The exudate of the boswellia tree contains terpenoids, oils, and gum resins. As the terpenoids, referred to collectively as boswellic acids, have been shown to be the active constituents in boswellia, extracts from commercial sources are standardized to boswellic acid content. Up to 16% of the oleo-resin is essential oil, primary alpha thujene and p-cymene. The gum resins are also known as guggals. The typical forms of boswellia used are gum resin preparation or ethanol extracts of the gum resin standardized to contain 10-15 micrograms/ml of 3-O-acetyl-11-keto-beta-boswellic acid.
Studies have shown that the boswellic acids have an anti-inflammatory action much like the conventional nonsteroidal anti-inflammatory drugs (NSAIDs) used for inflammatory conditions. Boswellia inhibits pro-inflammatory mediators in the body, specifically leukotrienes via inhibition of 5-lipoxygenase, the key enzyme involved in the biosynthesis of pro-inflammatory leukotrienes. In contrast to NSAIDs, which are well known to disrupt glycosaminoglycan synthesis, thus accelerating articular damage in arthritic conditions, boswellic acids have been shown to significantly reduce glycosaminoglycan degradation. Consequently, long-term use of boswellia does not lead to irritation or ulceration of the stomach. Recent studies also suggest that boswellic acids exert significant anticancer, antimicrobial and immune-potentiating effects.
Owing to its pharmacological actions, boswellia may be effective in various healthcare applications. Clinical studies using herbal formulas containing boswellia have yielded good results in both osteoarthritis and rheumatoid arthritis. The inhibition of both leukotriene biosynthesis and subsequent excessive humoral inflammatory response may also be one of the primary mechanisms by which boswellia has been shown to be a safe and effective therapy in asthma and inflammatory bowel diseases such as colitis, Chron’s disease and ileitis.
No toxic reactions to boswellia have been reported and no known reason exists to expect a toxic reaction to boswellia sp. Similarly, there are no known contraindications with diseases or conditions. No drug/nutrient/herb interactions are known to occur and there is no known reason to suggest a theoretically clinically significant interaction. Additionally, no adverse side-effects due to boswellic acids have been reported.
Typical dosage varies depending upon the form being used and the health care application for which it is being used.
Studies have shown that the boswellic acids have an anti-inflammatory action much like the conventional nonsteroidal anti-inflammatory drugs (NSAIDs) used for inflammatory conditions. Boswellia inhibits pro-inflammatory mediators in the body, specifically leukotrienes via inhibition of 5-lipoxygenase, the key enzyme of leukotriene synthesis. As opposed to NSAIDs, boswellia does not decrease glycosaminoglycan biosynthesis nor does long-term use of boswellia lead to irritation or ulceration of the stomach. Controlled, double blind studies have shown that boswellia extracts are very helpful for inflammatory bowel conditions including ulcerative colitis and Crohn’s disease. Recent studies also suggest that boswellic acids exert significant anti-cancer, anti-microbial and immune-potentiating effects.
Clinical studies using herbal formulas containing boswellia have yielded good results in both osteoarthritis and rheumatoid arthritis. In contrast to non-steroidal anti-inflammatory drugs, which are well known to disrupt glycosaminoglycan synthesis, thus accelerating articular damage in arthritic conditions, boswellic acids have been shown to significantly reduce glycosaminoglycan degradation while inhibiting 5-lipoxygenase, key enzyme involved in the biosynthesis of pro-inflammatory leukotrienes.
Asthma is characterized by chronic bronchial airway inflammation resulting in increased mucus production and airway hyper-responsiveness. The underlying process appears to be an out-of-balance immune activity: overactive humoral immunity and underactive cell-mediated immunity. Boswellic acids have been shown to inhibit leukotriene biosynthesis, thus lessening excessive humoral inflammatory response.
Boswellic acids have been shown to inhibit 5-lipoxygenase, the key enzyme involved in the synthesis of inflammatory leukotrienes, which are a key contributing factor in the initiation and progression of inflammatory bowel disease. Boswellia serrata gum resin preparations have been shown to be a safe and effective therapy in colitis, Crohn’s disease and ileitis. In one study in which the efficacy and safety of boswellia extract was compared to mesalazine for the treatment of Crohn’s disease, boswellia was found to be more effective in reducing disease activity than mesalazine.
In inflammatory and bronchoconstrictive conditions the standard dosage of boswellia extract is 400 mg three times daily, although some studies have produced good results using 300 mg three times daily.
Extracts should be standardized to contain 10-15 micrograms/ml since boswellia’s anti-inflammatory action is dose-dependent.
No adverse side-effects due to boswellic acids have been reported.
No known toxic reactions.
No known contraindications.
No interactions are known to occur, and there is no known reason to suggest a theoretical clinically significant reaction to boswellia.
The resin of the Boswella serrata tree is collected towards the end of October. Transverse incisions are made in the upper and lower portions of the tree trunk to be exposed and then segments of bark six to eight inches wide are peeled off. The gum that exudes from the resulting wound is collected for the next 10 to 12 days.
The exudate of the boswellia tree contains oils, terpenoids, and gum:
In the ancient Ayurvedic medical texts of India, salai gugul, the gummy exudate from boswellia, is one of a group of gum resins collectively referred to as guggals. Historically, the guggals were recommended for a variety of conditions including osteo and rheumatoid arthritis, abdominal pain, diarrhea, dysentery, asthma, bronchitis and other pulmonary diseases, ringworm, pimples, sores, tumors, cancers, dysmenorrhea, stimulation of menstrual flow, syphilis, and as a diuretic.
Pliny, in the 1st century A.D., mentions frankincense as an antidote to hemlock. In the 10th century, Avicenna recommended frankincense for tumors, ulcers, vomiting, dysentery and fevers. In China, it was used in the treatment of leprosy.
The religious use of frankincense was common in ancient Persia, Babylon and Assyria. The ceremonial incense of the Jews was compounded of equal parts of four 'sweet scents,' one of which was frankincense, which is frequently mentioned in the Pentateuch, the first five books of the Bible.
According to Herodotus, the Arabs brought 1,000 talents of frankincense to Darius annually as tribute, and this amount of frankincense was offered on the great altar of the temple in Babylon each year during the feast of Bel. Herodotus describes the use of frankincense combined with other ingredients into a paste to perfume the hands among the women of Scythia, a usage also alluded to in the Bible (Judith 10, verses 3 and 4), and one which continues today.
Among the Greeks, frankincense was the most common incense offered to the gods. Among the Romans, frankincense (alluded to as mascula thura by Virgil in the Ecologues) was used not only in religious ceremonies, but also on state occasions and in domestic life.
Today, frankincense is used both as incense and in cosmetics. Kohl, the black powder used by Egyptian women to paint their eyelids, has been made charred frankincense, or other odoriferous resin mixed with frankincense, since ancient times. Frankincense is also melted to make a depilatory. Frankincense is a primary constituent of the incense now used in Christian churches in Europe.. In Rome, Olibanum alone is employed; in the Russian church, Benzoin is chiefly employed.
In an in vivo animal study (1971), boswellia gum resin caused "marked sedative and analgesic effects." A possible mechanism of action for these effects was demonstrated in a later in vitro study (1993) in which antibody-coated sheep erythrocytes were added to pooled guinea-pig serum. In this study, boswellic acids inhibited C3-convertase of the classical complement pathway, thus inhibiting immunohaemolysis, and also exhibited weak inhibitory effects on individual components of the complement system. Another in vitro study (1996), in which beta-boswellic acid demonstrated significant inhibition of both the classical and alternate complement systems, confirmed these actions.
In in vivo experiments (1988), oral administration of an alcohol extract of salai guggal was shown to strongly inhibit antibody production and cellular response to sheep red blood cells in mice and to inhibit the infiltration of polymorphonuclear leucocytes and reduce the volume of pleural exudates in carrageenan-induced pleurisy in rats.
Later in vitro experiments (1993) elucidated the mechanism of these anti-inflammatory effects. In these experiments, boswellic acids were found to inhibit leukotriene synthesis via 5-lipoxygenase, but did not affect the 12-lipoxygenase or cyclooxygenase activities, nor did they prevent peroxidation of arachidonic acid by iron or ascorbate. Boswellic acids were therefore shown to be specific, non-redox inhibitors of leukotriene synthesis, either interacting directly with 5-lipoxygenase or blocking its translocation.
In 1998, an in vivo study of guinea pigs with experimental autoimmune encephalomyelitis (EAE) confirmed that boswellic acids act as selective, non-redox, potent inhibitors of the biosynthesis of leukotrienes. Intraperitoneal dosage (20 mg/kg) of boswellic acids significantly reduced clinical symptoms in guinea pigs with EAE.
Pentacyclic triterpenes from the 11-keto-boswellic acid series have recently (2000) been identified as the active principal ingredients of boswellia resin responsible for inhibiting the key enzyme of leukotriene synthesis, 5-lipoxygenase (5-LO). Of these boswellic acids, 3-O-acetyl-11-keto-beta-boswellic acid (AKBA) is the most potent inhibitor of 5-LO. In vitro testing has further clarified that boswellic acids' inhibition of leukotriene biosynthesis via impairing 5-LO is dose-dependent. While extracts of boswellic acids in concentrations greater than 10-15 micrograms/ml inhibit 5-LO product formation, extracts containing lower concentrations (1-10 micrograms/ml) not only did not inhibit, but actually protentiated 5-LO product formation, especially the biosynthesis of 5(S)-HETE. Extract standardization is therefore vitally important for therapeutic effectiveness.
In contrast to non-steriodal anti-inflammatory drugs, which are well known to disrupt glycosaminoglycan synthesis, thus accelerating articular damage in arthritic conditions, boswellic acids have been shown to significantly reduce glycosaminoglycan degradation. A 1989 in vivo study that compared boswellia extract to ketoprofen found that boswellia markedly reduced degradation of glycosaminoglycans in male albino rats whereas, in the ketoprofen-treated animals, a significant reduction in glycosaminoglycan biosynthesis was observed.
Several species of boswellia have exhibited anti-microbial activity:
Methanol and aqueous extracts of Boswellia dalziellii stem bark were found to exhibit broad spectrum inhibiting activity against bacteria, both Gram-positive and Gram-negative, and fungi.
Methanol and aqueous extracts of Boswellia carterii were found to significantly inhibit (>/90% inhibition at 100 microg/mL) hepatitis C virus (HCV) protease.
A possible mechanism of action is boswellic acids' stimulation of the mitogen-activated protein kinases p42 and p38 and mobilization of intracellular Ca(2+). Via these actions, extracts of Boswellia serrata gum resins and the boswellic acids, particularly the keto boswellic acids (11-keto-beta-boswellic acid and 3-O-acetyl-11-beta-keto boswellic acid) were shown to be potent activators of human polymorphonuclear leukocytes.
Several studies, two in vitro and one in vivo, suggest that boswellic acids have anti-carcinogenic effects.
In one in vitro study, boswellic acids from Boswellia serrata gum resin inhibited the synthesis of DNA, RNA and protein in human leukemia HL-60 cells in a dose-dependent manner with 3-O-acetyl-11-beta-boswellic acid (AKBA) having the most pronounced inhibitory effects. Another in vitro study found that boswellic acid acetate (BC4), a compound isolated from Boswellia carterii was a potent inducer of differentiation and apoptosis of leukemia cells with 90% of cells showing morphological changes. BC4 strongly inhibited all cell lines tested in a dose- and time-dependent manner. In HL-60 cells, 20 micro/ml of BC-4 decreased viable cell number by 60% at 24 hours, and at 3 days, virtually no viable cells remained.
In the in vivo study, topical application of a menthol extract of Boswellia serrata gum resin to the backs of DMBA-initiated mice markedly inhibited TPA-induced increases in skin inflammation, epidermal proliferation, and tumor-promotion. Addition of Boswellia serrata extract to the diet of the mice for 10-24 weeks reduced the accumulation of parametrial fat pad weight under the abdomen, and inhibited azoxymethane-induced formation of aberrant crypt foci by 46%.
Boswellic acid extracts have demonstrated anti-arthritic effects in a several experimental animal studies. Two mechanisms of action, both of which support the health and repair of joint tissues, explain these beneficial effects: inhibition of 5-lipoxygenase, the key enzyme involved in the biosynthesis of pro-inflammatory leukotrienes and prevention of glycosaminoglycan degradation. Clinical studies using herbal formulas containing boswellia have yielded good results in both osteoarthritis and rheumatoid arthritis. As noted above, in contrast to non-steriodal anti-inflammatory drugs, which are well known to disrupt glycosaminoglycan synthesis, thus accelerating articular damage in arthritic conditions, boswellic acids have been shown to significantly reduce glycosaminoglycan degradation.
Asthma is characterized by chronic bronchial airway inflammation resulting in increased mucus production and airway hyper-responsiveness. The underlying process appears to be an out-of-balance immune activity: overactive humoral immunity and underactive cell-mediated immunity. Boswellic acids have been shown to inhibit leukotriene biosynthesis, thus lessening excessive humoral inflammatory response. In a double-blind, placebo-controlled study of 80 patients, 40 (23 males, 17 females) were given a boswellia gum resin preparation of 300 mg, 3 times daily for 6 weeks. 70% of patients given boswellia extract showed significant improvement as evidenced by disappearance of physical symptoms (dyspnea, rhonchi, increase in FEV1, FVC and PERF, decreases in ESR and eosinophil count) and lower number of attacks. In contrast, only 27% of patients in the control group showed improvement.
The inflammatory process is associated with increased formation of leukotrienes causing chemotaxis, chemokinesis, synthesis of superoxide radicals and release of lyosomal enzymes by phagocytes. Boswellic acids, specifically, the biologically active ingredients of the gum resin of Boswellia serrata, have been shown to be specific, nonredox, noncompetitive inhibitors of 5-lipozygenase, the key enzyme of leukotriene biosynthesis. Boswellic acids have therefore been studied for their potential therapeutic effectiveness in ulcerative colitis, chronic colitis, experimental ileitis, and Chron disease. Boswellia serrata gum resin preparations have been shown to be a safe and effective therapy in all of these inflammatory bowel conditions.
In a 1997 study, patients with ulcerative colitis grade II and III were given Boswellia serrata gum resin preparation (350 mg, 3 times daily for 6 weeks) or sulfasalazine (1 g, 3 times daily). In patients given boswellia, improvement was noted in all parameters tested with results being similar to those given sulfasalazine. Among patients given boswellia, 82% went into remission compared to 75% of those given sulfasalazine.
A more recent (2001) study led by the same principal investigators evaluated 30 patients (17 males, 13 females ranging in age from 18 to 48 years) with chronic colitis. Twenty patients were given a preparation of the gum resin of Boswellia serrata (900 mg daily divided in 3 doses for 6 weeks), and 10 patients were given sulfasalazine (3 gm daily divided in 3 doses for 6 weeks). Among the 20 patients treated with boswellia, 18 showed improvement and 14 went into remission. Among the 10 treated with sulfasalazine, 6 showed improvement and 4 went into remission.
Of the four primary boswellic acids, 3-O-acetyl-11-keto-beta-boswellic acid (AKBA) has been determined to be the most potent inhibitor of 5-LO. Recent (2001) studies of experimental ileitis and Chron disease have used an AKBA extract called H15.
In a study of Spraque-Dawley rats with indomethacin-induced ileitis, H15 significantly attenuated tissue injury scores and resulted in a dose-dependent decrease in rolling (up to 90%) and adherent (up to 98%) leukocytes.
The efficacy and safety of H15 was compared to mesalazine for the treatment of Chron's disease in a randomized, double-blind, placebo-controlled trial in which 44 patients were treated with H15 and 39 with mesalazine. The Chron Disease Activity Index given at enrollment and at the end of therapy was used to measure outcome. Among patients given H15, the CDAI was reduced by 90 and after therapy with mesalazine by 53 scores in the mean. Researchers concluded, "Considering both safety and efficacy of Boswellia serrata extract H15, it appears to be superior over mesalazine in terms of a benefit-risk evaluation."
Gum resin preparation or ethanol extracts of the gum resin standardized to contain 10-15 micrograms/ml of 3-O-acetyl-11-keto-beta-boswellic acid.
In inflammatory and bronchoconstrictive conditions the standard dosage of boswellia extract is 400mg three times daily, although some studies have produced good results using 300 mg three times daily.
Extracts should be standardized to contain 10-15 micrograms/ml of 3-O-acetyl-11-keto-beta-boswellic acid. In vitro testing has shown that boswellia's inhibition of leukotriene biosynthesis by impairing 5-lipoxygenase is dose-dependent. While extracts in concentrations greater than 10-15 micrograms/ml have been shown to inhibit 5-LO product formation, extracts containing lower concentrations (1-10 micrograms/ml) not only did not inhibit, but actually potentiated 5-LO product formation, especially the biosynthesis of 5(S)-HETE.
No adverse side-effects due to boswellic acids have been reported.
No drug/nutrient/herb interactions are known to occur, and there is no known reason to suggest a theoretical clinically significant reaction to boswellia.
No toxic reactions to boswellia have been reported, and no known reason exists to expect a toxic reaction to boswellia sp.
No known interactions or contraindications with diseases or conditions have been reported, and there is no known reason to expect a clinically significant adverse reaction to boswellia sp.