Frankincense and Autoimmune Disease

Frankincense and Autoimmune Disease

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 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 lies 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.  Also, 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 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).


Multiple sclerosis

An additional study looked at the effects of Boswellia on cognitive impairment in multiple sclerosis (MS). With MS being a disease that effects 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 effects 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 frankincense 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 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 in maintaining 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 (frankincense) 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.
          What is autoimmune?

          What is autoimmune?



          Autoimmune disease prevalence has been on a continuous rise, and is estimated to continue to increase at a rate of 19% per year.  That number is outrageous and quite frankly scary! To understand why this rate continues to rise and to combat it, means we need to pinpoint what is autoimmune?

          Approximately 1 out of 9 women have an autoimmune disease and 1 out of 12 adults.  There are about 50 million Americans suffering from 80-100 different autoimmune diseases. The scary thing is, only about 24 autoimmune diseases have actual known mechanisms.  I can’t tell you how many people I know, that have come to me, since I started my blog, and told me they have an autoimmune disease.  I see this surge to be an epidemic in the medical community and we truly need to understand the how and the why behind it. Let’s dig deeper as to why there is a rise in autoimmune- and how we can attempt to minimize it.

          What is autoimmune?

          How about a simple formula?

          Genetic predisposition + environmental trigger + intestinal permeability = autoimmunity

          With this formula we can control 2 out 3 of these, thus preventing autoimmunity and the development of autoimmune disease.  When we put all three factors together we obviously get autoimmunity.  Autoimmunity is when the immune system is directed at a self-antigen or self -tissue.

          Remember, autoimmunity is the mechanism, but autoimmune disease is the disease that results from the mechanism when a tissue or organ is being destroyed.

          So, I want to start by defining a few key players in the immune system:

          • Antibodies: proteins that are made by the immune system that bind to foreign material and fight them
          • B-cells: are responsible for making antibodies
          • T-cells – have 2 subtypes, CD4 (helper cells) and CD8 (killer cells). CD4 helpers are telling all the other cells what to do.
          • Antigen- a toxin or other foreign substance which induces an immune response in the body
          • Macrophage – Macro means big and PHAGE means eater, so we have our big eater cells- and they pretty much each anything.
          • Cytokines – large groups of proteins and peptides that are secreted by cells in the immune system and work as messengers to regulate immunity and inflammation

          Let’s start at the root of how we develop immune cells within the body.  Usually when B and T cells are made in the bone marrow they go through a testing process while they are STILL in the bone marrow. If they are specific for self, they kill themselves- this is autoreactive, and obviously meant to protect us from developing an autoimmune disease. This process is called CENTRAL TOLERANCE. Clearly our fascinating human body has a mechanism to control for autoimmunity, so what’s the problem… why do we see a continuous rise?  Well, let’s start with focusing on the complexities of the body and how things can go wrong.

          While our body has a mechanism to automatically kill immune cells that are specific to self tissue, some of the cells escape tolerance before dying off!!!

          Because this happens we need a SECOND mechanism for tolerance. What this means is we basically need TWO signals to activate a T-cell.

          The first signal is when a macrophage presents an autoimmune antigen to a T-cell.

          The second signal is when CD 86 on the macrophage binds to CD 28 on the T-cell.

          Let’s talk about how we get CD-86…. If a pathogen or virus enters the blood stream, that signals danger to our macrophage and so it sends out the troops (CD-86) and puts CD-86 on it’s surface. Basically, it’s like its waving the white flag to our T-cell, and so it activates the T-cell to attack. If we don’t have CD86 the T-cell will just die off

          So what’s the difference between autoimmunity and inflammation… Let’s break that down:

          Inflammation Autoimmune disease
          Non-specific innate immune system involved Specific immune system involved
          Macrophages, neutrophils and mast cells – produce pro-inflammatory cytokines IL1, IL6 and TNF-alpha Activates B cells and T cells – produce IL17 and TH1 and IFN gamma autoantibodies produced to specific antigens
          We get tissue damage as a result of chronic inflammation We develop autoimmunity as a result

          Again…. Not only do we want to know What is autoimmune…. but how do we get autoimmune disease?


          Let’s dig in and summarize three mechanisms:

          1. Preferential tolerance: preventable
          2. Bystander effect: nothing you can do to prevent this
          3. Molecular mimicry: nothing you can do to prevent this

          Let’s start with the complex mechanisms that explain…. what is autoimmune?

          Bystander effect, what does that actually mean? Well, really it is what it sounds like. In this case we get extra CD-86 which keeps the T-cells turned on. Your body is fighting something foreign and your SELF gets in the way and your body fights BOTH as a bystander.  This is the most common mechanism of how we get autoimmune disease.

           This happens when your body simultaneously responds to a foreign antigen-VIRUS and self antigen… YOU!

           As a response to a virus our body signals danger to our macrophages who are like little monsters that are released to eat up the bad guys.  Macrophages are always eating things, but when it eats a SELF antigen you have a problem.  The macrophage can then present this self-antigen to our immune system, and if your immune system is already turned on due to an infection – it may see that antigen with a danger signal and respond. As a result, the body is attacking itself as well as the virus. This is why we call this a BYSTANDER effect.

           The second mechanism that helps us get to the root of answering, what is autoimmune is….


          Molecular mimicry: this is when a foreign antigen (virus) imitates a self-antigen causing the immune system to think its attacking something foreign when really, it’s attacking itself.

          Lastly, stressors and mental emotional problems can trigger autoimmune disease.  Let’s talk about how anxiety can trigger autoimmunity.  High levels of anxiety increase IL-6 levels resulting in an increase in TNF-alpha. There are pro-inflammatory cytokines that result due to inflammation. Now in a normal situation, your T-cells that are self-specific SHOULD be producing TGF-Beta, but in the presence of IL-6 and TNF-alpha- instead of producing TGF-beta which is protective, the T-cells actually produce TH-17 which is pathogenic or BAD! 

          An additional contributor to development of autoimmune disease has to do with the hormone cortisol.  In normal conditions, our cortisol levels peak when we wake up and slowly drop throughout the day until it’s time for bed and that’s how we go to sleep.  In some individuals, who lead highly stressful lifestyles, have a flat lined cortisol level, and they never get that peak. That is a BIG problem! That peak is essential to regulating our immune system, because this is another mechanism by which autoreactive cells die. When we get that peak first thing in the morning, our body kills off those autoreactive cells that escape the bone marrow.  Without that peak because of imbalanced hormonal function, those autoreactive t-cells can get into the periphery and cause autoimmune disease.

          So now that we have answered WHAT IS AUTOIMMUNE – the question is why are we seeing such a rise and increase in incidence of autoimmune?

          A main reason is because of how closely the gut effects the immune system, this is hypothesized as the primary reason for the growing epidemic in developing autoimmune disease.  Our gut microbiome is responsible for producing TGF-beta (Remember that is protective and balances our immune system).  We know that TGF-Beta is the primary cytokine that keeps autoimmune disease under control.  If we have leaky gut, or an altered gut function we reduce TGF-Beta and thus alter that mechanism that controls autoimmunity.


          So, lets focus on 5 preventable and modifiable risk factors that can lead to autoimmune development:

          1. Dietary habits: For people who are eating a standard American diet – the prevalence of autoimmune disease is elevated. This diet is high in processed foods, additives, high in sugar and trans fats, and promotes inflammation.
          2. Environmental surrounding: We have changed our lifestyle and spend majority of our time indoors leading to very low vitamin D levels- we will talk more about this in future posts on vitamin D and its relation to immunity.
          3. Too clean – we are so scared of dirt! We don’t garden anymore so we have no exposure to soil bacteria. Everyone is so worried about “getting sick” that vwe are getting even more sick! Our infectious habits have changed.
          4. Pollution – more chemical exposure in our atmosphere, in our food supply, diesel exhaust, personal care products, makeup.
          5. Excessive stress: This will continue to impact autoimmunity through various mechanisms. Our lives have become so fast paced and high stress.


          It’s important to understand the underlying mechanisms of the immune system and how autoimmune develops.


          How can we manage our disease if we don’t understand what is autoimmune?


          All in all, we talked about the mechanisms by which autoimmune disease develops. While we can’t alter our genetic predisposition to autoimmune disease, we can certainly change its expression.  We have the ability to control and prevent or delay the onset.  When you think about the question we are answering, WHAT IS AUTOIMMUNE, I want you to remember the simple formula we talked about early on:


          Genetic predisposition + environmental trigger + intestinal permeability = autoimmunity


          Keep in mind the environmental triggers we discussed and exposure to various toxins that can alter our immune health. But just as important, gut health is key! Majority of our immune system begins in the gut, so what we expose to our intestinal environment impacts overall health prevention and disease development.  When you hear the phrase, you are what you eat, it’s true! Eat healthy, vegetables that are lively and full of nutritious benefits- then you will be the same, Lively and nutritious!  Eat processed foods full of chemicals and garbage, your body will feel like garbage, be sluggish and be more prone to developing disease.


          Autoimmune disease is on the rise and unfortunately will continue to rise because of our ever changing and convenient lifestyle we have created as human beings. Keep educating yourself and implementing what you learn. I am an avid believer that even the slightest change will make a difference. We can only control what we can control- so take your health into your own hands and make a change. Stop your disease before it stops you, and if you have already developed it and understand how it came to be- take control and delay progression. Balance your overall health with nutrition and medicine and live your best life!


          Subscribe below to get my summary of the top infections that have been correlated to autoimmune disease. Be aware of what these infections are and balance your immune system.  Remember how autoimmunity develops and how it impacts our immune system.  Stay tuned for a summary on how to boost our immune system and prevent the development of autoimmune disease!