella asiatica, Convolvulus

pluricaulis, Emblica officinalis, Tambra bhasma, unripe plantain banana, Piper longum,

TABLE 22.3 (continued)

Antiulcerogenic Activity of Some Medicinal Plants

Drugs

(Common/Ayurvedic Name) Experimental Models Mechanism of Action Ref.

Sitavirya drugs

a. Asparagus racemosus, Fam. Liliaceae

(Satawari)

Fresh juice of roots

b. Glycyrrhiza glabra, Fam. Leguminosae

(Mulhatti)

Water decoction of roots

c. Holarrhene antidysenterica Wall., Fam.

Apocynaceae (Kurachi) water

decoction of barks

d. Ficus religiosa, Fam. Urticaceae

(Peepalbanti)

Water decoction of barks

PL- and CRS-induced GU

in rats

PL- and CRS-induced GU

in rats

PL- and CRS-induced GU,

CYS-induced DU in rats

PL- and CRS-induced GU

and CYS-induced DU in

rats

No effect on acidpepsin

secretion and

promotes mucosal

defensive factors by

enhancing mucin

secretion and life span

of mucosal cells

86

Tectona grandis L.

Fam. Verbenaceae (Sagwan)

Ethanolic fraction of trunk bark and wood

chips

Pylorus ligation (PL)

restraint stress (RS)- and

prendnisolone-induced

GU in rats

Histamine (HIST)-

induced GU and DU in

guinea pigs (GP)

No effect on acid-pepsin

secretion but caused an

increase in mucin

secretion

87

Withania somnifera, Fam. Solanaceae

(Aswagandha)

(Roots)

SG-1 [total Me OH-H2O (1:1)]

SG-2 (sitoindosides VII, VIII, and

withaferin-A)

RS-induced GU in rats Antistress activity 88

Tables 22.3 and 22.4.

are summarized in Table 22.3. Some of these drugs have been chemically characterized

406 Scientific Basis for Ayurvedic Therapies

TABLE 22.4

Ulcer Protective Effect of Some Active Constituents Isolated From Herbal Drugs

Plants

Active

Constituents Models Mode of Action Ref.

Aegle marmelos

Correa, Fam.

rutaceae (Bael

(seeds)

Luvangetin -do- — 89

Asparagus

racemosus,

Fam. Liliaceae

(Satawari)

Standardized

extract to active

saponins

CRS-, EtOH-, ASP- and

PL-induced GU in rats

No effect on acid

pepsin secretion,

increase in mucin

secretion and life

span of mucosal cells

90

Azadhiracta indica,

Fam. Meliaceae

(Neem)

Nimbidin ASP-, prednisolone,

indomethacin-,

serotonin stress-, and

acetic acid-induced GU

in rats; HIST-induced

DU in GP CYSinduced

DU in rats

— 91

Emblica officinalis

Gaertn.,

Fam. Euphorbiaceae

(Amla)

methanolic extract

Standardized to

the tannoids,

emblicanin A and

B

CRS-, EtOH-, ASP-, and

PL-induced GU in rats

and aceticacid–

induced

healing model

Decreased the acid

and pepsin secretion

and increased mucus

secretion

22

Garcinia indica,

Fam. Guttiferae

(Kumkum)

Fruit rind

Garcinol Water-immersion

stress

Free-radical scavenger 92

Ocimum basilum,

Fam. Leguminosae

(Tulsi)

Fixed oil ASP-, indomethacin-,

EtOH-, Hist-, reserpine,

Serotonin-, PL-, and

stress-induced GU

in rats

Antisecretory 93

Shilajit Fulvic acid,

4¢- methoxy 6

carbomethoxybiphenyl

PL-, PL+ASP-, and RS–

induced GU and CYSinduced

DU in rats

Per se decrease in acidpepsin

secretion and

cell shedding,

tendency to increase

mucin secretion, but

reversed the increase

in cell shedding and

decrease in mucin

secretion induced by

ASP

94

Tectona grandis L.,

Fam. Verbenaceae

(Sagwan)

(Trunk bark and

wood chips)

Lapachol Immobilization stress

(IS)- and ASP-induced

GU in rats; CYS-and

HIST-induced DU in

rats and GP,

respectively

Per se no significant

effect on both

offensive and

defensive factors but

reversed the ASPinduced

increase in

peptic activity and

decrease in sialic acid

and mucin secretion

95

Zingiber officinale

Roscoe. (Ginger)

(Adrak)

6-Gingesulphonic

acid, 6-shogaol,

and ar-curcumene

— Gastric motility 76, 77, 96

Ferula foetida, Bacopa monniera, Eclipta alba, Garcinia cambogia, Pongamia pinnata, Tectona

grandis, Withania somnifera, and Satavari mandur. These therapies are relatively safe and

effective.

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23

Alzheimer’s Disease

Divya Shangari Vohora and Lakshmi Chandra Mishra

23.1 Introduction

Mental diseases and mental temperaments have been extensively described in Ayurveda

(e.g., nervous disorders [

vata vyadhi

], epilepsy [

Apasmara

], insanity, psychosis [

unmada

],

loss of consciousness, fainting [

murccha, moha, tamaka

], impairment in functioning of mind

[

Pramoha

], amnesia [

Vismriti

], etc.)

1,2

Alzheimer’s disease (AD) is a neurodegenerative

disorder associated with the progressively worsening of cognitive functions and behavioral

disturbances; it is the most common form of primary dementia and mortality in the

geriatric population. Although there is no precise equivalent for AD in Ayurveda, cognitive

dysfunction has been described in convulsive disorders

1,3

and with the aging process,

which is known to be associated with physical and mental disability.

4,5

Thus it can be seen

CONTENTS

that in spite of the terminological differences between the Ayurvedic and the modern

systems of medicine, there are areas of similarity between the two. It is necessary to bridge

the terminology gap between the Eastern and Western concepts and management for a

better understanding and control of cognitive disorders. The present review is aimed

toward this objective.

23.2 Clinical Description

The major clinical manifestations of AD are memory disturbances, spatial and temporal

disorientation, and getting lost in familiar surroundings. As the disease progresses, aphasia,

apraxia, acalculia, and sleepwalking may develop.

6

23.3 Epidemiology

AD is a worldwide problem that affects 5 million people in the U.S.

7

As the life span is

increasing, AD is becoming a more common disorder. Approximately 10% of the population

older than 65 years are affected.

6

In a recent report, AD was listed as the eighth cause

of death in the U.S. in 2000.

8

23.4 Etiology and Pathophysiology

In Ayurveda, AD is considered age related with no specific etiology except that the

vata

dosa

is involved. Conventional medicine is using several working hypotheses to find an

effective treatment for AD and develop prevention strategies. These hypotheses include

defective beta-amyloid (Abeta) protein metabolism; abnormalities of glutamatergic, adrenergic,

serotonergic, dopaminergic, and cholinergic neurotransmission; and the potential

involvement of inflammatory, oxidative, and hormonal pathways.

9–12

Another

suggested possible cause is a diet containing excessive intake of sugar, refined carbohydrates

(with high glycemic index), and animal products (with high content of saturated

fats), and a decrease intake of unrefined seeds (cereals, legumes, and oleaginous

seeds), vegetables (with high fibrous content, vitamins, polyphenols, and other antioxidant

substances [e.g., phytoestrogens]), and seafood (rich in omega-3 fatty acids).

13

The

other causative factors hypothesized are insulin resistance, decreased endothelial production

of nitric oxide, free-radical excess, inflammatory metabolites, homocysteine

deficiency, and estrogen deficiency.

13

In a prospective analysis of risk factors, increasing age, lack of education, and the

apolipoprotein E epsilon4 allele were found to be significantly associated with increased

risk of AD. On the other hand, use of nonsteroidal anti-inflammatory drugs (NSAIDs),

wine, and regular physical activity were found to be significantly associated with reduced

risk of AD.

14

Some evidence suggests that oxidative damage of brain tissue may be

involved in pathogenesis, which precedes the occurrence of symptoms and the formation

of amyloid-containing plaques and neurofibrillary tangles.

15

Genetic factors may also be involved, but they do not explain in full the etiopathogensis

of AD, implying a role for environmental factors.

16

The discovery of pathogenic mutations

in the beta-amyloid peptide (beta-APP) and the presenilin genes provides strong support

for the genetic hypothesis because Abeta production and deposition contribute to the

etiology of AD.

17

There is some evidence that alterations in the lysosomal system may have a role in the

pathogenesis of AD.

18

The lysosomal system contributes to protein deposits associated

with different types of age-related neurodegeneration. Lysosomes are highly susceptible

to free-radical oxidative stress in the aging brain and leads to the gradual loss of metabolic

activity over the life span of an individual.

19

23.5 Clinical Examination and Diagnosis

Ayurvedic examination primarily consists of an eight-point examination to determine

the vitiated

dosas,

body constitution, and manifestations of the disease to determine

difficulty in learning, spatial and temporal disorientation, and decline in daily living

activities (e.g., eating and difficulty in grooming, dressing, and undressing). Patients

generally begin to feel spatially lost in familiar surroundings. It is important to rule out

the other causes of dementia such as metabolic causes (e.g., diabetes, medicationinduced

psychiatric illness) before treating the patient with cholinesterase inhibitors.

Because many causes of dementia are rare and can be excluded by careful historical

information, serial examination, and some structural examination, an accurate diagnosis

can be made by using clinical criteria.

6

23.6 Clinical Course and Prognosis

AD is a uniformly progressive disease. It ultimately results in irreversible debilitating

cognitive impairment in patients. Although some medications appear to produce transient

improvement, there is no medication available that can halt the progression of

AD.

19

23.7 Management

Ayurveda uses natural products (drugs of plant, animal, and mineral origin) for the

treatment of all physical and mental ailments, including cognitive dysfunction. There are

two approaches: one is aimed at general or total well-being, including mental exercises

appropriate treatment (Chapter 2). Patients are examined for memory disturbances,

(memory games, reading, card games) and meditation, whereas the other specifically

targets intellect (

medha

) and memory (

smriti

). Ayurvedic

rasayana tantra

, which describes

these approaches, was defined by the Ayurvedic physician Susruta (500

B

.

C

.) as the measure

that prolongs longevity, develops positive health and mental faculties, and imparts resistance

and immunity against disease.

4

These measures do not appear to differ from the

adaptogenic,

20

immunomodulatory,

21

and antioxidant

22

therapeutic approaches used in

modern medicine. The host-oriented approach of

rasayana

drugs is believed to vitalize the

digestion and metabolism and improve microcirculation and tissue perfusion

5

to elicit the

desired therapeutic effects.

23.7.1 Brain Tonics (

Medhya Rasayana

)

Abhang

23

reviewed the past, present, and future of

medhya rasayana

drugs: a special class

of

rasayana

agents that rejuvenate mental faculties, intellect, and memory. In ancient

India most of the education was imparted by oral instructions. The students retained

and recalled this knowledge by repeated recitation. Therefore, intelligence was considered

synonymous with memory, and drugs that helped reduce time for learning (memorizing)

the lesson were developed from natural sources. Many such products,

particularly of plant origin, have been described in Ayurvedic texts. Some of these are

particularly reputed for

medhya rasayana

properties since ancient times of great

Ayurvedic physicians Charaka (400

B

.

C

.) and Susruta (500

B

.

C

.). The following brain

vitalizers have been mentioned in

Charak Samhita

24

:

1. Expressed juice of Indian pennywort (

Centella asiatica

)

2. Powder of licorice (

Glycyrrhiza glabra

) with milk

3. Juice of

guduchi

(

Tinospora cordifolia

)

4. Paste made from small leaves of

shankhpushpi

(

Convolvulus pluricaulis

) mixed with

its roots and flowers

A large number of Indian medicinal plants are attributed with brain tonic and memoryenhancing

effects. These plants are rarely used singly and are mostly incorporated in

polyherbal formulations containing 4 to 20 ingredients. The latter may occasionally include

mineral-origin drugs in addition to medicinal plants. Polypharmacy appears to be the rule

(rather than exception) in Ayurveda as in other traditional systems of medicine practiced

in India (e.g., Unani-Tibb and Siddha). It is claimed that such combinations enhance

activity and mitigate side effects of individual components.

Some plant ingredients are common to many formulations. A look at the composition

of 6 polyherbal formulations, marketed in India for memory enhancing effects, revealed

In conventional medicine, the only drugs currently approved for the treatment of AD

are cholinomimetics, such as tacrine, which have the pharmacologic profile of acetylcholinesterase

(AChE) inhibitors.

12,25,26

Tacrine has been shown to affect some measures of

memory performance, but the magnitude of improvement was very modest.

27

The side

effects of tacrine, such as abdominal cramping, nausea, vomiting, and diarrhea, may be

significant and dose limiting. Considerable research is being conducted in other areas,

such as using selective anti-inflammatory drugs (selective cyclooxgenase-2 [COX-2] inhib-

the presence of 32 medicinal plant ingredients (Table 23.1).

itors) to reduce inflammatory activity in the brain and antioxidants.

7,11,15

Other areas of

research are antiamyloid strategies (e.g., immunization, aggregation inhibitors, secretase

inhibitors), transition metal chelators (e.g., clioquinol), lipid-lowering agents, antihypertensives,

vitamins, and neurotransmitter receptors.

9

Studies on herbal materials with AChE inhibitory properties have shown some

promise.

28,29

Ayurveda has many formulations and herbomineral drugs discussed

below that are used to improve cognitive functions. The precise biochemical mechanism

of action of these herbs is not clear. It is likely that antioxidant and antiinflammatory

properties of these herbs may be responsible for their beneficial effect

in the treatment of AD.

 

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)