Scientific Basis for Ayurvedic Therapies -26

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

The drug was effective when given either before or after

enterotoxin binding and when given either intraluminally or parenterally; it did not inhibit

the stimulation of adenylate cyclase by cholera enterotoxin and caused no histological

damage to intestinal mucosa.

 Berberine also markedly inhibited the secretory response of

E. coli heat-stable enterotoxin in the infant mouse model. Although the mechanism of

Name of Formulation Activity Dose Adjuvant Ref.

Gangadhara curna Digestive,

appetiser,

antidiarrheal

1–3 g three

times/day

Jaggery, buttermilk

and honey

6

Hingvashtaka curna Carminative,

digestive,

antidysenteric

1–2 g two

times/day

Warm water before

meals

5

Agnimukha curna Carminative,

digestive,

antidysenteric

1–3 g two

times/day

Buttermilk 5

Bilvadi curna Carminative,

digestive,

antidysenteric

2–6 g two

times/day

Buttermilk (50–100

ml)

8

Kutajaghana vati Antidysenteric 250–500 mg two

times/day

Buttermilk (50–100

ml)

11

Jatiphaladi vati Antimotility,

Antispasmodic

60–120 mg three

times/day

Buttermilk and

water

8

Karpura vati Antimotility,

Antispasmodic

120–240 mg two

times/day

Honey 8

Kutajarishta Digestive,

antidysenteric

15–30 ml two

times/day

Equal quantity of

water

8

Kutajavaleha Antidysenteric 5–10 g three

times/day

Water 8

Sankha bhasma, Kapardika bhasma,

or Pravala bhasma

Antiflatulent,

digestive, and

intestinal

adsorbant

0.25–0.5 g two

times/day

Lemon juice before

meals

46

Agasthisutaraja rasa Antidiarrheal 60–120 mg three

times/day

Cumin, nutmeg

powders

5

Kanakasundara rasa Antidiarrheal 60–120 mg three

times/day

Buttermilk 8

action of the drug is not yet known, these data provide a rationale for its apparent clinical

usefulness in treating acute diarrheal disease.47

21.2.10.3 Medicinal Herbs (Boerhaavia diffusa, Berberis aristata, Tinospora cordifolia,

Terminalia chebula, and Zingiber officinale)

The antiamoebic effect of a crude drug formulation against Entamoeba histolytica was

studied. The formula is composed of five medicinal herbs: Boerhaavia diffusa, Berberis

aristata, Tinospora cordifolia, Terminalia chebula, and Zingiber officinale. The dried and pulverized

plants were extracted in ethanol together and individually. In vitro amebicidal

activity was studied to determine the minimal inhibitory concentration (MIC) values of

all the constituent extracts as well as the whole formulation. The formulation had an MIC

of 1000 mg/ml as compared with 10 mg/ml of metronidazole. In experimental cecal amebiasis

in rats, the formulation had a curative rate of 89%; with the average degree of

infection (ADI) reduced to 0.4 in a group dosed with 500 mg/kg/day as compared with

an ADI of 3.8 for the sham-treated control group of rats. Metronidazole had a cure rate

of 89% (ADI = 0.4) at a dose of 100 mg/kg/day and cured the infection completely (ADI

= 0) when the dosage was doubled to 200 mg/kg/day. There were varying degrees of

inhibition of the following enzyme activities of crude extracts of axenically cultured

amoebae: deoxyribonuclease, ribonuclease, aldolase, alkaline phosphatase, acid phosphatase,

alpha-amylase, and protease.48

Ayurvedic plants having inhibitory activity on enteropathogenic bacteria are shown in

References

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Table 21.2.

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28. Shoba, F.G. and Thomas, M., Study of antidiarrhoeal activity of four medicinal plants in castoroil

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29. Rani, S. et al., Anti-diarrhoeal evaluation of Clerodendrum phlomidis Linn. leaf extract in rats,

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30. Bajad, S. et al., Antidiarrheal activity of piperine in mice, Planta Medica, 67(3), 284, 2001.

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36. Srivastava, D.N. and Bhatt, K.R., Effect of Neblon on transit time of ingesta in and gut of

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38. Jain, P.K. et al., Clinical trial of arka mula tvaka bark of Calotropis procera, on atisar and

pravahika – a preliminary study, J. Res. Ayurveda Siddha, (1, 3, and 4), 88, 1985.

39. Saroja, P.R., Sivaprakasam, K., and Veluchamy, G., Role of Chundaivattral Churnam in the

management of (non-specific diarrhoea) Athisaram, J. Res. Ayurveda Siddha, 3-4, 128, 1998.

40. Jing, M. et al., Study on the mechanism of Valeriana officinalis for infantile viral diarrhea, Yunnan

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41. Rabbani, G.H. et al., Clinical studies in persistent diarrhea: dietary management with green

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by acute diarrhea: a clinical trial, Acta Paediatr., 86(10), 1047, 1997.

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44. Anon., Epidemic Dysentery Fact Sheet No. 108, Division of Emerging and other Communi-

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46. Anon., The Ayurvedic Formulary of India, Vol. 1, Part 1, Ministry of Health and family Welfare,

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www.healthlibrary.com/reading/ncure/chap44.htm.

22

Gastroduodenal Ulcers

Krishnamurthy Sairam and Sailaja Vani Batchu

  407

22.1 Introduction

In Ayurveda, peptic ulcers or gastroduodenal ulcers generally refer to parinamasula. It

is the disease of the gastrointestinal tract, especially the stomach. Abdominal pain during

digestion is the main symptom in these diseases. Earlier Ayurvedic classics like Charaka

Samhita and Sushrut Samhita mentioned abdominal pain as relating to digestion but not

as a separate clinical entity.1,2 For the first time, in 7th century A.D., Madhavakar

described this disease separately with the name parinamashula in his famous treatise,

Madhava Nidana, which mainly deals with the etiology and pathology of different diseases.

He has given a precise description of parinamasula, but Vijayarakshita, the commentary

of Madhava Nidana, later elaborated it. This disease has been mentioned in all

the later books like Bhavaprakash, Yogaratnakar, Sharangadhara Samhita, and Chakradatta.3–5

Apart from the stress placed on food habits and personal hygiene, some herbal drugs

have also been mentioned in the treatment of this disease. The gastric ulcer (GU) remains

a major global health problem, eluding satisfactory therapeutic regimen. Modern medicine

has not adequately evaluated the usefulness of natural drugs in ulcer therapy,

although studies have been reported.

It is now assumed that the antiulcer drugs ultimately balance the aggressive factors

(acid, pepsin, H. pylori, bile salts) and defensive factors (mucin secretion, cellular mucus,

bicarbonate secretion, mucosal blood flow, cell turnover, etc.).6 New etiological factors,

such as involvement of free radicals7 and H. pylori,8,9 have gained attention. Resistance of

H. pylori to antimicrobials10 and poor patient compliance due to multiple doses11 are

reported to be major causes for the failure of antiulcer therapy. This necessitates using

newer antibacterials and reducing doses during therapy. Antiulcer drugs with antioxidant

and antibacterial effects would be superior to combined therapies.12 These attributes are

found with herbal drugs.

In this chapter, literature on Ayurvedic therapies of GUs and duodenal ulcers (DUs) is

reviewed and compared with therapies in conventional medicine. Many similarities

between the two systems are noted.

22.2 Clinical Description, History, and Epidemiology

According to Ayurveda, abdominal pain that is aggravated during digestion is known as

parinamashula. Various synonyms of parinamashula mentioned in the texts (i.e.,

annadravashula, paktishula, annavidahajashula, etc.) are related to food and digestive factors.

According to Ayurveda, the word parinama implies digestion. It actually starts after the

emptying of the stomach. The word shula refers to pain. Hence the pain that occurs during

the digestion period is called parinamashula.

Similarly, in conventional medicine, peptic ulcer disease (PUD) is described to be associated

with epigastric pain exacerbated by fasting and improvement with food. The patient

has a history of alterations in bowel habits, especially diarrhea or constipation.13

As discussed earlier, the GU or DU has not been recognized as a separate clinical entity,

making information on history and epidemiology limited.

22.3 Etiology

When we compare and contrast GUs and DUs, both seem to be very much similar. PUD,

according to the modern concept, is a multifactorial disease.13 The causes include genetic,

dietetic, psychological (stress and emotional factors), endocrine, and drug-induced infections.

The common result of all these initiating factors is a breakage in mucous membrane

of either the stomach or duodenum (common sites). There may be a difference in incidence,

placement of ulcer, symptomatology, or prognosis of DUs and GUs, but the presence or

absence of an ulcer is determined by a delicate interplay between the aggressive factors

(acid and pepsin) and defensive factors (mucosal resistance).1

The defense mechanism of the gastrointestinal mucosa against aggressive factors, such

as hydrochloric acid, bile acid, free radicals, H. pylori colonization, nonsteroidal antiinflammatory

drugs (NSAIDs), etc., mainly consists of functional, humoral, and neuronal

factors.14 These coincide with the Ayurvedic concept of PUDs, where it is believed to be

an imbalance between kapha and pitta. The important factors responsible for ulcerogenesis

are described below.

22.3.1 Offensive Factors

Pitta represents the aggressive factors such as acid and pepsin. Vata is the main factor in

production of pain and represents the neuronal part of acid secretion. The symptomatology

of parinamashula and PUD have similar symptoms such as pain in the epigastrium and

other sites, nausea, vomiting, and pain relieving with intake of food (in DUs) or after

digestion (i.e., in an empty stomach or with vomiting [in GUs], heartburn, abdominal

pain, etc.)

22.3.1.1 Acid and Pepsin Secretion

The role of hydrochloric acid in the pathogenesis of gastric ulcer is well established.15

Many commonly used antiulcer agents heal ulcers by blocking acid secretion.

22.3.1.2 H. pylori colonization

H. pylori, a gram-negative bacterium, is found in more than 90% of DU cases and 75% of

GU cases.16 Clinical outcomes associated with H. pylori infection include GU, DU, gastric

adrenocarcinoma, and gastric-mucosa–associated lymphoid tissue lymphoma. The pathogenicity

of H. pylori depends on bacterial and host factors.16 Even though there have been

advances in eradication of H. pylori in peptic ulcer patients by using multiple therapies,

there are several reports on the limitations of such treatments, such as resistance to H. pylori11

and poor patient compliance due to multiple doses.12 Further treatment can be accompanied

by nausea, diarrhea, abdominal pain, and pseudomembraneous colitis.17 These adverse

effects contribute to patient noncompliance and reduce the efficacy of therapy.

22.3.1.3 Histamine

Histamine has been found in the gastric wall and is a powerful stimulant for gastric

secretion. Histamine blockers such as ranitidine have been reported to prevent even

psychological stress-induced gastric ulceration.18

22.3.1.4 Drugs (NSAIDs)

NSAIDs are widely prescribed for treating many conditions. The risk of ulcer complications,

such as bleeding, perforation, and death, is increased approximately fourfold in

NSAID users. NSAIDs disrupt the GI mucosal-protective and acid-limiting properties of

prostaglandins (PGs) and also have a direct topical irritant effect. NSAIDs induce gastric

damage through generation of reactive oxygen species.19 Adverse side effects may be

significantly reduced through the use of cyclooxgenase-2 (COX-2)–specific inhibitors.20

22.3.1.5 Free Radicals

Free radicals are defined as chemical species possessing unpaired electrons. The role of

oxygen-derived free radicals has been demonstrated in acute and chronic ulceration.21

Several natural drugs have been reported to have antioxidant activity, which contributes

to their activity.22–24

22.3.2 Gastric Mucosal Defense Mechanisms

The role of kapha is that of mucosal defensive mechanism and was clearly mentioned in the

pathogenesis of parinamashula in 7th century A.D. According to modern medicine, the malfunctioning

of certain defensive (protective) mechanisms of the GI tract mucosa are the

important determinants in the development of ulcers. These mechanisms are presented here.

22.3.2.1 Mucus-Bicarbonate Barrier

The entire surface of the gastric mucosa is covered by a continuous layer of mucus gel,

which has a variable thickness of less than 500 mm.25 Mucus is made up of glycoprotein

and contains sulfhydryl groups (-SH), which protect the mucosa from free-radical–induced

injury.26 Mucus provides a mixing barrier at the mucosal surface and also prevents the

activation of pepsinogen to pepsin apart from providing a microenvironment for repair

and restitution.27

22.3.2.2 Gastric Mucosal Renewal and Restitution

The rapid proliferation of gastric mucosa plays an important role in mucosal protection

during normal state and after mucosal damage.28

22.3.2.3 Gastric Motility

Gastric motility changes have been reported to cause both gastric and duodenal ulceration.

29 Incompetence of the pyloric sphincter and delayed gastric emptying may lead to

stasis and delayed clearing of refluxed duodenal contents; these actions can lead to increase

gastric release and a subsequently higher rate of acid secretion.

22.3.2.4 Mucosal and Submucosal Blood Flow

Constituents of mucosal blood flow are important in mucosal defense. They play a vital

role in protecting the mucosa by delivering oxygen, nutrients, and bicarbonate to the cells.

They also remove hydrogen ions that have penetrated the mucus-bicarbonate and epithelial

barrier.30

22.3.2.5 Prostaglandins

PGs, namely, prostaglandin E and prostaglandin I (PGE and PGI), have been shown to

protect against experimental necrotic damage. PGs increase gastric mucosal blood flow,

mucus, and bicarbonate secretion and strengthen the mucus bicarbonate barrier. Thus,

inhibition of the production predisposes the stomach to injury. The beneficial effects of

COX-2 inhibitors are still controversial.31

22.3.2.6 Antioxidants

Antioxidants are stated to be any substance, even present at low concentrations compared

with those of an oxidizable substrate, that significantly delays or prevents oxidation of

that substrate. Uncontrolled oxidation in aerobic organisms produces oxidative stress, cell

damage, and eventually cell death. An array of cellular defense systems exists to counterbalance

reactive oxygen species (ROS).32 Antioxidants neutralize free radicals, thus

protecting essential micro- and macromolecules in the body from the oxidative damage.

22.3.3 Other Causative Factors

Other causative factors can be broadly divided into three types: diet (ahara), lifestyle

(vihara), and seasonal (kala) factors.

22.3.3.1 Dietetic Factors (Ahara)

Excessive use of sour, salty, pungent, spicy, astringent, and dry foods; alcohol intake; oil;

mustard; pulses (e.g., peas, beans); and a nonvegetarian diet may all lead to ulcer development.

Consuming food before digesting a previous meal, eating incompatible food, and

being gluttonous may also cause peptic ulcers.

There are also recent reports from modern medicine on the influence of food on the

genesis of GUs and DUs.34–36 Factors such as being a male, having a family history of

ulcers, having an O-blood type, skipping breakfast or more than one meal, drinking

excessive amount of coffee, and smoking cigarettes were reported to be associated with

increased incidences of DUs.37

22.3.3.2 Lifestyle Factors (Vihara)

Lifestyle factors include the following:

1. Physical factors — Examples include excessive exercise, hard work, excessive

sexual indulgence, excessive exposure to sun or fire, waking up at night, and

suppressing natural urges.

2. Mental factors — Examples include anger, grief, anxiety, and depression.

3. Psychological factors — Lifestyle factors can be equated with psychological factors.

Although there has not been much information on patterns of life on ulcers

in conventional medicine, there are reports on the psychological changes, which

are an immediate fallout of these physical factors.

4. Stressful life events — According to modern medicine, these events have been

associated with the onset or symptom exacerbation of some of the most common

chronic disorders of the digestive system, including functional GI disorders,

inflammatory bowel disease, gastroesophageal reflux disease, and PUD.38 There

is considerable evidence that supports the role of stressful life events in the

etiology of PUD. These mechanisms involve both the cortical and subcortical

levels.39 Many investigators have suggested the role of ROS in stress-induced

ulcers.40

5. Cigarette smoking — This is a major lifestyle risk factor for the development and

recurrence of peptic ulcers. The association between ulcerative disease and smoking

cannot be explained on the basis of an effect on gastric secretion of acid or

pepsin, blood flow, or pancreatic secretion.

6. Seasonal factors (kala) — Seasonal factors, including rainy season, autumn, spring,

cold weather, evening time, midday, midnight, and sunrise, may trigger ulcer

development.

22.4 Pathogenesis

According to Ayurveda, in his description of the gastroduodenal ulcers, Madhavakar

has not mentioned the specific etiological factors. However, he did state that all the

exogenous and endogenous factors that cause the vitiation of vata are responsible for

the initiation of pathogenesis of ulcers; kapha and pitta are also involved.33 Hence the

provocating factors mentioned in reference to shularoga were found to be relevant for

gastrodudenal ulcers. Because of the indulgence in specific etiological factors, the dosas

may start accumulating at their own sites followed by vitiation. The vitiation of any one

of these dosas may disturb other dosas. Even when one of the three dosas is in a state of

vitiation, the biofire (i.e., agni) tends to be deranged, hindering the process of digestion

and leading to the formation of defective juices from inadequate digestion of food (ahara

rasa).

The stomach (amashaya) is the site of specific kaphas (kledakakapha, pachakapitta, and

samanavata). According to Ayurveda, kledakakapha protects the stomach from the ill effects

of pachakapitta. The role of samana vata is to stimulate the pachakapitta. So, the eroding

effect of pitta is counteracted by kledakakapha and vata maintains the motility and movements

of the stomach. Because of indulgence in etiological factors, the displaced kapha

from its site admixtures with the pitta and is inactivated with the help of vata, which

produces the pain during the period of digestion. Parinamashula is a tridoshik disease,

but pitta is the predomint dosa, as it plays important role during the period of digestion

(i.e., parinamakala).

22.5 Clinical Examination

The cardinal feature of this disease, according to Ayurveda, is pain in the abdomen during

the process of food digestion. Important sites of the pain are the epigastrium (kukshi), flanks

(jathara parshwe), umbilical region (nabhau), retrosternal region (stanantare), and back (prishtamoola

pradesha); the pain sometimes occurs in all the above mentioned sites simultaneously

(sarveshu). There are seven clinical types mentioned, but basically they are derived from the

permutations and combinations of three dosic states. Pain may be aggravated through the

consumption of a specific variety rice (raktashali) and may be relieved by taking a meal and

vomiting. As in modern medicine, the food habits and other personal clinical history features

(e.g., previous drug intake) are taken into consideration, and modern techniques such as

radiological and histological examinations are routinely done.

22.6 Clinical Course and Prognosis

The characters of pain are burning (daha), dull aching (swalpa ruk), flatulence (borborygmi),

trembling (vepana), and acute continuous pain (dirgha santata ruk). Borborygmi is due to vata

with systemic features of flatulence, constipation, and restlessness. These symptoms can be

relieved by a hot and fatty diet. Burning sensation due to pitta with systemic features of

thirst, restlessness, and excessive perspiration can be aggravated (shula vriddhi) by sour and

salty food intake. Dull aching and continuous acute pain due to kapha with systemic features

including nausea, drowsiness, and vomiting can be vitiated by pungent and bitter food.

The dual (dwandaja) type and triple (tridoshaja) type are clinical mixtures of abovementioned

three types of parinamashula. The tridoshaja variety is associated with excessive

weakness and markedly diminished digestive capacity; it is considered incurable.

22.7 Therapy

In Ayurveda, the whole armamentarium of treatment of any disease has been broadly

divided into two types: biopurificatory (samshodhana) and palliative (samshamana), along

with avoidance of causative factors (nidana parivarjana):

1. Samshodhan therapy41,42 — This type of treatment is used in strong and suitable

persons who can bear the impact of various procedures like langhan, vaman,

virechan, anuvasan, and niruha vasti.

2. Samshamana — Limited drugs have been mentioned41,42 for this type of treatment

3. Nidana parivarjana — Also known as the withdrawal from the etiological factors,

nidana parivarjana is considered to be crucial in the treatment of this disease.

(see Tables 22.1 and 22.2).

The main principle of treatment of parinamashula is aimed at the following: (1) alleviation

of excited vata, (2) controlling or reducing the hyperactivity of pitta, and (3) repairing and

maintaining the integrity of the rasavaha srotas situated at the site of lesion by increasing

the kapha.

22.7.1 Diet and Regularized Lifestyle (Pathya ahara and Vihara)

Bajra, wheat, Indian gooseberry (amalaki), milk, buttermilk, and all bitter and sweet foods

are compatible. Mental and physical rest are also helpful to control the symptoms of the

disease. Anger, grief, waking up at night, and excessive exposure to sun, cereals (e.g.,

blackgram, sesame), excessive sour and salty foods, alcohol, and foods that are heavy for

digestion are all considered incompatible for a proper lifestyle and diet.

22.7.2 Conventional Therapies

Conventional drugs are reviewed here to understand their mechanism of action, which

can be correlated with Ayurvedic drugs discussed later. This section also highlights their

TABLE 22.1

Single Herbal Drugs

Drug Form of Drug Dosage

Patola Ghee prepared with fruits 25 ml twice daily with milk

Shatavari Root powder

Ghee prepared with roots

3-4 g three times with milk

25 ml twice daily with milk or hot water

Yashtimadhu Root powder 4–5 g three times daily

Aswagandha Root powder 4–5 g three times daily

Bhringaraja Powder of whole plant 4–5 g four times daily

Amalaki Powder of fruit pulp 1 g twice daily

Aparajita Root paste 4–5 g twice daily

TABLE 22.2

Compound Ayurvedic Formulas Used in the

Treatment of Gastroduodenal Ulcers

Preparation Type Name of Preparation

Churna [powder] Avipattikara churna

Amalaki Rasayan

Avaleha Kushmandavaleha

Dadimavaleha

Gutika [pill] Shankha vati

Mahashankha vati

Bhasma [ash] Shankha bhasma

Varata bhasma

Shambooka bhasma

Lauha [iron preparations] Saptamrita lauha

Dhatri lauha

Mandur Shatavari mandur

Rasaushadhi Sutashekhara ras

Kamadudha ras

Pravala panchamrit

Khanda Narikelakhanda

balance of therapeutic efficiency to adverse effects, drug interactions, and the need for

alternative strategies.

22.7.2.1 Antacids

The effect of antacids on the stomach is due to partial neutralization of gastric HCl and

inhibition of pepsin. Although adverse effects with antacids are minimal, significant

adverse reactions can occur with long-term use.43

22.7.2.2 Histamine H2-Receptor Antagonists

Histamine H2-receptor antagonists (H2RAs) competitively inhibit histamine action at all

H2 receptors. Their main clinical use is as inhibitors of gastric-acid secretion. There are

reports suggesting non–acid-related effects contributing to the activity of H2RAs defying

the previously held view as only antisecretory drugs.44 Reports suggest that the central

nervous system (CNS) may be partially responsible for antiulcerogenic activities of

H2RAs.45 This correlates well with the Ayurvedic view of influence of psychological factors

and the use of adaptogens (rasayanas) for ulcer therapy. Human gastric carcinoid was

detected during the development of tolerance and rebound acid secretion during the longterm

treatment with H2RAs.46

22.7.2.3 Proton Pump Inhibitors (PPIs)

Proton pump inhibitors (PPIs) act by irreversible interaction with the SH group of the H+-

K+adenosine triphosphatase (ATPase), forming a disulphide bond. Reported side effects

include headache, diarrhea, skin rash, and reversible abnormalities in biochemical liver

function tests. Long-term inhibition has been reported to produce gastric carcinoma,47

achlorhydria, and hypergastrenemia.48 Omeprazole has been reported to reduce the secretion,

synthesis, and gene expression of pepsinogen, which may create problems in the

protein digestion and result in diarrhea.49 There are reports of potential CNS side effects

after PPI treatment, which need further evaluation.50 PPIs have also been reported to have

some drug interactions. Recently, lansaprasole has been reported to potentiate vecuronium-

induced paralysis in patients.51

22.8 Preventive Measures

Preventive measures essentially include dietary intervention and lifestyle changes based

22.9 Scientific Basis of Ayurvedic Therapies

Because the etiological factors for gastroduodenal ulcers in Ayurveda and conventional

medicine are similar (e.g., imbalance of offensive [vata] and defensive factors [kapha]),

animal models used to evaluate modern medicine are often used to evaluate Ayurvedic

therapies.

on the factors as suggested in Ayurveda (see Sections 22.4 and Section 22.7).

The upcoming review of some selected drugs gives an elaborate and clear view of how

modern evaluation models are suitably used for screening natural drugs. The success of

Ayurvedic drugs in the commercial market depends on stringent evaluation followed

closely in line with modern experimentation and clinical evaluation. One of the major

hurdles is to clearly define the composition of Ayurvedic drugs and the identification of

active ingredients. Without the knowledge of active ingredients, the product cannot be

standardized or the amount of active ingredient cannot be quantified and would fall short

of drug enforcement standards. Investigations not taken to this level will be of academic

interest only and not of any practical value. This review gives major trust for drugs that

have been actively quantified or have been standardized for active ingredients.

22.9.1 Animal Studies

22.9.1.1 Musa sapientum var. paradisiaca (Unripe Plantain Banana)

Plantain banana has been subjected to extensive experimental and clinical studies. Dried

powder of banana pulp (DRBP) was effective against experimental ulcers.52 The antiulcer

activity of DRBP was reported to be due to its predominant effect on mucosal defensive

factors rather than on the offensive acid-pepsin secretion.53–55

Ethanolic extract of banana was reported to increase the accumulation of eicosonoids

like PGE, prostaglandin I2 (PGI2), and leukotrienes B4, and C4/D4 (LTB4, C4/D4) in the human

gastric and colonic mucosal incubates.56 Many active principles such as steryl-aclyglycosides,

and sitoindosides I-IV were isolated and characterized from many vegetables and

bananas and were reported to have antiulcerogenic activity both in animal and human

models.57–59 Methanolic extract of banana was reported to have an antioxidant effect but

was devoid of anti-H. pylori activity in vitro.24

22.9.1.2 Tambrabhasma

Herbomineral preparations have been widely mentioned in Ayurveda.60 Tambrabhasma

(TMB), a traditional preparation of copper (containing CuO ≥ 44.45% £ 66.13%, Fe2 O3

< 6.03%, and S < 2.75%) has been advocated for use in amlapitta. Tambrabhasma showed

antiulcer activity against experimental GUs and DUs. The activity of tambrabhasma was

ascribed due to a decrease in offensive acid-pepsin secretion and an increase in defensive

factors; the effect was also free from toxicity.61,62

22.9.1.3 Mahakasya Drugs

A water decoction of ginger, which makes up one of the constituents of mahakasyaya drugs,

along with a water decoction of Piper longum and a colloidal solution of Ferula foetida, has

been reported to protect against cold-restraint stress, aspirin, and pyloric-ligation–induced

GUs in rats. Although increase in offensive acid-pepsin secretion was observed in this

study, the increase in defensive mucin secretion was sufficient enough to protect against

experimental ulcers.63

22.9.1.4 Bacopa monniera (Bramhi)

Bacopa monniera Wettst. (syn. Herpestis monniera L.; scrophulariaceae) is classified as a medhya

rasayana, a class of plant drugs used to promote mental health and improve memory and

intellect.64 It is a classic example where an adaptogenic drug has antiulcer activity. It is

intriguing that Bacopa monniera has shown both anxiolytic and antidepressant activity.65–67

Bacopa monniera contains active chemicals, such as bacoside A, which have been reported to

be responsible for facilitation of memory68 and the antiulcerogenic effect.69

Fresh juice of Bacopa monniera and its standardized methanolic extract, containing 35%

of bacoside A,23 has been reported to have an antiulcerogenic effect. Bacopa monniera extract

(20 mg/kg) showed no effect on offensive factors, but it increased the defensive factors.

Bacopa monniera showed significant antioxidant effect per se in stressed animals. In vitro

studies with H. pylori showed significant inhibition at the concentration of 1000 (mg/ml

of Bacopa monniera extract.70 Even though effective antimicrobial therapy is available to

eradicate H. pylori infection, current therapies require patients to ingest multiple agents

several times a day for at least 1 week, leading to noncompliance of treatment schedules.

An antiulcer agent having anti-H. pylori activity can have better compliance among

patients and can also decrease incidences of drug interactions. Bacopa monniera extract also

increased in vitro accumulation of PGs on human colonic mucosa cells.70

22.9.2 Clinical Studies

22.9.2.1 DRBP

The clinical effectiveness of DRBP was confirmed by radiological and endoscopic studies in

the several clinical trials. DRBP was found to decrease or delay the relapse of peptic ulcer

for 6 to 12 months after a 3-month continuous treatment at the dose level of 1 g four times/

day. It became commercially available as Musapep® after phase IV clinical trials. A doubleblind

study71 done at multiple centers has shown that about 40 to 70% of endoscopically

proved DUs healed after 12 weeks of treatment with DRBP, as compared with about 16%

with placebo. In another clinical study72 with Musapep in nonulcer dyspepsia (NUD), there

was a reported 75% relief in symptoms after 8 weeks of treatment compared with 20% in

the control. The authors advocated that the therapeutic trials with this dose justified the use

of DRBP on clinical grounds to be safe and effective in the treatment of NUD.

22.9.2.2 Satavari mandur

Effect of Satavari mandur was studied in 40 cases of parinamashula, including 10 cases of

peptic ulcer, 15 cases of erosive mucosal disorder, and 15 cases of NUD. The improvement

was assessed by clinical and radiological or endoscopic findings, together with the biochemical

study of gastric juice in eight patients. The drug was given in a dose of 3 g/day

in two divided doses with ghee for 2 months in NUD cases and 3 months in peptic ulcer

cases. A significant improvement was observed in all the groups, but it was more prominent

in ulcer dyspepsia than NUD. Satavari mandur showed significant improvement in

healing ulcers (marked healing of 50%, partial healing of 30% in ulcer group) as well as

significant improvement in symptoms. The biochemical study of gastric juice in eight

patients showed a significant increase in mucosal defensive factors such as decreased cell

shedding, increased individual carbohydrates, and increased total carbohydrate to protein

ratio. These findings indicate the drug was promoting the mucosal defensive mechanism

rather than affecting the acid and pepsin secretion.41

22.9.2.3 Eclipta alba (Bhringaraja)

 

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)