Frankincense, Inflammation and Autoimmune Disease

Margo R. Flanagan

American College of Healthcare Sciences

 

Abstract

Frankincense has long been known for its medicinal properties and documented use as a drug dating as far back as 1500 BC. Recent research studies have uncovered the mechanism of action by which Frankincense is able to inhibit the cascade of events leading to inflammation with little or no side effects. In animal and human studies, the key agent, acetyl-11-keto-beta-boswellic-acid found in the gum resin of Frankincense has repeatedly shown its strength in its ability to halt inflammation. Autoimmune diseases are incurable, chronic, inflammatory conditions requiring long-term drug therapies. The conventional drugs used to control the hallmark destructive inflammatory process of autoimmune diseases often have significant side effects. This paper assesses the use of Frankincense to aid in the reduction of inflammation associated with autoimmune diseases.

Introduction

Autoimmune diseases affect 50 million Americans and place a considerable cost burden on the healthcare system. There has been an alarming increase in autoimmune diseases being seen all around the world since the 1970’s that researchers attribute to environmental and genetic events (American Autoimmune Related Diseases Association, 2011). Currently there is no curative treatment for autoimmune diseases. Given this, treatment is long-term and focused on symptom management. Modern drug therapies such as non-steroidal anti-inflammatory drugs (NSAIDs) and immunosuppressive agents can cause considerable side effects impacting quality of life. Additionally, these medications can be costly with diminished effect over time.

Frankincense has been used for hundreds of years in India, Africa and in Ayurvedic Medicine to treat many different diseases including chronic inflammatory conditions. Both autoimmune disease and Complementary and Alternative Medicine (CAM) therapies to treat them such as Frankincense (Boswellia sp.) are vastly under researched areas. This paper assesses the use of Frankincense to aid in the reduction of inflammation associated with autoimmune diseases.

Results

Historical Background

The history of Frankincense dates back thousands of years, the most noted story of it as a gift to the baby Jesus from the 3 Wise Men. The papyrus Ebers, discovered between the legs of a mummy is one of the oldest documents with Frankincense depicted as a treatment for medical conditions (Ammon, 2006). Ancient medical texts for Ayurvedic Science include the use of the tree gum resin “guggals” to treat arthritis (Siddiqui 2011). From ancient times to the 1st and 2nd century A.D., Ayurvedic medicine specifically discusses Frankincense Boswellia Serrata for the treatment of inflammation and pain (Ammon, 2006). 20th century Europe also saw the use of Frankincense as a drug but for unexplained reasons documented use of it as a treatment for medical conditions faded in the time after. Its resurgence as an anti-inflammatory agent was due to the discovery in 1991 of the action mechanism of Boswellia sp. to inhibit the synthesis of the proinflammatory enzyme, 5-lipoxygenase (5-LO) (Ammon, 2006).

Composition of Frankincense

Frankincense is produced when the Boswellia species of tree found in areas of India, Africa and the Middle East are tapped and the gum resin is collected (Siddiqui, 2011). The species of trees that produce “true Frankincense” include B.sacra, B.carterii, B.frereana, B.serrata and B.papyfera (Ammon 2006). Each species differs not only in its location and harvesting but also in chemical composition. The active constituents of the gum resin extracts include 30-60% resin, 5-10% essential oils and the rest polysaccharides (Siddiqui, 2011). The resin contains pentacyclic triterpenes or Boswellic Acids (BA). Of the four BAs, acetyl-11-keto-β-Boswellic acid (AKBA) is considered the strongest inhibitor of proinflammatory enzymes that play key roles in the cascade of events that occur during an inflammatory process (Siddiqui, 2011).

Action Mechanisms of Frankincense on Inflammation

Inflammatory mediators interacting with Frankincense are the proinflammatory cytokines Interleukin 1 (IL-1), Tumor Necrosis Factor (TNF-alpha) and Interleukin-6 (IL-6), leukotrienes, phospholipids, arachadonic acid (ADA), 5-LO and components of the complement system (Madame Curie Bioscience Database, 2013). Depending on the autoimmune disease, the mediators of inflammation play key roles in immune dysfunction, with the BAs of Frankincense resin working to regulate it.

The action mechanism of AKBA is similar to NSAIDs but concerns a different pathway of biochemical responses to inflammation. When injury occurs cells release histamine to dilate capillaries and increase blood flow. Mast cells produce the chemical mediators leukotrienes, which kick up the immune response causing neutrophils to adhere to the endothelium awaiting migration. Activated macrophages and lymphocytes produce cytokines IL-1, IL-6 and TNF-α. IL-1 and TNF-α cause acute phase reactions that increase white blood cell production and the liver to produce acute phase proteins such as fibrin, complement and c-reactive protein. Phospholipids are activated by tissue injury hydrolyzing ADA causing chemotaxis, increasing development of leukotrienes and activation of the “5 lipoxygenase pathway” (Yadav, Prasad, Sung, Gelovani, Guha & Krishnan, 2011).

In vitro studies, systematic reviews and meta analyses consistently show that boswellic acids inhibit the synthesis of the pro-inflammatory enzyme 5-LO thus halting the further production of inflammatory leukotrienes and subsequent inflammation to the area (Ernst, 2008).

Modern Therapy vs. Frankincense

Proinflammatory cytokines IL-1, IL-6 and TNF-α are targets for treatment of autoimmune diseases as inhibiting their action halts inflammation. Successful drug therapies are already in use but create complications when interacting with biological systems over time (Astrakhantseva, Efimov, Srutskaya, Kruglov & Nedospasov, 2014).

Glucocorticoids and NSAIDs are the most widely prescribed medications for many autoimmune diseases but are well known to cause side effects ranging from gastrointestinal and cardiac problems to development of Cushing’s syndrome and diabetes (Su, Duan, Chen, Huang, Shang, Yu, Wei et al., 2015).

A randomized, double blind placebo controlled cross-over study after 32 weeks of oral consumption of Frankincense showed pain reduction without significant side effects (Prabhavathi, Chandra, Soanker & Rani, 2014).

Studies of animal and human models with oral consumption of Boswellia extracts repeatedly show protective effect and positive results for reducing inflammation in conditions of ulcerative colitis and Crohn’s disease with little to no side effects (Yadav, Prasad, Sung, Gelovani, Guha & Krishnan, 2011).

Studies show oral consumption of Frankincense is an effective treatment in Type 1 diabetes for reducing blood glucose levels with an added protection for liver and kidneys. Further evidence compiled shows no effect on blood pressure, heart rate or respirations with low toxicity (Hamidpour, Hamidpour, Hamidpour & Shahlari, 2013)

Discussion

Autoimmune diseases number just under a hundred different types affecting upwards of 50 million Americans. For women, autoimmune disease is the number one cause of morbidity (American Autoimmune Related Diseases Association, 2011). These chronic, incurable conditions put stress and staggering costs on the healthcare system with their complexities regarding diagnosis through unusual patient complaints and need to visit physicians from multiple disciplines. Physicians find there is considerable struggle to provide optimum symptom management and quality of life for patients. As the underlying process contributing to disease progression in autoimmune diseases is inflammation, physicians seek to reduce the immune response with steroids, NSAIDs and newer pharmaceuticals known to have considerable side effects. Patients unable to manage both disease symptoms and drug side effects end up with a reduced quality of life setting the stage for more health issues related to stress.

To better understand what goes wrong in autoimmunity, one must understand the normal process of the human body in response to tissue damage. Inflammation is a complex process and defense mechanism of the body to repair cell injury utilizing hundreds of mediators. Infection, chemical or physical injury can start the following inflammatory reaction. The capillaries begin to dilate and increase the blood flow to the area. Microvascular structural changes cause plasma proteins to move out of the blood stream. Leukocytes migrate through the endothelium, a thin layer of epithelial squamous cells lining blood and lymphatic vessels and accumulate at the site of injury (Markiewski & Lambris, 2007). The injury is repaired and the process stops.

Autoimmune disease is defined as an abnormal immune response resulting in tissue damage and inflammation when the body attacks itself creating a chronic inflammatory condition. It is not known exactly what causes an autoimmunity to occur but it is speculated that dysregulation of cytokine production plays a key role. Cytokines are small proteins produced by activated lymphocytes, monocytes and macrophages. The key mediators in the chronic inflammatory response that are affected by the boswellic acids of Frankincense include the proinflammatory cytokines TNF-α, IL-1 and IL-6, leukotrienes (produced by all leukocytes and mast cells) and pro-inflammatory enzymes of which, 5-LO is greatly inhibited.

Frankincense has been used for hundreds of years to treat many conditions including chronic inflammatory diseases and is an effective CAM therapy for reducing inflammation. The active constituents of the gum resin extracts of Frankincense (Boswellia species) contain 30-60% resin and 5-10% essential oils (Siddiqui, 2011). Found within the resin of Frankincense are tetracyclic triterpenic acids and four boswellic acids of which AKBA is considered the most potent inhibitor of pro-inflammatory enzymes, mainly 5-LO.

Increasing numbers of people suffering with autoimmune diseases are turning to CAM therapies to manage their symptoms. Dissatisfaction with current modes of treatment and numerous prescription medications with side effects are the driver for seeking alternative treatment. Frankincense has shown itself to be a remarkable inhibitor of the 5-lipoxygenase pathway sufficiently decreasing inflammation WITHOUT noted side effects.

Limitations cannot be overlooked. Evidence compiled in systematic reviews and meta-analyses assessing the effectiveness of Frankincense state the pharmacokinetics and optimal dose of Frankincense is unknown (Ernst, 2008). Route of administration, dosing and safety for long term use need to be established through large controlled human clinical research trials.

Conclusions and Recommendations

Frankincense has been used throughout history for a variety of illnesses including chronic inflammatory conditions. The anti-inflammatory effects of the gum resin of Frankincense have shown it to be a promising CAM therapy for use in the reduction of pain and inflammation associated with autoimmune diseases with little to no side effects. Autoimmune disease is rapidly becoming a health care crisis and public health priority and those suffering with one of the 80 to 100 various diseases searching for more natural ways to manage the disease progression.

Clinical trials of Frankincense show analgesic activity both in humans and in vitro comparable to NSAIDs but further investigation with larger clinical trials are necessary to build evidence based medicine protocols, study the effectiveness, determine appropriate routes of administration, dosing and safety of treatment for long-term use.

References

Ammon, H. P. T. (2006). Boswellic Acids in Chronic Inflammatory Diseases. Planta Med.Oct;72(12), . Retrieved from http://myachsclass.org/re/DotNextLaunch.asp?

Ernst, E. (2008). Frankincense: Systematic review. BMJ, 337(dec17 2), a2813–a2813. doi:10.1136/bmj.a2813

Astrakhantseva, I.V., Efimov, G. A., Drutskay, M. S., Kruglov, A. S. & Nedospasov, S. A. (2014). Modern Anti-Cytokine Therapy of Autoimmune Diseases. Biochemistry (Moscow), 79(12), 1308-1321. Doi:10.1134/S0006297914120049

Hamidpour, R., Hamidpour, S., Hamidpour, M., & Shahlari, H. (2013). Frankincense (Boswellia species): From the selection of traditional applications to the novel phytotherapy for the prevention and treatment of serious diseases. Journal of Traditional and Complementary Medicine, 3(4), 221. doi:10.4103/2225-4110.119723

Markiewski, M. M., & Lambris, J. D. (2007). The role of complement in inflammatory diseases from behind the scenes into the spotlight. The American Journal of Pathology, 171(3), 715–727.doi:10.2353/ajpath.2007.070166

Prabhavathi, K., Shobha Jagish Chandra, U., Soanker, R., & Usha Rani, P. (2014). A randomized, double blind, placebo controlled, cross-over study to evaluate the analgesic activity of Boswellia serrata in healthy volunteers using mechanical pain model. Indian Journal of Pharmacology, 46(5), 475. doi:10.4103/0253-7613.140570

Santamaria, P. (2013). Madame Curie Bioscience Database. Austin, TX: Landes Bioscience.

Siddiqui, M. Z. (2011). Boswellia Serrata, A Potential Antiinflammatory Agent: An Overview. Indian Journal of Pharmaceutical Sciences, May/June(73(3)), 255–26 doi:10.4103/0250-474X.93507

Su, S., Duan, J., Chen, T., Huang, X., Shang, E., Yu, L., … Tang, Y. (2015). Frankincense and myrrh suppress inflammation via regulation of the metabolic profiling and the MAPK signaling pathway. Scientific Reports, 5, 13668. doi:10.1038/srep13668

Yadav, V., Prasad, S., Sung, B., Gelovani, J., Guha, S. & Krishnan, S. (2011). Boswellic acid inhibits growth and metastasis of human colorectal cancer in orthotopic mouse model by downregulating inflammatory, proliferative, invasive and angiogenic biomarkers. International Journal of Cancer: 130, June. doi: 10.1002/ijc.26251

 

 

 

One Reply to “Frankincense, Inflammation and Autoimmune Disease”

  1. Interesting. Lots of hard work went into this paper. Frankincense sounds like an encouraging option to conventional anti-inflammatory treatment. When will the medical field become open to “natural” remedies.

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