Scientific Basis for Ayurvedic Therapies -23

Scientific Basis for

Ayurvedic Therapies 

edited by

Brahmasree Lakshmi Chandra Mishra

Hyperacidity (Amlapitta)

Shankar K. Mitra and Paramesh R. Rangesh

19.1 Introduction

Hyperacidity (

amlapitta

) is a disease caused by the excessive formation of acid in the

stomach associated with the symptom of burning sensation in the throat and heart area.

This condition appears in many diseases ranging from gastritis and peptic ulcer disease

(PUD) to the currently named gastroesophageal reflux disease (GERD).

Gastritis includes myriad disorders that involve inflammatory changes in the gastric

mucosa, including erosive gastritis caused by a noxious irritant, reflux gastritis from

exposure to bile and pancreatic fluids, hemorrhagic gastritis, infectious gastritis, and

gastric mucosal atrophy. PUD refers to a discrete mucosal defect in the portions of the

gastrointestinal (GI) tract (gastric or duodenal) exposed to acid and pepsin secretion.

Presentations of gastritis and PUD usually are indistinguishable, and the management is

generally the same. GERD is a digestive disorder that affects the lower esophageal sphincter

(LES), the muscle connecting the esophagus with the stomach. Many people, including

pregnant women, suffer from heartburn or acid indigestion caused by GERD. Doctors

believe that some people suffer from GERD due to a condition called hiatal hernia. In

most cases, heartburn can be relieved through diet and lifestyle changes; some people

may require medication or surgery.

Amlapitta

is more generally classified as a GI disorder, which is due to imbalance in

enzyme secretions. Caraka describes some of the common causes for such as deranged

digestive enzymes. Fasting, overeating while having indigestion, practicing irregular eating

habits, consuming unsuitable foods, eating in an unsupportive atmosphere or at the

wrong time, or eating foods that have been improperly prepared will all produce acid

indigestion.

1

19.2 Definition

A

mlapitta

is defined as the digestive secretions (

pitta

) that have undergone an acidic and

acrid state.

2

Gastroesophageal refers to the stomach and esophagus and reflux means to flow back

or return. Therefore, gastroesophageal reflux is the return of the stomach’s contents into

the esophagus.

19.3 Clinical Description

Hyperacidity is characterized by reflux of acid juice from the stomach, vomiting, a burning

pain in the chest region, and headache.

2

As described in conventional medicine, the most prevalent symptom is a burning pain

in the area of the lower chest or upper abdomen. The pain of an ulcer can last anywhere

from 30 min to a few hours. Additional symptoms that may be experienced are weight

loss, a decrease in appetite, anemia, nausea, and vomiting. There may be times when the

pain of an ulcer seems to be gone and then it suddenly returns. Pain associated with ulcers

affect different people in different ways. Some people experience pain immediately after

eating, whereas others may not be bothered for several hours. It is beneficial to figure out

what may be responsible for producing excess stomach acid so these symptoms can be

avoided.

19.4 History and Epidemiology

Hyperacidity is not described in detail in most of the ancient Ayurvedic literatures, including

those of Caraka, Susruta, and Vagbhata that belong to the period

circa

1500

B

.

C

. to 600

A

.

D

. However, Caraka has mentioned, while explaining irritable colon (

grahani

) disease,

that this condition is the outcome of endotoxin, and the horsegram (

Dolicos biflorus

) seeds

are known to be aggravating the disease.

1

For the first time, Kashyapa (

circa

800

A

.

D

.) has

described this disease separately. Madhava (1000

A

.

D

.) has given details about this disease.

3

Looking back at the history of conventional medicine, PUD was a rare and generally

unrecognized cause of symptoms and complications or death until the early 19th century.

Despite sporadic case reports beginning in late 18th century, PUD did not become widely

appreciated until early 20th century. The first 6 decades saw the dominance of surgery in

the treatment of PUD. With the introduction of acid-suppressive drugs like histamine-2

blockers in the 1970s, the treatment of PUD was revolutionized. By the 1980s, the advent

of

Helicobacter pylori

brought about a dramatic twist and possibly the cure.

Reflux disease is common. Approximately 15 to 20% of adults experience heartburn at

least once a week. Obesity (body mass index [BMI] >30 kg/m

2

), alcohol consumption (>7

standard drinks/week), and a first-degree relative with heartburn increase the risk of

having reflux symptoms. Patients with connective tissue diseases, such as scleroderma,

and chronic respiratory disease, such as asthma and cystic fibrosis, institutionalized and

intellectually handicapped patients. Patients nursed in a supine position for prolonged

periods are at increased risk of reflux disease.

4

19.5 Etiology

According to Ayurvedic medicine, hyperacidity is caused by eating foods that are excessively

sour, hot, and spicy; increasing the intake of alcohol; and eating oily, fried, or irritant

foods. Violation of rules for eating and lifestyle changes, including overeating, having an

incompatible diet, eating irritant and contaminated food, eating when suffering from

indigestion, increasing the intake of horse gram, living in temperate climate, and experiencing

factors that increase

pitta

(e.g., negative emotions and control of natural urges) are

causes this disease.

1

Dietary and lifestyle choices may contribute to GERD. Certain foods and beverages,

including chocolate, peppermint, fried or fatty foods, coffee, or alcoholic beverages, may

weaken the LES, causing reflux and heartburn. Studies show that cigarette smoking relaxes

the LES. Obesity and pregnancy can also cause GERD.

4

19.6 Pathogenesis and Pathology

In Ayurveda, hyperacidity may be an expression of excessive digestive enzymes

(

pachaka pitta

) due to stimulation from

vata

. This excessive enzyme secretion will dry

the mucous (

kaphadhara kala

) lining of the stomach, leading to irritation, hypersecretion,

acidity, and eventually ulceration. There are two common causes of this type of

vata

stimulation:

1.

Samana vata

— This type of

vata

normally stimulates the digestive enzymes while

eating. It is the controller of digestion and relates the state of mind. If one is

stressed and hurried during a meal, skips a meal, or eats fast, nondigestible food,

these stressors will affect the quality of digestion.

2.

Apana vata

— This type of

vata

is in the intestinal tract. It is often siphoned upward

through the enteric cycle into the liver and digestive organs. This reversed flow of

the

apana

vata

can excessively stimulate the digestive enzyme in the stomach and

irritate the stomach lining. Subsequently,

apana

vata

can then be drawn upward from

an already aggravated

pitta

. Also,

apana

vata

may increase as a result of stress,

wherein the nervous system is under such extreme influence that

apana

vata

is drawn

upward for nervous system support. Along the way, the

apana

would stimulate the

digestive enzyme and leave the seat of

vata

in the intestines depleted.

2

Pitta

is at the root of such a disorder. This is typically seen in a

pitta

constitution with

a

pitta

imbalance.

Pitta

constitution types are the ones who eat fast without awareness

and have a very hectic lifestyle.

Pitta

, which increases by the etiological factors (especially

with its acid state), results in hyperacidity. This state of

pitta

is burnt out to cause acid

eructation.

Thus hyperacidity is a hypersecretory disorder of the stomach and duodenum. It

involves the pathological state of

pitta

locally and blood systemically.

19.7 Diagnosis

The diagnosis of this condition is made by identifying a combination of signs and symptoms

such as indigestion (

avipaka

), bitter and acid regurgitation (

tikta-amlodgara

), substernal

burning (

hritkantha daha

), hypersalivation (

utklesha

), fatigue, and increased stress (

klama

).

19.7.1 Classification

Amlapitta

is classified into two types: regurgitation through the mouth (

urdhvaga amlapitta

)

and a similar type of movement in the lower GI tract (

adhoga amlapitta

). Based on the

association of the

dosa

involvement, there are three types:

vata

,

kapha

and

vata

kapha

.

2

19.7.1.1 Hyperacidity Affecting the Upper GI Tract (Regurgitation through the Mouth)

Clinical features of this type are regurgitation of excessive sour, slimy, meat soup (with

green, yellow, bluish, dark, blood-stained contents) and vomiting of bitter and sour contents

despite having an empty or full stomach. Heartburn rising from the stomach or

lower abdomen that continues to the chest and toward the neck, headache, a burning and

hot feeling in the sole and palm, and distaste (usually associated with fever) are the other

associated problems.

19.7.1.2 Hyperacidity Affecting the Lower GI Tract

This condition is characterized by the passing of loose stools with burning pain, excessive

thirst, vertigo, stupor, hypersalivation, skin rashes, hypersweating, and horripilations.

19.7.1.3 Hyperacidity Due to Vata

This condition, in addition to the above symptoms, presents abdominal pain, tremors,

horripilations, blackouts, delirious talk, stupor, and fatigue.

19.7.1.4 Hyperacidity Due to Kapha

This condition, in addition to the above symptoms, also has expectoration of sputum,

heaviness of the body, loss of taste, vomiting, weakness, itching all over the body, and

excessive sleep.

2

19.7.2 Clinical Features of GERD

19.7.2.1 Heartburn

This is the hallmark symptom of reflux disease. It is characterized by a burning feeling

below the sternum, rising from the stomach or lower chest toward the neck. It is

typically provoked by meals, especially those containing fatty and highly spicy food;

bending forward; straining; or lying down. It is usually eased or relieved by antacids.

19.7.2.2 Regurgitation

This is the other characteristic symptom of reflux disease. Regurgitated material is

usually tasted and reswallowed but is sometimes so voluminous that it may be mistaken

for "vomiting.” Some patients may experience regurgitation as their predominant symptom.

19.7.2.3 Water Brash

Esophageal acidification may cause such sudden and brisk stimulation of salivation that

the patient's mouth fills with saliva.

19.7.2.4 Atypical Symptoms

Reflux may cause a number of other symptoms not easily identified as being due to reflux.

These include angina-like chest pain, excessive belching, dyspepsia and nonspecific queasiness,

uneasiness, or nausea.

19.7.3 Complications of Reflux Disease

19.7.3.1 Respiratory Symptoms

Reflux has been incriminated as a cause of respiratory and laryngeal diseases such as

asthma, chronic cough, laryngitis, and sinusitis. Coughing, wheezing, hoarseness, or a

sore throat may occur and are occasionally the presenting symptoms. It is uncertain how

important reflux is in causing these nonspecific symptoms, but this applies probably only

in a minority.

19.7.3.2 Dysphagia

Dysphagia is common but is usually variable and due either to defective esophageal

peristalsis or heightened esophageal sensitivity. Dysphagia that is associated with symptoms

of bolus impaction is highly suggestive of a stricture.

19.7.3.3 Odynophagia (Painful Swallowing)

This may be a prominent symptom due to excessive sensitivity of the esophageal mucosa.

It is usually associated with severe esophagitis.

19.7.3.4 Bleeding from Esophagitis

Hematemesis may be a presenting symptom but is rarely severe. Occasionally, iron deficiency

may result.

5

19.8 Clinical Course and Prognosis

Hyperacidity is amenable to treatment if treated early. It becomes palliative if delayed and

is difficult to cure in patients not observing preventive follow-up.

2

19.9 Therapy

In Ayurveda, the following procedures are used in treating hyperacidity:

1. Emesis therapy (vamana) with the water extracts of snakeguard (

Trichosanthes

dioica

) and neem (

Azadirachta indica

) followed by purgation (

virecana

) with powders

of trivrit (

Operculina turpethum

) or any one of the following:

avipattikara curna

,

amalakyadi curna

,

abhayarishta

, or

triphala curna

.

2. If the burning pain is intensive, the patient is advised to apply whole body

massage with

candana taila or lakshadi taila.

3. In conditions of regurgitation through the mouth, purgation is advised. In case

of lower GI symptoms due to hyperacidity, emesis is the choice.6

19.9.1 Lifestyle Changes

Three factors are essential for good and balanced digestion. First, food must be fresh and

grown locally, or at least seasonally, and prepared with a caring and loving attitude.

Second, food must be eaten with attention and awareness. Our sense of taste both prepares

and ignites the digestive process before food ever reaches the stomach, as does our sense

of composure and calm. Being distracted with books, driving, computers, and phones

during a meal negates any hope of a balanced digestive process. Third, eating is best done

during pitta period, between 10 A.M. and 2 P.M.; this is when the enzymes are the strongest

and digestion will be the most effective. Eating at other times will eventually compromise

the body’s ability to digest and assimilate nutrition and give energy over a long period.

19.9.2 Home Remedies for Hyperacidity

1. Take tender coconut (Cocus nucifera) water. A dose of 100 to 500 ml should be

taken twice/day.

2. Take the powdered fruit rind of emblic myrobalan (Emblica officinalis). A dose of

3 to 6 g should be taken with 100 to 250 ml milk twice/day.

3. Mix a gruel of rice corn, raw sugar, and honey in equal quantity. A dose of 100

to 200 g should be taken twice/day.

4. Take powdered fruit rind of chebulic myrobalan (Terminalia chebula) and whole

plant of thistles (Eclipta alba) in equal quantity. A dose of 3 to 6 g should be taken

with 12 g of jaggery and warm water twice/day.

5. Take dried rhizome of turmeric (Curcuma longa), leaf of snakeguard (Trichosanthes

dioica), and fruit rind of emblic myrobalan (Emblica offcinalis) in equal parts and

make the powder. A dose of 3 to 6 g should be taken with the fresh juice of ginger

and 30 drops of papaya latex twice/day.

6. Prepare a decoction from the equal parts of stem of tinospora (Tinospora cordifolia),

fruit of neem, leaf of snakeguard, and triphala. A dose of 14 to 28 ml should be

taken twice/day.

7. Prepare a decoction of equal parts of dried ginger, fruit of coriander, and leaf of

snakeguard. A dose of 14 to 28 ml should be taken twice/day.

8. Prepare a decoction of equal parts of leaves of snakeguard and vasaka, dried ginger,

stem of tinospora, and rhizome of katuki (Picrorhiza curroa). A dose of 14 to 28 ml

should be taken with 4 to 6 g honey twice/day.

9. Prepare mahasurdarshan churna, containing triphala (Emblica officinalis, Terminalia

belerica, Terminalia chebula), guduci (Tinospora cordifolia), katuka (Picrorrhiza kurroa),

fumaria (Fumaria officinalis), lime juice, etc. A dose of 1/2 tsp three times/day after

meals is recommended.

10. Prepare avipattikara churna, containing ginger, black pepper, triphala, nut grass

(Cyperus rotundus), embelia fruits (Embelia ribes), cardamom (Elettaria cardamomum),

clove (Syzygium aromaticum), cinnamon (Cinnamomum cassia), and sugar.

This is the medicine of choice in treating hyperacidity. A dose of 1 tsp before meals

three times/day with lemon juice is recommended.

11. Use aloe vera (Aloe littoralis). Prepare 1 tbsp of fresh gel from the plant and take

three times/day.

12. Drink coriander (Coriandrum sativum) and cumin (Cuminum cyminum) tea.

13. Take 1 tsp of psyllium (Plantago ovata) 1 h after meals with 8 oz of warm water.

14. Prepare a milk decoction of 1 tsp emblica myrobalan (Emblica officinalis), 1 tsp raw

sugar, 1 cup of milk, and 1 cup of water. Boil to 1 cup. Drink as a tea with meals

or anytime three times/day.

15. Prepare a decoction of fenugreek (Trigonella foenum-graecum), honey, 1/2 tsp of

powder with 1/2 tsp of turmeric on an empty stomach with warm water or warm

milk.

16. Prepare a licorice (Glycyrrhiza glabra) ghee. Make the decoction with 1 tsp of licorice

in 2 cups of water. Boil to 1 cup. Add 1 cup ghee and 1 cup water. Boil off water.

Take 1/2 tsp three times/day on an empty stomach with hot water. This ghee can

be used in cooking.7

Compound formulas commonly used to treat hyperacidity are listed in Table 19.1.

19.10 Scientific Basis

The scientific studies relating to the treatment of GERD through natural products are

diverse, which include not only the studies on gastric acidity, but also those which are

suggestive of antiulcer activity. Some of the current studies on therapeutic procedures as

well as the plants and herbomineral preparations are listed below.

19.10.1 Fat Preparations (Snehapana)

Various dehydrated butter (ghee) or oil preparations have been prescribed in Ayurveda

for the management of parinama sula. Ghee in the duodenum inhibits gastric acid secretion;

gastric inhibitory peptide (GIP) has been proposed as a candidate for this enterogastrone

action. Moreover, extracts of various indigenous herbs are mixed in Ayurvedic ghee and

oil preparations, making these preparations more useful. Utility of ghee and oil preparations

in PUD is discussed below.

Snehapana of dadimadya ghrta (2 oz/day for 2 to 6 weeks) exhibited symptomatic relief

in peptic ulcer syndrome. A significant reduction in gastric acidity was observed particularly

in cases of nonulcer dyspepsia (NUD).9

TABLE 19.1

Common Ayurvedic Formulas Used To Treat Hyperacidity

Name of Formulation Activity Dose Adjuvant Ref.

Avipattikara curna Digestive, pacifies pitta 3–6 g twice/day before

meals

Warm water 6

Dhatri loha Carminative, hemetinic 0.5–1 g twice/day Ghee 8

Kamadudha rasa Antacid 250–500 mg twice/day

before meals

Honey and

Water

8

Sankha bhasma, Kapardika

bhasma, or Pravala bhasma

Antacid, antispasmodic 250–500 mg twice/day

before meals

Honey and

water

8

Sutasekhara rasa Antacid, antispasmodic 250–500 mg twice/day

before meals

Honey and

water

8

Narikela khanda Antacid, antiflatulent 6–12 g twice/day before

meals

Milk 8

Dadimadya ghrta or accha ghrta produced excellent results in 60% of cases with peptic

ulcer syndrome (15-patient case study) when given in dose of 50 g/day for 2 to 3 weeks.

Experimental studies10 also confirmed the protective action of ghrta against histamineinduced

ulcers.

In a control study, researchers have evaluated the efficacy of panchakarma (snehana and

subsequent virecana) in 30 patients with parinama sula. A dose of 30 ml of dadimadya ghrta

was given to the first group of 15 patients on the first day followed by a daily increase of

30 ml for 7 days. Thereafter, virecana with avipattakara curna was given. A control group

of 15 patients was treated with shankha vati (6 tablets/day) for the same duration. Cases

of both groups were followed for 3 months. Approximately 60% of the snehana-virecana

group was completely cured from the disease for the whole period of follow-up along

with radiological ulcer healing and reduction in gastric acidity. Other cases of this group

had different degrees of relief. Patients of the control group were not completely cured.

This cure probably works by virtue of elimination of vata and pitta dosa along with woundhealing

effects.10

Tikta ghrta (astangahrdaya) was taken in doses of 40 ml/day. Results showed complete

symptomatic relief in 82% of cases with parinama sula (38-patient case study). The study

lacks laboratory or radiological evidence of improvement.10

Indukanta ghrta (sahasrayoga) was tested in 46 patients with parinama sula (28 with duodenal

ulcer [DU], 10 with gastric ulcer, and 8 with hyperchlorhydria). Snehapana was given

according to the agnibala of the patients for the first 7 days followed by Svedana (2 days).

Virecana with castor oil (1 day) was followed by samsarjana karma for the next 3 days.

During the samana period of 7 days, indukanta ghrta was given in doses of 30 ml/day.

Complete symptomatic relief was observed in 84% of cases of this series. However, a

gastric acid secretion augmented histamine test, barium meal, or endoscopial study has

not been included in the evaluation of results.10

Kusadi ghrta has been studied in patients with peptic ulcers (18 with DU and 2 with

gastric ulcer). A dose of 25 g of ghrta per day was given for 1 month. Apart from clinical

improvement, ghrta reduced gastric acid secretion in the Fractional Test Meal test and

caused complete ulcer healing confirmed radiologically in 65% of patients.10

Many single and combined herbs, herbominerals, and fat preparations have been found

effective in treating PUD. Amalaki, madhuyasthi, satavari, and bhringaraja appear more useful

among herbs. Real efficacy can be proved only by comparative and controlled study

adopting endoscopic evaluation. These herbs have shown ulcer-healing property even on

these parameters. Moreover, these herbs are cheap and nontoxic even with long-term use.10

19.10.2 Herbs, Herbal Preparations, Rasas, and Bhasmas

19.10.2.1 Emblica officinalis (Indian Gooseberry)

Dhatri lauha, frequently used in amlapitta and parinama sula, consists of two herbs (amalaki

and madhuyasthi) and one mineral (iron). This preparation has been found to alleviate the

common clinical complaints like epigastric pain, acid eructation, epigastric and retrosternal

burning in the majority of patients with amlapitta along with an appreciable reduction in

free and total acidity.12 Fruits of amalaki, apart from having proven efficacy in experimental

study, relieved the symptoms significantly in patients with amlapitta having hyperchlorhydria

when given in doses of 3 g three times/day for 7 days. However, this study

consisted of only a few patients.10

In a clinical trial on amalaki in a large series of patients with DU (27 cases) and NUD

(12 cases), amalaki was given in a dose 9 to 13.5 g/day (in three divided doses) for an

initial 2 weeks. This was followed by a dose of 6 to 9 g/day (two divided doses) for the

rest of total duration of 3 months to the patients of both groups. Gastric acid secretion

was measured by an AHT. Pepsin and mucin were also estimated in gastric juice. A

significant decrease in acid and pepsin secretion was observed. Complete radiological

healing was reported in peptic-ulcer patients. Marked symptomatic relief was found in

most of the patients (78-patient case study) with the use of amalaki. Moreover, the drug

exhibited prophylactic effect against the histamine-induced ulcer in albino rats. Furthermore,

amalaki exhibited some anabolic activity evidenced by weight gain and also an

increase in hemoglobin concentration.13 Both the prophylactic and curative properties of

amalaki rasayana have been observed in another study on experimental peptic ulcer.14

Amalaki powder produced 66% symptomatic improvement, significant reduction in gastric

acidity response (AHT), and endoscopic healing in 57% of cases with DU. However, there

were only seven trial cases.10

19.10.2.2 Glycyrrhiza glabra (Licorice)

The second and important ingredient of dhatri lauha is madhuyasthi or licorice. The antiulcerogenic

effect of madhuyasthi was observed against both the pyloric ligation and histamine-

induced ulcers. The drug powder in doses of 18 g/day in three divided doses

exhibited marked response in 80% of patients with DU (10-case study) within a week.

Further clinical and experimental study was done on madhuyasthi.15 The powder of the

drug was given to 10 patients with NUD (6 g/day) and 15 patients with DU (6 g/day)

for 1 to 3 months. Excellent response was reported in 30% of patients and good response

was seen in 50% of patients with NUD. After 2 months of therapy in the duodenal ulcer

group, pain was relieved completely in 56% of cases, whereas a burning sensation was

reported in 78% of the cases. Complete radiological healing was observed in 50% of cases

and partial in 40% of cases. No reduction in gastric acidity response was observed.

Experimentally, madhuyasthi did not produce significant acid reduction. Haridra (Curcuma

longa), babula (Acacla arabica), and aparajita (Clitoria ternatia) reduced acidity significantly

in albino rats. Two herbs of dhatri lauha, amalaki and madhuyasthi, have been found quite

effective for both types of patients, i.e., DU and NUD.10

19.10.2.3 Asparagus racemosus (Asparagus)

A clinical study has reported good response in 80% of patients with DU with the use of

satavari (asparagus) powder in a dose of 20 g/day in three divided doses for 4 weeks.

Free and total gastric acidity was reduced significantly in 15 patients with DU having

hyperacidity. Workers also have observed a significant decline in free and total acidity of

gastric juice of albino rats with satavari. In a double-blind, randomized drug trial, researchers

have observed suppression of heartburn, nausea, or vomiting in 100% of cases and

pain in 83% of cases with DU with the use of satavari powder (6 g/day for 6 weeks).

Complete ulcer healing was observed in 50% of cases radiologically and in 62% of cases

endoscopically. The drug also reduced hyperchlorhydria of these patients. Workers

observed slightly better results with satavari in comparison with amalaki, but the study

was conducted on only eight and seven patients, respectively.

A group of researchers have observed antiulcerogenic effect of satavari and bhringaraja

in aspirin (200 mg/kg body weight for 4 days)-induced ulcers in albino rats. There was

a decrease in ulcer score and severity in both the groups, along with reduction in gastric

acidity and peptic activity and an increase in mucin activity. Continuity and thickness of

gastric mucosa was maintained in comparison with aspirin-treated gastric mucosa. Histochemically,

mucin content of gastric mucosa was increased in both the groups. Clinically,

both the drugs (satavari and bhringaraja) exhibited radiological (in 83 and 67% of cases,

respectively) as well as endoscopical healing (in 55 and 50% of patients, respectively)

along with significant reduction in hyperacidity pattern. However, again the number of

patients was fewer: only six in satavari group and nine in bhringaraja group.

Another group has observed significant symptomatic improvement in 26 patients with

proved DU disease with the use of satavari root powder (12 g/day for 6 weeks). Satavari

inhibited basal acid output by 32%, histamine-induced maximum output by 38%, and

alcohol-induced output by only 32%. Approximately 75% of patients had radiologic and

endoscopic evidence of ulcer healing. The drug was not found to possess antacid property

in vitro. Direct healing effect was proposed probably by enhancement of mucosal barrier,

prolongation of life span of mucosal cells, or cytoprotection.10

The antiulcerogenic activity of juice of fresh roots of asparagus has been reported against

cold-restraint stress and pylorus ligation-induced gastric ulcers. The activity was reported

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

mucin secretion. Mucin secretion was quantified in terms of TC:P ratio in the gastric juice.

The strengthening of the mucin barrier led to a further decrease in the dexoribonucleic acid

(DNA) content of the gastric juice, indicating a decrease in cell shedding.16 In continuation

of earlier experimental work, a satavari containing Ayurvedic preparation, satavari mandur,

has undergone clinical trails and shown promising results. It has been observed that when

given satavari mandur at the dose of 1.5 g twice daily for a month, the preparation not only

produced significant improvement in symptoms of peptic ulcer, but also healed endoscopically

proved cases of ulcer dyspepsia by 75%. The biochemical estimations of offensive acidpepsin

and defensive mucin secretion and cell shedding before and after treatment with

satavari mandur showed a tendency to decrease acid-pepsin secretion. The estimations also

showed a significant decrease in cell shedding and an increase in mucin secretion indicating

satavari mandur’s predominant effect on mucosal defensive factors.10

19.10.2.4 Eclipta alba (Thistles)

Bhringaraja is used as a soaking agent for various Ayurvedic antiulcer preparations. As early

as in 1968 researchers have reported the efficacy of Eclipta alba in treating hyperchlorhydria.17

Later on, in a clinical trial done on 22 patients with NUD and 8 patients with DU, researchers

observed a significant reduction in gastric acidity when bhringaraja (whole plant) was given

in syrup form in a dose of 20 ml/day (20 g crude drug) in three divided doses for 6 weeks.

Approximately 90% of dyspeptic patients were cured, whereas about 87% of ulcer patients

improved. Seeing its efficacy, a team of scientists further evaluated its effectiveness in NUD

and DU in a large series of 60 cases (35 of NUD and 25 of DU). The powder of whole herb

was given in a daily dose of 30 g (in three divided doses) for 1 month to the NUD group

and for 3 months to the DU group. The drug exhibited marked symptomatic relief in the

majority of the patients and reduced gastric acidity significantly in both groups. Approximately

80% of patients with NUD responded well to this therapy. Radiological improvement

was observed in 75% of cases out of 12 patients with DU who came for follow-up. Approximately

48% of patients of this series gained excellent relief with bhringaraja. Later another

group further confirmed the effectivity of bhringaraja in 60% of cases (935-patient case study)

with DU when given in dose of 30 g/day for 3 to 6 months.10

19.10.2.5 Trichosanthes dioica (Snakeguard)

Patoladi kasaya (prepeptone), consisting of patola, haritaki, bibhitaka, amalaki, kutaki, cirayata,

amrta, pittapapada, sunthi, and bhringaraja, exhibited complete improvement in 50% of cases

and partial improvement in 40% of cases with PUD (10-patient case study). The decoction

was given in doses of 30 ml/day in three divided doses for 3 weeks. It decreased the acid

response in hypersecretors and normalized the acid response in hyposecretors. Best results

were observed in patients with kaphaja parinama sula.

Another patoladi kasaya consisting of only four herbs, patola, sunthi, amrta, and kutaki,

was given in a follow-up study of 33 operated cases of DU. The drug kept the patients

symptom- and complication-free when given in doses of 40 ml/day in two divided doses.

It normalized both the hyper- and hypoacidity of these patients.

The efficacy of a single herb, patola, was studied in 20 patients with DU. Its decoction

was given in doses of 150 ml/day (60 g crude drug) in three divided doses for three weeks.

Drug exhibited marked clinical improvement and reduction in gastric hyperacidity. Excellent

response with complete ulcer healing (radiological) was observed in 50% of patients,

and good response in 35% of patients. Effectively of patola in DU (excellent response in

45% of 20 cases) has been further reported.10

19.10.2.6 Adhatoda vasica (Vasaka)

Vasaka in Ayurveda is indicated in bleeding disorders. PUD may cause hematemesis.

Therefore, this drug was tried in 20 patients with DU. Approximately 60 ml of syrup

(30 g crude drug) was given daily in four divided doses for 6 weeks. Clinical improvement

along with reduction in gastric acidity was observed in 85% of patients in this

series. Moreover, the drug also decreased gastric acid secretion in albino rats. The drug

was not tried in patients with DU.18,19

19.10.2.7 Cocos nucifera (Coconut)

Coconut water has been reported to possess protective action against aspirin- and histamine-

induced gastric mucosal damage. Its kernal reduced the gastric acidity and improved

the clinical features in patients with DU. Narikela khanda, a famous preparation for parinama

sula, was given in a dose 60 g/day in five divided doses for three weeks to eight patients

of PUD. Approximately 62% of patients got complete relief, whereas the reamining cases

got partial improvement. Best results were obtained in the paittika type of parinama sula.

Two researchers evaluated the effectivity of an Ayurvedic compound preparation consisting

of narikela lavana, trisankha bhasma, and avipittikara curna in 60 cases of amlapitta.

The compound clinically exhibited good response in 57% of cases and fair response in

26% of cases.10

19.10.2.8 Tamra bhasma (Copper Calx)

The use of herbomineral preparations in Ayurveda is well documented. Tamra bhasma, a

traditional preparation of copper, has been suggested for its use in amlapitta. An earlier

published study has given the composition of tamra bhasma as CuO < 44.45%, Fe2O3 <

6.03%, and S < 2.75%.20

Extensive studies have been undertaken to unravel the antiulcerogenic activity of

tamrabhasma. It has been shown to possess ulcer-protective activity against various

gastric ulcers in 8-h immobilized, 4-h pylorous-ligated, and aspirin-induced rats and

histamine-induced gastric and DUs in guinea pigs. The activity was due to both a

decrease in offensive acid-pepsin and an increase in defensive mucin secretion.21 Further

evaluation of tamra bhasma from different sources were compared with pure compound

and mixture of major ingredients of tamra bhasma for antiulcerogenic activity. Results

revealed that tamra bhasma preparation was better than pure copper compound or a

mixture of known ingredients.

Quantitative differences in tamra bhasma preparation also showed the importance of

pharmaceutical processing in the therapeutic activity of tamra bhasma.22 Tamra bhasma has

an overall solubility in water of approximately 1% and 12 ng/ml of CuO forms a saturated

solution at 50°C. This implies that when used orally it would have a local effect rather

than being systemically absorbed, reducing the possibility of systemic toxicity with copper.

Toxicity studies have shown that TMB was safe, and even 1000 times of the effective

antiulcer dose was tolerable in rats.

Tamra bhasma was also found to have an antiulcerogenic effect against aspirin-induced

ulcers without affecting the anti-inflammatory activity of aspirin. Tamra bhasma seemed

to have prolonged effect, as the protective effect of tamra bhasma lasted up to 5 days after

discontinuation of treatment. An aspirin–copper combination may reduce ulcerogenic

activity of aspirin without affecting its anti-inflammatory effect. Researchers have reported

the gastric protective effect of tamra bhasma against cold restraint stress-induced gastric

ulcers in rats and guinea pigs and its healing effect against acetic acid-induced gastric

ulcers in rats. Tamra bhasma was reported to increase prostaglandins (PGEs) and decrease

leukotrine C4 (LTC4) in human gastric and colonic mucosal incubates. The mucosal protective

effects of tamra bhasma and CuCl2 could be due to their effect on endogenous PGEs

and LTs. Tamra bhasma showed better and potent effect when compared with CuCl2 on

PGEs release both in gastric and colonic incubates, suggesting that other ingredients of

TMB add to its effects. Tamra bhasma significantly protected rats against ethanol-induced

ulcers, and the effect was ascribed to decrease in LTC4/D4 synthesis.23

Tamra bhasma has also been reported to increase the defensive mucopolysaccharides,

including sialomucin and fucose. It has also been reported to decrease DNA in gastric juice,

suggesting decrease in cell shedding and increase in life span of mucosal cells, with no

change in mucosal DNA and incorporation of [3H]-thymidine uptake in mucosal tissues,

indicating absence of activity on cell proliferation. The effect of TMB on offensive acid-pepsin

secretion and LTs and defensive mucus secretion, mucosal glycoproteins, prostaglandin, and

cell shedding may contribute to its ulcer protective activity.24

Tamra bhasma (1 mg/kg) has shown antiulcerogenic effect in 8-h immobilized, 4-h pylorous

ligated, aspirin-induced and histamine-induced gastric ulcers in albino rats and guinea

pigs. The drug decreases total acid and pepsin output and increases carbohydrate protein

ratio, indicating an increase in mucosal barrier. Acute and subacute toxicity of the drug

was not observed.25 Tamra bhasma has better and prolonged antiulcer effect than pure

copper preparation. Moreover, it does not antagonize the anti-inflammatory effect of

aspirin. It has been suggested to take it on alternate days or even twice a week only with

all beneficial effects in PUD.10

19.10.2.9 Sutasekhara Rasa

Sutasekhara rasa, an herbomineral mercury preparation, is widely used for the treatment

of amlapitta and parinama sula. It contains copper, aconite, datura, and certain other herbs

like bhringaraja. Two types of sutasekhara rasa, those with gold and those without gold, are

popular in treating DUs.

Two researchers evaluated the efficacy of modified sutasekhara rasa (devoid of gold and

copper) in seven patients with NUD and three with DU. The drug was given in doses of

600 mg/day for 6 weeks. Excellent response was reported in 85% of patients with NUD

and in 67% of patients with DU.

A team of researchers, in a comparative clinical trial done on 63 patients with parinama

sula (DU), did not observe any significant difference in the effectivity of sutasekhara rasa

with gold and without gold. Gold preparation (375 mg/day in three divided doses)

exhibited relief in 70% of patients, whereas preparation without gold (750 mg/day in three

divided doses) produced relief in 67% of patients in 45 days. Results were assessed only

on symptomatic improvement and reduction in acid secretion (FTM) and not on radiological

and endoscopical ulcer-healing criteria. They have recommended the use of

sutasekhara rasa without gold because of the high cost and long-term toxicity of sutasekhara

rasa with gold.26 Another group has reported the relief in patients with DU after a course

of sutasekhara rasa for 42 days. Workers believe that this preparation acts probably by

modifying the homeostatic regulation of hormonal stimulation of Hy ion secretion.27

Recently, sutasekhara rasa (without gold, 600 mg/day) along with ashvangandha powder

(Withania somnifera, 6 g/day) exhibited symptomatic radiological and endoscopical

improvement. It also exhibited along with a reduction in gastric acidity (FTM) in all the

four treated patients with DU in 6 weeks; sutasekhara rasa alone improved three out of

four patients. Similarly, sutasekhara rasa and asvangandha separately exhibited good

response in four out of five patients, whereas their combination showed response in all

the five treated cases with NUD. The number of trial cases in each group was very low.

A substantial inference cannot be drawn. Even then, this study highlights the utility of

antianxiety indigenous herbs (medhya drugs) as an adjuvant in the management of PUD.10

There are many plants used in antiulcer herbal formulations that have not yet been

individually investigated for their efficacy in this condition. A group of researchers has

reported the antiulcer effect of an herbal formulation, UL-409, consisting of six medicinal

plants: Glycyrrhiza glabra L. (root), Saussurea lappa C.B. Clarke (root), Aegle marmelos Corr.

(fruit), Foeniculum vulgare Mill. (seed), Rosa damascena Mill. (flower petals), and Santalum

album L. (stem). This herbal formulation was found to increase the stomach mucus and

decrease the acid volume, free and total acid content, in rats. Moreover, this formulation

significantly prevented the occurrence of stress-induced ulceration and significantly inhibited

gastric ulceration induced by ethanol, aspirin, pylorus-ligation, histamine, and

indomethacin in rats and guinea pigs. It was found to have antiulcer activity due to a

modulation of defensive factors, thereby improving gastric cytoprotection.28,29

A clinical trial was conducted in 56 patients with peptic ulcers, as confirmed by endoscopy,

with UL-409. Results showed the formulation’s beneficial effect in patients with

PUD without any side effects in any of the patients.30

In another clinical trail,31 patients with H. pylori infection (UL-409) showed clinical

improvements without any side effects.

19.11 Future Ayurvedic Formulas

A variety of botanical products have been reported to possess antiulcer activity (especially

from ethnopharmacological studies), but the documented literature has centered primarily

on pharmacological action in experimental animals. Except for a few phytogenic compounds

(i.e., liquorice and chilli), limited clinical data are available to support the use of

herbs as gastroprotective agents and, thus, the data on efficacy and safety are limited.

Despite this, there are several botanical products with potential therapeutic applications

because of their high efficacy and low toxicity. Finally, it should be noted that substances,

such as flavonoids, aescin, aloe gel, and many others, that possess both anti-inflammatory

and antiulcer activity are of particular therapeutic importance. This is because most of the

anti-inflammatory drugs used in modern medicine are ulcerogenic.

Several plants and herbs are used in folk medicine to treat gastrointestinal disorders,

including peptic ulcers. Recently, there has been a growing interest in identifying new

antiulcer agents from plant sources.

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2. Madhava, Madhavanidanam, Part II, Upadhyaya, Y., Ed., Chowkhamba Sanskrit Series Office,

Varanasi, U.P. India, 1973, chap. 51, p. 171.

3. Dhyani, S.C., Kaya Chikitsa, 1st ed., Ayurvedic & Tibbi Academy, Lucknow, U.P. India, 1991,

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23. Goel, R.K., Tavares, I.A., and Bennett, A., Effects of cupric chloride and tamrabhasma, a

traditional Indian preparation of copper, on eicosanoid production by human gastric and

colonic mucosa, J. Pharm. Pharmacol., 44(10), 862, 1992.

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12(11), 49, 2001.

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)