Mar 27, 2023
Mar 27, 2023
A detailed description and differential diagnosis of a group of disorders involving respiratory distress (dyspnea) is given in all three of the major Ayurvedic compendiums.
These diseases are collectively known as svasa roga, of which five varieties are described. These include: maha svasa, urdhva svasa, chinna svasa, ksudra svasa, and tamaka svasa. The last variety, tamaka svasa, corresponds to chronic persistent bronchial asthma of allopathic medicine.
In Ayurveda, it is considered the only type of respiratory distress which can be controlled, and then only with diligence on the part of the patient and physician. In striking similarity to the modern allopathic description, tamaka svasa is defined in Ayurveda as a chronic and recurring condition characterized by dyspnea, cough, airflow obstruction, and wheezing.
Although the concept of atrophy and hyperactivity were unknown, Ayurveda was clear on its understanding of this condition as multifactorial, including environmental and emotional factors.
The prevalence of both adult and childhood asthma is reported to be increasing worldwide. Up to 10% of people have experienced a documented episode of asthma. In the United States, approximately 12 million individuals have been diagnosed with asthma. Between 1982 and 1992 the prevalence of asthma increased from 34.7 to 49.4 per 1000. In addition the death rate from this condition actually increased from 13.4 to 18.8 per million. The mortality rate was five times higher in African Americans than in Caucasians.
Vagbhata gives a clear explanation of the causes and evolution of asthma. In all cases there is an antecedent period of aggravation of both Vata and Kapha doshas. A very great number of factors can be responsible for aggravating these two doshas, and to list them all would not be possible. However several vitiating factors are specifically mentioned by Vagbhata and therefore merit mention. He cites chronic diarrhea due to indigestion which goes untreated, excessive vomiting, poisons, anemia, fevers, excessive exposure to dust, smoke or strong wind, trauma to the vital organs, and drinking very cold water.
At this early stage in the disease process, if these signs and symptoms are recognized and properly treated by pacification and elimination of the aggravated doshas, the disease (asthma) will not appear. However, if left untreated and if further aggravated, Kapha will obstruct the movement of Vata in the chest area. Due to this obstruction, Vata spills out of its normal channels (srotas) and spreads in all directions, carrying with it the vitiated Kapha dosha. As a result, the three major channels in the chest region become blocked and, to a greater or lesser degree, dysfunctional. These channels are Prana Vaha Srota (governs respiration), Anna Vaha Srota (governs digestion of food), and Udaka Vaha Srota (governs water distribution). At this point the disease is no longer in its incipient stage and asthma --tamaka svasa-- has manifested.
The role of psychological stress in asthma is important but not yet completely understood. Not only is there emerging evidence that stress can precipitate asthmatic exacerbations but also that it may be an independent risk factor in the prevalence of the disease. The mechanisms involved in this association have not yet been fully defined and may involve increased production of proinflammatory cytokines.
Signs and Symptoms
The signs and symptoms of this disease are vividly enumerated in both the Caraka Samhita and the Astanga Hridayam and are worth noting:
Although a full description of the other four types of svasa roga (dyspnea, or difficult breathing) is beyond the scope of this paper, a few comments are in order. Ksudra svasa is the mildest form of svasa roga it roughly corresponds to mild intermittent asthma and is said to be curable. Tamaka svasa (asthma) is the next mildest form of svasa roga yet it is considered difficult to cure. It roughly corresponds to mild persistent asthma in the modern allopathic classification scheme. Cure is possible if the disease is of recent origin or if it occurs in an otherwise strong and health individual. In a weak individual only palliation (i.e. alleviation) should be attempted. The other three types of svasa roga, namely maha svasa, urdhva svasa, and chinna svasa loosely correspond to other more severe forms of obstructive pulmonary disease, are incurable, and in time result in the premature demise of the patient.
While an individual's constitutional type must always be kept in mind when developing a treatment plan for any disease, asthma is nevertheless generally treated by pacifying Vata and Kapha doshas. The treatment will always include two main strategies:
However asthma is highly variable in its course and clinicians need to tailor their treatment plans to the needs of each individual patient. The general Ayurvedic principle is to initially gain control of the disease as quickly possible with strong Vata and Kapha purification measures which are then followed with appropriate herbal therapies.
Oleation and Fomentation Procedures
Patients must first undergo oleation therapy (snehana) this includes both external and internal forms of oil treatment. External oleation by daily oil massage should be administered first, for 7-10 days. The best oils in tamaka svasa are: narayana oil, talispatra oil, amra oil (from mango seeds), or chandrabala oil. Next, patients undergo internal oleation with daily intake of an appropriate unctuous substance for 3-7 days this is usually pure or medicated cow's ghee which should be at least six months old. During this period, patients have simultaneous sweat, or fomentation, therapy (swedana). This usually includes both general "steam box" treatments as well as pinda sweda . The latter therapy involves the placement of hot boluses of rice and special herbs wrapped in a cloth over certain points of the body. These points are called marma sthula and are similar to the Chinese acupuncture points.
Following snehana and swedana therapies, a one-time virechana , or laxative therapy, is administered. Castor oil (Ricinis communis) in a dose of 2-3 tablespoons is generally used for this.
Therapeutic Vomiting Procedure
Finally, vamana, or therapeutic vomiting therapy should be initiated this is the most important therapy in diseases involving respiratory distress. This usually involves three consecutive mornings when, following a light breakfast, patients are given an emetic herb (i.e. madana phala) and then asked to fill the stomach with cool water or milk to induce vomiting. Correctly performed, this is not at all uncomfortable and does not produce nausea. Weaker, very elderly, acutely ill, or cardiac patients however should not be given vamana therapy.
After completing these purificatory treatments, patients are given herbal therapies. The most efficacious in my experience are the following.
Ayurvedic Herbal Medicines
Tylophora asthmatica or Tylophora indica (antamoola) is an Ayurvedic medicine claimed to treat respiratory disorders in which mucus accumulation is a symptom. The leaves are used for asthma, bronchitis, common cold, dysentery, and rheumatism. It is believed to have cathartic, diaphoretic, emetic, and expectorant effects. This indigenous plant is recognized as a bronchodilator.
Shivpuri et al. conducted several studies on the treatment of asthma with Tylophora indica. In the preliminary uncontrolled study there was a relief of symptoms lasting a few weeks in 40-50% of patients who chewed 1 leaf /day for 36 days. Two follow up crossover, controlled, double blinded studies were performed by Shivpuri et al. with leaves and an alcoholic extract of Tylophora . Results showed complete to moderate relief of symptoms as compared to placebo: 62% chewing leaves vs. 28% placebo and 58% alcohol extract vs. 31% placebo. Also, relief of symptoms lasted 812 weeks in some patients. Patients who chewed leaves experienced a high incidence of side effects: sore mouth, vomiting, and loss of taste. Side effects were less pronounced with use of the alcoholic extract. In a controlled, unblinded study, Shivpuri showed that 71% of asthmatics had increased bronchial tolerance to an inhaled antigen 2 days after treatment with leaves. On follow-up, nine patients continued to demonstrate protection against inhalation challenges from 9 to 48 days after stopping treatment.
In two crossover, double blind studies by Thiruvendagan et al., patients showed reduction in nocturnal dyspnea after receiving a powdered leaf capsule as compared to placebo, but none demonstrated significant difference in other symptoms as compared to placebo or a capsule of standard medication containing ephedrine, theophylline, and phenobarbitone. There was a steady increase in maximum breathing capacity (MBC), vital capacity (VC) and PEF over 7 days with the Tylophora capsule as compared to placebo. These effects also differed from those of the standard medication that produced quick but transient rises in values. However, Gupta et al. acquired opposite results to the above studies. In his double blind study, no statistically significant difference was noted in symptom scores and pulmonary function tests after patients took powdered Tylophora leaf or placebo.
In 1975, Haranath et al. studied the mode of action of aqueous extract of Tylophora asthmatica. Tylophora prevented anaphylaxis and reduced Schultz -Dale reactions in guinea pigs. Tylophora also produced an initial leukocytosis followed by a reduced lymphocyte and eosinophil count in dogs. It had mild, brief antispasmodic action on contractions in tissues induced by histamine, Ach, and serotonin (5HT). This suggests that its primary action is not the antagonism of histamine or choline. Also, it apparently has no betaagonist effects because it produced a fall in blood pressure despite addition of propranolol.
Gore et al. studied the physiological basis of Tylophora by comparing its effects to a known bronchodilator (isoprenaline). In asthmatic patients there was a significant improvement in lung function tests. There also was an increase in urinary 17ketosteroid levels and decreased absolute eosinophil count.
Udupa et al. examined the effects of extracts of Tylophora on adrenal gland and the pituitaryadrenal axis in rats. Extracts of Tylophora increased the weight of adrenals and decreased cholesterol and vitamin C contents. It also antagonized dexamethasone / hypophysectomy-induced suppression of pituitary on adrenal activity. These results indirectly suggest that Tylophora indica might act by direct a stimulation of adrenals.
The major ingredient in Tylophora is tylophorine, an alkaloid. Gopalakrishnan investigated this alkaloid for its antiinflammatory and immunological effects. The results showed that pre-treatment with tylophorine provided 70% protection against anaphylaxis in guinea pigs. It also inhibited SchultzDale reactions and immunocytoadherence. Immunocytoadherence or rosette formation is the method by which antigen is bound to red cells and these cells adhere in vitro to lymphoid cells with corresponding antibody. Tylophorine inhibited mast cell degranulation by diazoxide (an agent that produces mast cell rupture by reducing cAMP levels in cells), but did not affect histamine release in mast cells incubated with tylophorine alone. Gopalakrishnan suggested that tylophorine might act by increasing cAMP levels.
Picrorrhiza kurroa, or kutki, is a small herb with tuberous roots that is used in Ayurvedic medicine for the treatment of liver and lung diseases (asthma, bronchitis), fever, anemia, dyspepsia, chronic dysentery, and arthritic conditions. It is claimed to have antiperiodic, cathartic, and laxative effects. It contains phenol glycoside androsin, kutkin, Dmannitol, vanillic acid, kutkiol, kutkisterol, and apocynin. The powdered root is used in medication and potentially has immuno-modulating activity in cell-mediated and humoral immunity.
In one study, 10 asthmatics were given powdered Picrorrhiza kurroa root b.i.d. for 14 days. Shah et al. noted an improvement in asthma symptoms in six asthmatics and improved lung function changes (FEV,) in four patients. Four patients had side effects ranging from headaches, nausea, vomiting, and abdominal pain to insomnia and giddiness.
Mahajand et al. demonstrated that pre-treatment powdered root of Picrorrhiza kurroa decreased sensitivity to histamine in guinea pigs. The severity and duration of allergic bronchospasm was reduced. Also, total histamine content in lung tissue was reduced. Pretreatment with Picrorrhiza inhibited histamine and slow reacting substances of anaphylaxis (SRSA) release in chopped lungs. Picrorrhiza kurroa also enhanced isoprenaline and adrenaline bronchodilator effects in the animals.
In a random doubleblind trial, 72 asthmatics were treated t.i.d. with Picrorrhiza kurroa root powder and placebo. Doshi et al. noted some initial clinical benefit. Despite this, there was no significant evidence of reduction in clinical attacks, need for bronchodilators, or improvement in lung function.
Dorsch et al. identified androsin, a phenol glycoside, as the active compound in Picrorrhiza kurroa. In a randomized, controlled, crossover study, it prevented allergen and PAFinduced bronchial obstruction in guinea pigs. Other unknown compounds inhibited PMN leukocyte histamine release.
Albizzia lebbek, or shirisha, is an indigenous tree used for bronchial asthma and bronchitis in Ayurvedic medicine. It contains saponins. Tripathi et al. studied asthmatic patients who were treated with this plant and showed reduced histamine levels and elevated cortisol levels. Treated guinea pigs also were protected from histamineinduced bronchospasm. As a consequence, Tripathi further explored the effects of histamine and Albizzia. In a 1979 controlled study, 18 guinea pigs were treated with distilled water, histamine, or histamine plus alcoholic extract of Albizzia lebbek bark. Plasma cortisol, catecholamine, and histaminase levels were measured and lungs and adrenals were examined. Histaminase levels were high in both groups but were highest in histaminetreated groups. The cortisol levels were high in the histamine group and highest in the Albizzia group. Catecholamine levels were highest in the histamine group, indicating stress. Histologically, the adrenals in the Albizziatreated group had larger cells and nuclei with many microvacuoles, indicating hyperactivity. Also, lung tissue in the Albizziatreated group appeared normal as compared to bronchospasm and luminal obstruction in the histamine group. Tripathi concluded that Albizzia counteracts the effects of histamine either by possibly neutralizing histamine directly or by causing increased cortisol production.
In 1981, Tripathi et al. examined the effect of histamine and Albizzia on catecholamines. Twentyfour guinea pigs were treated with control, histamine, or histamine plus Albizzia lebbek extract for 7 days. Adrenal glands were examined for medullary noradrenaline and adrenaline granules. Catecholamine levels were high in the histamine group and near control levels in Albizziatreated group. Also, granule and medullary size and number were increased in histaminetreated group and resembled the control group in the Albizzia treated group. In the previous study, plasma histaminase levels were increased in the Albizziatreated group. Tripathi stated that the reduction in catecholamine levels in Albizzia treated groups may be due to production of histaminase (see previous study) or a possible antihistaminic activity in the plant itself. Also, the previous study noted a rise in cortisol level with Albizzia that Tripathi believed might help in suppressing histamineinduced reactions such as the increase in catecholamines.
Johri et al. examined the effects of Albizzia seed extract and pure saponin fraction on rat peritoneal mast cells. Active and passive anaphylaxis were induced in rats and their mast cells were collected. Results showed that ruptured mast cell numbers were reduced with the Albizzia extract and fraction and with disodium cromoglycate (DSCG). Johri concluded that Albizzia and its saponin derivatives protected mast cells from allergeninduced degranulation similar to disodium cromoglycate, and may potentially have mast cell stabilizing activity similar to that of DSCG.
Adhatoda vasica (vasaka or malabar nut) is used in India for cough, bronchitis, bronchial asthma, glandular tumors, consumption, diarrhea, dysentery, cough, fever, jaundice, and tuberculosis. Its leaves were smoked. Its leaves and roots were prescribed by Ayurvedic practitioners as a mucolytic, antitussive, antispasmodic, and expectorant. In other cultures, the fruit is used for bronchitis and the root is used for asthma, bilious nausea, bronchitis, fever, gonorrhea, and sore eyes. The essential oil is claimed to have expectorant, antitubercular, and antihelmintic effects. Active chemicals are considered to be alkaloids, vasicine, vasicinone, and vasicinol.
The pharmacological action of the alkaloids in Adhatoda vasica were studied as early as 1959. Amin and Mehta studied vasicinone for its action on guinea pig trachea and perfused lung and on intact guinea pigs. Vasicinone antagonized histamineinduced constriction, but was less effective than adrenaline. A quinazol4one ring is found in vasicine and vasicinone and may be responsible for the action of Adhatoda. Vasicinone is the autooxidation product of vasicine.Cambridge et al. stated that in vitro tests showed relaxation of guinea pig trachea rings by vasicinone and quinazol4one at about 1/2000 the activity of adrenaline.Vasicinone was 1/700 and quinazol4one was 1/3800 as active as adrenaline against histamineinduced contraction. In in vivo studies of anesthetized guinea pigs, vasicine produced bronchoconstriction at high doses. Vasicine and vasicinone were found to have a weak antihistaminic effect which was of short duration. Vasicinone had less antihistaminic activity than vasicine and the effect decreased at higher doses.
Lahiri and Pradhan studied vasicinol, an alkaloid from the roots of Adhatoda vasica. The results were compared to those of vasicine and vasicinone. Vasicinol caused a transient fall in blood pressure in cats, guinea pigs, and rats and the effect was reversed by atropine in cats. It caused negative inotropic and chronotropic effects on guinea pig hearts that were blocked by atropine. Cat respiration was slightly increased and blocked by atropine. It also potentiated AChinduced bronchospasm but inhibited the action of histamine. No contraction in guinea pig tracheal chain was noted. Vasicinol contracted guinea pig ileum, enhanced the contraction caused by Ach, and was blocked by atropine. It also potentiated ACh contractions in frog rectus abdominus. No analgesic or toxic qualities were noted. Similar results were seen with vasicine except it had no effect on guinea pig ileum and relaxed the tracheal chain at low dose. Vasicinone had no effect on blood pressure and respiration in cats. It relaxed the tracheal chain and slightly contracted the ileum with potentiation of ACh and blockage by atropine. These results indicate that vasicinol has a cholinergic nature. The therapeutic effect of Adhatoda may be explained by vasicinol's antagonism of histamineinduced bronchoconstriction. Also, vasicinone acts as a bronchodilator, whereas vasicine bronchoconstricts at high dose. As discussed, Arvin attributes the beneficial effects of Adhatoda to the autooxidation of vasicine to vasicinone.
To clarify the action of vasicine and vasicinone, Gupta et al. studied their effects in vivo and in vitro.Vasicine reduced blood pressure in a dosedependent manner in dogs that remained unaltered by pressors, carotid denervation, or vagotomy. Vasicine had negative inotropic and chronotropic effects that were greater in combination with vasicinone. Vasicine also had direct vasodilatory effects. Vasicinone alone had no cardiovascular effects. Vasicine stimulated respiration in anesthetized dogs in a dosedependent manner. The respiratory effects were reduced in carotid sinus denervated, vagotomized, decerebrated, and atropinepretreated animals. Respiratory stimulation was also seen in rabbits. Vasicine increased ciliary movements when applied to frog esophagus and inhibited bronchial secretions in dog tracheas. Vasicinone had no effect. No antitussive activity was noted with either alkaloid.
Gupta concludes that the effects of Adhatoda vasica can be attributed to the bronchodilatory effects and increased ciliary movements by vasicine, and potentiation of bronchodilatory effects and antagonism of cardiac depression by vasicinone.27 By stimulating respiration, vasicine probably improves ventilation and helps expel tracheobronchial secretion, adding to the claims of expectorant activity in Adhatoda vasica.
Coleus forskholii is an Ayurvedic anti-asthmatic herb. It has bronchodilator effects. It is considered to be an antispasmodic, diaphoretic, sedative, anodyne, antidotal, antiseptic, antitussive, carminative, expectorant, febrifuge, pectoral, preventative (cold), and tonic. In Korea, leaves are used for colds, cough, and dyspepsia. It is claimed to increase intracellular cyclic adenosine monophosphate (cAMP) by acting directly on the catalytic subunit of the adenylate cyclase system. This may offer an advantage by bypassing psurface receptors and overcoming tachyphylaxis.
In a randomized, doubleblind, controlled, fourperiod, crossover study, Bauer et al. studied the effects of dry colforsin powder in 16 asthmatics. Colforsin or forskolin is a derivative of Coleus forskholii. Specific airway conductance was measured after exposure to fenoterol, a known betaagonist bronchodilator, and colforsin capsules. Fenoterol metered dose inhaler (MDI) showed a greater increase in airway conductance, followed by dry powdered fenoterol capsules, and then colforsin. The dry powdered colforsin (forskolin) showed measurable bronchodilation in asthmatics by elevated FEV-1 values. After 30 min, colforsin showed 16 - 2% changes in FEV, as compared to fenoterol MDI and capsules (29 - 3% and 30 - 3%, respectively). After 120 min, fenoterol airway conductance and FEV, was unchanged, but colforsinaffected values returned to baseline. No serious side effects were observed in patients. Mild to moderate tremor, restlessness, and palpitations were reported after use of fenoterol MDI and fenoterol capsules. Colforsin capsule and placebo-treated groups experienced less severe side effects. A decrease in potassium levels was noted after fenoterol use but no change was observed in colforsin or placebotreated patients.
Kaik et al. demonstrated in a doubleblind crossover study that forskolin had bronchodilating effects that were initially as good as fenoterol in healthy nonsmokers.At 3 and 5 min, forskolin protected against AChinduced bronchoconstriction as effectively as fenoterol, but at 15 and 30 min, fenoterol was stronger.
Solanuum xanthocarpum, or kantakari, is commonly used in Ayurveda as a bronchodilator, expectorant, and antitussive. The entire plant is used and contains saponin-like alkaloids
Bector and Puri treated a total of 60 patients with different types of chronic obstructive pulmonary disease with 2 grams bid of the powdered whole plant.In the 22 chronic bronchitis patients, improvement in cough frequency and severity was noted in 3-20 days. In 16 chronic asthmatics, 13 reported slight improvement in the severity of asthmatic attacks. Significant improvement was reported in 10 patients with unproductive nonspecific cough. No change was noted in status asthmaticus.
In another study by Bector, et al. 305 asthmatic patients were treated with a powdered form of the whole plant in a dose of 1 gram tid for one month. Fifty percent of the patients reported subjective improvement in their respiratory status without any reported adverse effects.
Information provided in this article is for the sole purpose of imparting education on Ayurveda and is not intended to diagnose, treat, cure or prevent any disease. If you have a medical condition, please consult your physician.
More by : Dr. Gaurang Joshi
|sir, my broncities allergy in last 2 year suffer many disease , homeophatic and allophethic madicine are used in 2 year but no relief sir suggested for me any medicine to remove broncities allergy.|
broncities allrgy me sirf khasi jyada uthti he or koi paresani nahi sir koi ilaj bataiye
|I am having asthama since last 35 years .pls suggest ayurvedic medicines to be taken and how could i get this .|
|I AM HAVING ASTHMA SINCE LAST 40 YRS. I TAKE AYURVEDIC MEDICINS, DO YOGA, TAKE INHALERS AND MUCH MORE. PL GUIDE ME FOR FURTHER AYURVEDIC MEDICINCES.|
|My son 3years old suffering asthma . suggest what type of medicine to be take for cure. pls advice|
|I started suffereing from Ashthma, my sleep is getting break around 4-30 AM daily .|
Can i get a cure facility at Udaipur rajasthan