Pregnancy and Autoimmune: How does it relate?

Pregnancy and Autoimmune: How does it relate?

This topic is near and dear to my heart as many of my conditions developed during or after pregnancy.  There is such a strong connection between the immune system and the endocrine system (hormones), and a reason why autoimmune conditions are so highly prevalent in women.  Before I begin to talk about the details, I want to give you a basic explanation of the immune system, which can be quite complex.  To try to simplify it, we have two major pathways:

  1. Cellular immunity (T-helper 1) 
  2. Humoral immunity (T-helper 2)

T-helper cells are a type of cell within the immune system that when they are activated signal other immune cells to “attack” the invader.  They are categorized differently based on how they are activated and what they release to kill:

  • Th1 pathway is activated by intracellular organisms and secrete certain immune cells to kill the organisms.
  • Th2 pathway is activated in response to antigenic stimuli from an extracellular organism and leads the body to secrete a different set of immune cells, and support the function of antibody-producing B cells.

Evidence has accumulated from animal models and human studies to suggest that Th1 cells are involved in the development of organ-specific autoimmune diseases, such as Hashimoto’s, MS, rheumatoid arthritis, and type 1 diabetes.  In these conditions Th1 is considered pathogenic or “bad” whereas Th-2 cells are more protective.  By contrast, Th2-cell predominance was found in patients with lupus, atopic dermatitis, and allergic diseases.

So why am I bringing all this up and how does it relate to pregnancy?

Levels of estrogen before and after menopause and levels of estriol and progesterone during pregnancy appear to affect autoimmune diseases.

Estrogen appears to push the immune system in the direction of the proinflammatory Th1 pathways, EXCEPT during pregnancy.  Because pregnancy is actually a high-estriol/high-progesterone state, estriol, functionally a weak estrogen, and progesterone clearly has anti-estrogen properties – we actually see an improvement because estrogen levels are actually low.  This is the potential reason why autoimmune diseases that involve over-expression of Th1 (e.g., rheumatoid arthritis, multiple sclerosis) frequently “go away” during pregnancy but “come back” during postpartum periods.

Thus, pregnancy appears to represent a unique situation for the immune system, switching from a Th1-dominant environment to an often Th2-dominant environment.

Although it has been almost universally held that pregnancy is a “high estrogen state,” it is in fact a time when ovarian production of hormones is suppressed and placental production of estrogens, primarily estriol, and progesterone is high. Estriol may block the effects of estradiol on the mother’s immune system, just as it blocks the negative effects of estrogen for the fetus. Progesterone has been shown to stimulate the Th2 system, which is responsible for activating B-cells and down-regulating Th1.

Rheumatoid Arthritis and MS improve during pregnancy as estriol and progesterone may function to inhibit presentation of antigens to Th1 cells, and increases the death (apoptosis) of activated immune cells.  Lupus a disease of up-regulated Th2, is variable in its response to pregnancy, sometimes getting better but often getting much worse.

In some autoimmune diseases, estrogen is thought to have a dual effect, where too much or too little estrogen may be equally detrimental to the normal functioning of the immune system. In any event, it would appear that the relationship of estrogen to diseases of autoimmunity is complex and not fully worked out at this point, and the presence of an estrogen-dominant environment that we live in further complicates the immune system’s attempts to shut down the reactive furnace.

This is why I try and avoid estrogens as much as possible with my Hashimoto’s as I don’t want to exacerbate the response!


Druet P, Sheela R, Pelletier L. Th1 and Th2 cells in autoimmunity. Clinical And Experimental Immunology[serial online]. July 1995;101 Suppl 1:9-12.

Jones, D. et al.  Institute for Functional Medicine (2010).  Textbook of Functional Medicine. Gig Harbor, WA.: Institute for Functional Medicine.

Zhang P, Chen H, Tu Y, et al. Analysis of Th1/Th2 response pattern for erythrodermic psoriasis. Journal Of Huazhong University Of Science And Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban [serial online]. August 2014;34(4):596-601

Is Estrogen bad for you?

Is Estrogen bad for you?

Estrogen, Estrogen…… I need you and I hate you all at the same time!

We talked about the effects of soy as an estrogen like compound on our bodies, but I didn’t really get into the complexity of this hormone.

Did you know that estrogen needs to be detoxified in our body through the same phase 1 pathway as drugs, toxins, and various food substances we ingest?

Our body really only needs a very small amount of estrogen in the body to function and communicate with other hormones. As a result, the body views estrogen as a potentially dangerous toxin and needs to get rid of it, in excess.

Estrogen is metabolized through three reactions.

  1. Liver enzyme, 1A1 which takes Estrogen —> E2 (2-OH)
  2. Liver enzyme, 1B1 which takes Estrogen —>E4 (4-OH)
  3. Liver enzyme, 2C which takes Estrogen —>E16 (16-OH)

This is complex so I’m going to do my best to simplify.

But I needed you to know the root of this so you can understand the rest…..

So let’s put this together.

These three molecules have the same dangerous potential as other phase I detoxification by-products.  They must therefore be rapidly detoxified using a number of phase II pathways. Because of the large number of P450 SNPs (single nucleotide polymorphisms), there is great variation in the human population. The differences in our bodies ability to detoxify in different proportions of 2E, 4E, and 16E have shown to potentially predict risk of different estrogen-related diseases, such as breast cancer.

As we’ve discuss before, different environmental factors have an impact on our liver enzymes and their ability to detoxify.  For example, we recently talked about Brassica vegetables and indol-3-carinol (I3C).  This compound I3C found in these vegetables actually boosts liver enzyme 1A1 to breakdown estrogen to the 2E metabolite.  On a different note, enzyme 1B1 that breaks estrogen to 4E metabolite, can be boosted or slowed down.  Chemicals in cigarette smoke can actually slow this down which would cause higher levels of estrogen in the body.  Ginseng is an herb that has also been showed to slowdown the ability to break down estrogen.  Lastly, the 2C enzyme actually converts to the strongest bi product 16E, and various drugs have an impact on this pathway.


So, you guys should understand detox goes through 2 pathways, phase 1 and phase 2.  We have described all the phase 1 metabolites that are formed, 2E, 4E, and 16E – well we still need to get rid of these so they don’t effect our hormones. That‘s done by Phase 2….

There are a lot of toxins that have been identified as “endocrine disrupters” that impact that bodies ability to do this.  I have experienced this on a number of occasions with protein shakes and protein bars! I’ve literally missed a period for 3 months after consuming protein bars daily for a week, wow!

So these toxins, can cause a higher ratios of 4E and 16E to be floating around our body. Why do we care, 4E is DNA damaging and 16E is a stronger metabolite with estrogen properties than estrogen itself.


 What kind of toxins… Well let’s start with pesticides

Pesticides were found to significantly increase the ratio of 16E to 2E. Additionally, flame retardants like Tetrabromobisphenol (BFR), act as endocrine disruptors due to estrogen like properties.  Investigators suggest that the ratio of 16E to 2E may provide a marker for analyzing breast cancer risk and for generating preventive nutritional strategies and interventions.

Due to structural similarities to Estradiol (E2), phytoestrogens found in soy bind to E2 receptors and can act as endocrine disruptors and produce adverse health effects (Rietjens et al., 2013)

Some of these enzymes detoxify estrogen at the 2 position, and others act at the 16 position.   There is thought that environment chemicals we ingest change the way our liver communicates with our body resulting in estrogen to be “detoxified” at the 16 position – which is the most harmful form.

This could explain why postmenopausal women with the highest circulating estradiol (E2) levels have the greatest frequency of breast cancer- although this isn’t conclusive.

Remember that very small amounts of estrogen appear to have large effects and that estrogen is viewed by the body as a toxin. 

From what we understand about detoxification in our body, it is important to not only keep our liver healthy so that we can metabolize the excess estrogen initially, but to eat and continue to replenish are necessary cofactors for phase 2 detox with plant based foods!

Intermittent Fasting and Athletic Performance

Intermittent Fasting and Athletic Performance

Intermittent fasting has gained popularity over the last several years. Understanding the mechanism by which the various macronutrients, metabolic parameters, and inflammatory markers are impacted by a fasting state, provides us greater insight into why we’ve seen an increase in this method of eating.  In addition, while the physiology of fasting has been scientifically demonstrated, it’s important to also gain an understanding of the impact on athletic performance and recovery.  Important parameters of intermittent fasting on athletic performance include weight loss, maintenance of muscle mass, and post exercise metabolism due to decreases in glycogen stores, low levels of insulin, increase in hormones responsible for lipolysis (fat breakdown), and an increase in free fatty acids (Paoli 2019, Gieske 2018).




Time-restricted eating or intermittent fasting is defined as an intake of food within a specified eating window that ranges from 3 to 12 hours daily.  Based on the research, the benefits of time restricted eating are observed when food intake is limited to a 6 to 9 hour eating window (Paoli 2019).  This method of eating is considered to have the potential for significant fat loss as it is associated with an increase in fat metabolism (Smith 2017).  Additionally, it has demonstrated improvements in various metabolic parameters such as reduction in total and LDL cholesterol and blood pressure (Malinowski 2019, Paoli 2019).  Other protocols include eating for a 24-hour period, followed by a 24 hour fast repeated 2 to 3 times a week (Malinowski 2019). The benefits of this protocol that have been observed include reducing visceral fat, increasing adiponectin, reduced LDL and leptin concentrations (Malinowski 2019).

A study done on mice compared 2 groups that ate either in an 8-hour window versus a 24-hour window over a 100-day period.  Both groups consumed the same amount of food, which is an important control factor in the study.  With that being said, in contrast to the mice that ate in an open eating window, those mice that ate within the restricted eating window were resistant to the development of obesity as well as other health biomarkers.  In addition, the restricted eating mice maintained a lower respiratory exchange ration which correlates to an increase in fat metabolism (Smith 2017).  With more than just a focus on weight loss, many athletes strive for overall improvement in body composition. The ultimate goal is to not only decrease fat mass, but to also increase muscle mass to improve athletic performance.  As it pertains to intermittent fasting, mixed results are reported regarding the ability to maintain lean body mass, and not negatively impact overall strength and lean body mass (Tinsley 2017).  




Time restricted feeding has been of special interest in sports and athletics because of reports that demonstrate its ability reduce weight and maintain muscle mass (Malinowski 2019).  A study by Moro et al. compared 2 groups of athletes that consumed their daily energy intake in either an 8-hour eating window or a 12-hour eating window.  What the results showed after 8 weeks was a decrease in fat in the time restricted eating group (TRF) compared to the normal diet group. However, the most favorable outcome was that while the TRF group lost more fat, both groups maintained the fat-free mass and muscle area of the arm and thigh. This demonstrates that TRF can reduce fat mass, while maintaining muscle mass (Moro 2016).  In addition to maintaining muscle and improving overall body composition, it is essential to understand the effects of time restricted eating in athletes on physical performance and endurance (Real-Hohn 2018).




While intermittent fasting and time restricted eating have gained popularity, it is important for athletes to appreciate how implementing this change in eating impacts metabolic adaptations, body composition, physical performance and overall endurance, and recovery.  For the majority of athletes, there is an overarching goal to reduce fat mass and improve body composition, while increasing overall lean muscle mass and athletic performance.  Recently it has been demonstrated that intermittent fasting combined with athletic training allows athletes to achieve this desired outcome, and additionally improves various metabolic parameters that have an effect on post exercise metabolism and recovery.


In reviewing the effect of fasting on fat oxidation it’s important to review the methods of fat oxidation.  There are 2 methods to fat oxidation, either through fasting intervals between meals or during aerobic exercise at a VO2 max of 45-55%.  This aspect is important for endurance athletes as the balance between lean body mass and fat mass is necessary to improve and maximize performance. When an athlete employs both of these strategies the question is whether we expect to see an additive effect or not.  Fat is a major fuel source during exercise when in a fasted state. With that being said, exercise intensity plays a critical role in the level of fat metabolism.  An analysis by Vicente-Salar et al. noted that at moderate to high intensity exercise, plasma free fatty acids were higher in the fasting group versus the fed group after 90 minutes of exercise.  Based on these findings the authors don’t support the notion of training while fasting to improve body composition and reduce fat mass. (Vicente-Salar 2015).  Additionally, a study done in wistar rats, compared endurance training for 40 minutes 5 days a week for 6 weeks while fasting to those that did not.  The results demonstrated and increase in the reduction in body weight and reduced fat content in the intermittent fasting group while exercise versus in those that did not exercise. Unfortunately, they did not measure lean fat mass to assess the impact on lean fat mass composition (Moraes 2017).  Fortunately, Tinsley et al. looked at the effects of time restricted eating in young men performing resistance training and its impact on lean fat mass.  The study was broken out into 2 groups, one that did resistance training with a normal diet and one that followed a time restricted diet. Those in the study group, did the restricted eating plan on the 4 days of the week where they were not performing resistance training. The restricted eating parameters consisted of a 4-hour window between 4:00 p.m. and midnight in which participants consumed their daily caloric intake.  Overall the study found that those in the time restricted group consumed an overall 667 fewer calories and a reduced intake of macronutrients across the board.  There were no significant changes in body weight or total body composition in either group over the course of 8 weeks. While this study does not demonstrate a benefit overall in athletic performance in the fasting group a major limitation is that the time-restricted group had no limitation or requirements on foods consumed.  This study also found that the restricted eating did not lead to any reduction in lean soft tissue, although it also hindered any growth observed as a result of resistance training.  Despite the lack of increase in lean tissue overall in the restricted eating group, it was found that muscular strength and endurance were equivalent or better than those following the normal diet (Tinsley 2017).  In order to truly assess the impact on lean tissue growth, there would need to be a standardization of appropriate macronutrient intake to maximize performance and assess a restricted eating state.  A key factor in maintaining athletic performance in a fasted state versus fed state is ensuring the macronutrient composition and energy intake it maintained (Chaouachi 2012).


In assessing the impact of endurance on fasted exercise, a study by Real-Hohn at al. tested the metabolism adaptations and the synergy of high-intensity exercise and intermittent fasting, the researchers found improvements in endurance and energy production.  The reported improvements in endurance were double in the fasting group versus the non-fasting group.  The intermittent fasting group that performed high intensity interval exercise presented significantly lower levels of NAD(P)H. This finding aligns with the notion that a lower level of NAD(P)H results in higher mitochondrial oxidation rate.  An additional measurement included mitochondria respiratory control rate (RCR), which is high in a healthy mitochondrion.  The results demonstrated improve oxygen flux and ATP production in the fasting groups that was statistically significant (p<0.05).


Of additional interest is to not only look at the effects of feeding state on endurance athletes, but its impact on high intensity interval training.  Sprint interval training (SIT) is a common mechanism in performing exercise training to improve VO2max, endurance performance and muscle metabolism.  Rocha da Silva et al. found no significant different when assessing SIT in the fasting versus fed state on parameters of peak, mean, and minimum power (2018). However, when assessing VO2, it was found to be higher, 60 minutes following SIT, in the fasted versus fed state.  Additionally, in the fasting state, respiratory exchange ratio (RER) was higher in the first 30 minutes post exercise, but lower 40-60 minutes post-exercise.  RER was higher across the board for those in the fed state.  This indicates that in the fasted state, fat was the main source of fuel, as opposed to the fed where glucose was the main source with an RER reported closer to 1.  Additionally, based on the findings one can conclude that while there isn’t a conclusive difference in overall performance in the fasting versus fed state, the fasting state stimulated a higher level of fat oxidation that occurred for 30 minutes post exercise (Rocha da Silva 2018).  Based on several reports the mechanism of fat oxidation from the fasted state seems to be most prominent in the post-exercise phase as opposed to during exercise.


It has been suggested the ingesting protein immediately before exercise may have a beneficial effect on post exercise energy expenditure, with an increase in fat oxidation and resting metabolism.  Gieske et al. looked at the effects of casein versus whey protein taken immediately before exercise in the fed state compared to a fasting individual to assess if a difference exists.  Interestingly, the results did identify an appreciable difference between the effects of exercise in the fasted state versus pre-exercise casein protein supplementation.  While this is one factor that demonstrates this difference, it’s important to compare all aspects of the benefits in each eating protocol (Gieske 2018). Also, a systemic review found that in exercise performance that lasts for >60 minutes, pre-exercise feeding enhanced performance as opposed to those in the fasted state (AIrd 2018).

In addition, to understanding the impact on how intermittent fasting effects metabolic parameters, the impact on anaerobic power and exercise performance is critical to know for athletes.  Nashrudin et al. observed the effects of intermittent fasting over a 10-day period to assess the bodies adaptation to the changes in dietary regimen.  They utilized Wingate anaerobic (WT) and prolonged high intensity time to exhaustion cycling test (HIT) to observed the effects of intermittent fasting versus a control group.  This study findings are critical in that it found that intermittent fasting reduced WT at day 2, and by day 4 performance returned to normal state. In addition, time to exhaustion (TTE) was decreased throughout the study period (10 days), but they began to observe a trend of recovery towards the end of the study period.  This is an important finding for athletes, to manage expectation of the impact on performance that will observed initially, and that continuous dietary restrictions through intermittent fasting beyond 10 days are important to see a long-standing effect (Nashrudin 2018).



In addition to its impact on athletic performance as measured by time to exhaustion as well as other parameters, fasting has also demonstrated an impact on inflammatory markers.  Fasting has a positive impact on inflammation as observed through a reduction in NF-Kappa Beta, which could potentially translate into improved recovery in some athletes (Paoli 2019).  An additional study found that pro-inflammatory factors homocysteine, interleukin-6, C-reactive protein were all reduced in 40 healthy participants that fasted intermittently during Ramadan (Malinowski 2019). Oxidative stress markers are also important factors in post exercise recovery, and it is implied that intermittent fasting combined with high intensity interval training demonstrates an additive and synergistic effect on oxidative stress markers (Real-Hohn 2018).


conclusion on INTERMITTENT FASTING in athletic performance


It is well known that nutrition and the impact on exercise metabolism and performance are continuously evolving with additional mechanisms to reach optimal impact.  As fasting exercise has produced an interest in athletes with is various observed benefits, it’s vital to break down the findings and extrapolate across the general population.  The data has clearly demonstrated that in a fasted state our primary source of energy is fat, as we shift from glycogenolysis, with an upregulation in fat oxidation.  Time-restricted eating has ample potential for fat mass loss because of what appears to be an associated up-regulation of fat metabolism. In comparison to maintaining an energy deficit chronically, this approach represents a lifestyle that is likely more sustainable (Smith 2017).  Also, the evidence is clear as it relates to other metabolic parameters, such as total and LDL cholesterol, blood pressure, and glucose levels, in that a benefit is clearly observed.

When assessing the benefits of intermittent fasting specifically on athletic performance and recovery, the data does not exhibit a benefit in this state. The data demonstrated minimal improvements in exercise performance, where most studies concluded equivalency.  This is a positive finding, in that we know there isn’t a negative effect as long as exercise performance was maintained at <60 minutes.  Based on the available research, when comparing endurance exercise versus high intensity interval training (HIIT), no significant differences in performance measures were observed in HIIT.

All in all, intermittent fasting in athletes demonstrates a beneficial impact on metabolic parameters and an increase in lipid oxidation, however, does not demonstrate an improvement in athletic performance and recovery.  It is important to note while the findings did not support improvement in athletic performance, a negative outcome was also not observed. Rather, in a fasted or fed state the results across the data were similar for performance and recovery.

Aird TP, Davies RW, Carson BP. Effects of fasted vs fed‐state exercise on performance and post‐

exercise metabolism: A systematic review and meta‐analysis. Scandinavian Journal of Medicine & Science in Sports. 2018;28(5):1476. Retrieved from: LINK


Chaouachi A, Leiper J, Chtourou H, Aziz A, Chamari K. The effects of Ramadan intermittent fasting on

athletic performance: Recommendations for the maintenance of physical fitness. Journal of

Sports Sciences. 2012;30(Supp 1):S53-S73. Retrieved from: LINK


Da Silva CR, Santana PV, Mendes PC, et al. Metabolic and cardiorespiratory acute responses to fasting

versus feeding during high-intensity interval training. Sport Sciences for Health.

2018;14(2):347. Retrieved from: LINK


Gieske BT, Stecker RA, Smith CR, et al. Metabolic impact of protein feeding prior to moderate-intensity

treadmill exercise in a fasted state: a pilot study. Journal of the International Society of Sports

Nutrition. 2018;(1). Retrieved from: LINK


Malinowski B, Zalewska K, Węsierska A, et al. Intermittent Fasting in Cardiovascular Disorders-An

Overview. Nutrients. 2019;11(3). Retrieved from: LINK


Moraes RCM de, Portari GV, Ferraz ASM, da Silva TEO, Marocolo M. Effects of intermittent fasting and

chronic swimming exercise on body composition and lipid metabolism. Applied Physiology,

Nutrition & Metabolism. 2017;42(12):1341-1346. Retrieved from: LINK


Moro T, Tinsley G, Bianco A, et al. Effects of eight weeks of time-restricted feeding (16/8) on basal

metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in

resistance-trained males. Journal Of Translational Medicine. 2016;14(1):290. LINK


Naharudin MNB, Yusof A. The effect of 10 days of intermittent fasting on Wingate anaerobic power and

prolonged high-intensity time-to-exhaustion cycling performance. European Journal of Sport Science. 2018;18(5):667-676. Retrieved from: interlibrary loan


Paoli A, Tinsley G, Bianco A, Moro T. The Influence of Meal Frequency and Timing on Health in Humans:

The Role of Fasting. Nutrients. 2019;11(4). Retrieved from: LINK


Real-Hohn A, Navegantes C, Ramos K, et al. The synergism of high-intensity intermittent exercise and

every-other-day intermittent fasting regimen on energy metabolism adaptations includes

hexokinase activity and mitochondrial efficiency. PLoS ONE. 2018;(12). Retrieved from: LINK


Smith ST, LeSarge JC, Lemon PWR. Time-Restricted Eating in Women – A Pilot Study. Western

Undergraduate Research Journal: Health & Natural Sciences. 2017;8(1):1. Retrieved from: LINK


Tinsley GM, Forsse JS, Butler NK, et al. Time-restricted feeding in young men performing resistance

training: A randomized controlled trial. European Journal of Sport Science. 2017;17(2):200-207. Retrieved from: LINK


Vicente-Salar N, Urdampilleta Otegui A, Roche Collado E. Endurance Training in Fasting Conditions:

Biological Adaptations and Body Weight Management. Nutricion Hospitalaria. 2015;32(6):2409-

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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!