• Donna Mazzola, PharmD

Frankincense and Autoimmune

Updated: Sep 30

Boswellia Seratta has been touted as the herb that can conquer it all. In the world of essential oils, it is known as the “king of oils”, but do people really understand the reasoning behind its value and impact on health and disease. Boswellia is a branching tree and native to the eastern world primarily in India and Africa. While there are several species of Boswellia, Boswellia Serrata is most commonly used for medicinal purposes. The portion of the tree that has been identified to have various medical benefits is the gum resin, commonly known as Indian Frankincense. This is extracted by pulling away from the bark of the tree, where the main constituents include boswellic acid and alpha and beta boswellic acid. In addition to these main constituents many terpenoids, flavonoids, and other phenolic compounds have been identified in the gum resin of the tree. Among the various boswellic acids 11-keto-Beta-boswellic acid (KBA) and acetyl-11-keto-Beta-boswellic acid (AKBA) have been observed to be active. Additionally, the gum resin contains up to 16% essential oil, which is extracted and utilized as the commonly known oil frankincense (Monograph 2019).

Several mechanisms have been reported demonstrating boswellia’s targets of action. This is important in order to understand how it can impact disease processes. First, it’s been demonstrated to inhibit the key enzyme in leukotriene synthesis, thus inhibiting arachidonic acid. This is its main anti-inflammatory action, through the inhibition of leukotriene synthesis via 5-lipoxygenase (Ammon 2010). It has also demonstrated action in reducing the elastase enzyme, where it’s activity is predominantly in the lungs decreasing the elasticity leading to emphysema. Lastly, boswellia inhibits the C2 convertase enzyme, which has a role in specific immunity related to the compliment pathway (Iram 2017). Additionally, from a kinetics standpoint, the elimination half-life is about 6 hours. This implies that boswellia should be taken every 6 hours to maintain plasma levels and therapeutic action (Iram 2017).

Understanding Boswellia’s various mechanisms of action and its impact on autoimmunity lie heavily in its anti-inflammatory effects. Many studies have looked into the effects of Boswellia extracts and acids on NF-Kappa Beta and various cytokines. The activation of the transcription factor of NF-Kappa-Beta has been shown to be inhibited by AKBA (acetyl-11-keto-Beta-boswellic acid), this leads to decreasing cytokines related to inflammation. Studies have demonstrated the reduction of TNF-alpha, IL1, IL2, Interferon, IL-6, and IL 12. Additionally, an upregulation of IL-4 and IL-10 which are beneficial in balancing the immune process. Additionally, the release of leukocytes and macrophages caused by oxygen radicals is inhibited by Boswellia extract as well as AKBA, which is an additional means of destruction to various tissue when chronic inflammation is present, as in many autoimmune conditions (Ammon 2010). While the mechanism of Boswellia extract and AKBA has been studied in vitro and presented, several studies have looked at its role in various autoimmune diseases, specifically in rheumatoid arthritis, multiple sclerosis, and ulcerative colitis.

Boswellia serrata has been involved in several studies for various anti-inflammatory benefits. However, specifically for rheumatoid arthritis, a clinical trial looking strictly at Boswellia alone for treatment and symptom improvement has not been done. However, a study was recently done in 2019 assessing the effect of Boswellia Serrata on inflammatory parameters and tumor necrosis factor in a rheumatoid arthritis animal model (Kumar 2019). The study broke out 36 rats into 6 groups. A normal control group, an arthritic control group, arthritic rats treated with indomethacin, and 3 groups treated with Boswellia at varying doses. The parameters measured included body weight, paw thickness, ankle diameter, and paw volume, along with an arthritic index and TNF-α (Kumar 2019). The study found that Boswellia at the highest dose of 180mg/kg demonstrated significant improvement in body weight and decreased ankle diameter and arthritic index. While changes in paw volume were observed, it was not statistically significant. However, overall improvement was comparable to indomethacin which is used as a standard of care in the initial treatment of RA. Previous studies have identified that Boswellia suppresses IL-1, TNK-alpha, and IFN-γ. This is important as these cytokines are typically elevated in chronic inflammation and in progressing rheumatoid arthritis. While the results of TNF-α were not statistically significant, histopathological results demonstrated improvement in inflammation, which translates as clinical significance (Kumar 2019).

An additional study looked at the effects of Boswellia on cognitive impairment in multiple sclerosis (MS). With MS being a disease that affects the central nervous system, it is frequently associated with cognitive impairment. It is estimated that 40-60% of patients diagnosed with MS suffer from a degree of cognitive impairment. While we’ve discussed the specific anti-inflammatory properties of Boswellia, it has also demonstrated neuroprotective activity whereby it increases the formation of new nerve networks. Additionally, it has shown an ability to block degenerative changes in the hippocampus, which directly affects memory processing (Majdinasab 2016). A study by Majdinasab et al. included 60 patients with MS who were deemed cognitively impaired based on the multiple sclerosis neuropsychological questionnaire (MSNQ) without existing depression or psychiatric disorders. The treatment group of 30 patients received a capsule containing 450 mg powder of Boswellia serrata (BS) twice daily for 2 months compared to a placebo arm. The study found that the patients treated with BS demonstrated improvement in visuospatial memory test as well as the verbal learning test, both of which were statistically significant (Majdinasab 2016).

With the understanding of the disease process associated with MS, whereby we see neuronal degeneration in gray matter and damage to white matter, there is a significant association and prevalence of cognitive impairment. These changes in brain matter are due to pro-inflammatory agents such as TNF-alpha, Interferon, and Interleukin, which are known to be elevated in MS patients. As we discussed, AKBA, the active constituent in Boswellia is responsible for its anti-inflammatory activity via the mechanism of inhibiting 5-lipooxygenase enzyme inhibitory activity. Additionally, studies have demonstrated a decrease in several pro-inflammatory cytokines. Another compound that has been isolated in the Boswellia resin is incensole-acetate. This compound inhibits NF-kB, and has anti-inflammatory effects in the CNS, which have exhibited effects in reducing anxiety and depression (Majdinasab 2016).

Lastly, in considering Boswellia in autoimmune disease, a study looked at the effect of Boswellia serrata on ulcerative colitis. Again, sticking with the theme of blocking leukotriene synthesis, Boswellia has demonstrated to have an impact on the chronic inflammatory disease of the colon. In ulcerative colitis, it is suggested that leukotrienes play an important role causing inflammation in the colon. In understanding the mechanism by which Boswellia blocks 5-lipoxygenase, the enzyme responsible for leukotriene biosynthesis, we can thereby suggest it would have a positive effect on maintaining the disease. A study was done by Gupta et al. comparing Boswellia serrata 350 mg three times a day for 6 weeks to standard therapy sulfasalazine 1 gram three times a day. The results of the study were quite promising in that 82% of the patients treated with Boswellia went into remission compared to the control group rate of 75%. This clearly further solidifies the anti-inflammatory mechanism by which Boswellia has an impact on various autoimmune conditions (Gupta 1997).

Based on these findings it is evident that Boswellia clearly possesses anti-inflammatory activity via multiple mechanisms of action. The constituents have the ability to not only impact leukotriene biosynthesis but minimizes the production of various pro-inflammatory cytokines. Inflammation and autoimmune disease go hand-in-hand, minimizing inflammation thereby delays disease progression and can lead to remission in many cases. The majority of pharmacological agents available for autoimmune disease treatments focus on blocking inflammatory pathways in order to keep the disease state under control. Understanding the mechanisms of autoimmunity, I would extrapolate this information and make it applicable to any autoimmune condition in which we understand there is an inflammatory process. Utilizing this treatment as an alternative to NSAIDs, anti-inflammatory agents, and immunosuppressive agents may be feasible in early disease management as it has minimal side effects that we would otherwise experience with standard therapy.


1. Monograph: Boswellia. Natural Medicines Database. Updated: 3/11/2019.

2. Iram F, Khan SA, Husain A. Phytochemistry and potential therapeutic actions of Boswellic acids: A mini-review. Asian Pacific Journal of Tropical Biomedicine. 2017;7(6):513-523.

3. Ammon HPT. Modulation of the immune system by Boswellia serrata extracts and boswellic acids. Phytomedicine: International Journal of Phytotherapy & Phytopharmacology. 2010;(11):862.

4. Kumar R, Singh S, Saksena A, Pal R, Jaiswal R, Kumar R. Effect of Boswellia serrata extract on acute inflammatory parameters and tumor necrosis factor-α in complete Freund’s adjuvant-induced animal model of rheumatoid arthritis. International Journal of Applied & Basic Medical Research. 2019;9(2):100.

5. Majdinasab N, Siahpush A, Mousavinejad SK, Malayeri A, Sajedi SA, Bizhanzadeh P. Effect of Boswellia serrata on cognitive impairment in multiple sclerosis patients. Journal of Herbal Medicine. 2016;6(3):119-127.

6. Gupta I, Parihar A, Malhotra P, et al. Effects of Boswellia serrata gum resin in patients with ulcerative colitis. European Journal Of Medical Research. 1997;2(1):37-43.

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