Boswellia Serrata - An Anti-inflammatory Supplement

[katabasis]

Around two weeks ago, I started taking Boswellia Serrata for my ME/CFS and it’s had some significant positive effects on my fatigue. I’ve seen this supplement mentioned before on these forums, but I figured I would share some of the facts I have learned about it (and theories I have come up with) in a more condensed form. I’d love for other people to look over my reasoning, since I am no biochemistry expert, and to share their own experiences with Boswellia.

Boswellia Serrata, also known as Indian Frankincense, is a species of resinous plant native to India and Pakistan. This plant’s gum resin plays a role in Ayurvedic Medicine, and more recently, Boswellia extracts have been shown to be effective for a variety of inflammatory conditions. The active components of Boswellia extract include derivatives of boswellic acid, especially 3-O-acetyl-11-keto-beta-boswellic acid (AKBA), as well as various terpenoid compound derivatives like acetyl-lupeolic acid, incensole acetate, serratol, and thujene.

The primary in vivo studies which show a statistically significant benefit from Boswellia in inflammatory conditions focus on osteoarthritis and asthma. The former study uses ‘5-Loxin’, which is a brand of extract standardized to 30% AKBA. Bioavailability of AKBA is poor, so I use the ‘SuperiorLabs’ brand which is standardized to 65% boswellic acids and also includes piperine, which has been shown to improve bioavailability. There is also another brand, ‘Aflapin’ which appears to improve its bioavailability by recombining AKBA with nonvolatile oils from the Boswellia plant.

I got the idea to try Boswellia after my ME/CFS doctor (Dr. Susan Levine) recommended I try fenofibrate. Her research (covered in this thread) has found evidence of dysregulation in the inflammatory pathways which utilize lipid inflammatory mediators. Fenofibrate is a PPAR-alpha agonist, which enhances lipolysis, and her rationale for why it may benefit ME/CFS sufferers is that by increasing the availability of fatty acids, the synthesis of anti-inflammatory compounds like resolvins and HEPE will be increased. However, after taking fenofibrate for only three days, its gastrointestinal side effects were too much for me - severe abdominal pain, diarrhea, and bloating. GI side effects are not uncommon with this drug, and I have a lot of GI issues - both in the IBS/motility spectrum as well as a recent brush with severe C. Diff for which I needed to receive an FMT. I stopped taking fenofibrate, and then tried palmitoylethanolamide, a supplement which also activates PPAR-alpha. I ended up having a similar reaction, though less severe.

I did some investigation, but there isn’t a lot of information in the literature about why fenofibrate causes these side effects. However I began to speculate - the lipid inflammatory mediators that fatty acids are used to synthesize include not only anti-inflammatory compounds but also pro-inflammatory compounds like leukotrienes, 5-HETE, 5-oxo-ETE, etc. Perhaps if increasing lipid inflammatory mediator synthesis was worsening my symptoms, reducing lipid inflammatory mediator synthesis would alleviate them. After a little digging, I found that Boswellia extract, particularly due to AKBA, is an inhibitor of 5-lipoxygenase (5-LOX), one of the enzymes which converts fatty acids to lipid inflammatory mediators, which prompted me to try purchase some.

5-LOX inhibition is not the only way by which Boswellia extract exerts its anti-inflammatory properties. AKBA also inhibits NF-kappa B, a cellular receptor regulating inflammatory and immune responses. Activators of NF-kappa B include TNF-alpha, reactive oxygen species, IL-1 beta, and bacterial LPS - all factors which have significant notoriety in ME/CFS discourse. AKBA also may actually bind directly with LPS. And finally, it turns out that incensole acetate, one of Boswellia’s terpenoids, inhibits the expression of TNF-alpha, IL-1 beta, and other cytokines, though most supplements do not appear to standardize for this compound.

After taking Boswellia extract for two weeks, I have noticed a significant reduction in my fatigue and PEM. I can withstand more mental and physical exertion without causing a crash, and when I do crash, it does not last long nor does it feel as catastrophic. The extract doesn’t seem to cause any side effects, and if anything my GI problems have been slightly better. I have always noticed a connection between the severity of my GI symptoms and the severity of my ME/CFS symptoms, and it seems to make sense that something that attenuates inflammation relating to LPS would benefit me. I also suspect that I may have some low-level autoimmunity in the gut - I have HLA-B27, high AMCA, high TNF-alpha, and high Ruminococcus gnavus, which may suggest Crohn’s, though my scopes have all been more or less normal. Nonetheless, Boswellia affects various inflammatory mediators that would have significance to that kind of issue.

It’s still a bit early to say whether these gains will have any staying power, but I can’t help but be optimistic. I would say that it’s worth a shot to try Boswellia Serrata extract, especially if you have hard evidence of inflammation from cytokine panels, or suspect autoimmune or GI involvement.

 

[Judee]

What brand are you using, @katabasis?

I take Source Natural's and that does seem to help with brain inflammation.

Also how often and at what dose are you taking it?

Thank you.

 

[katabasis]

What brand are you using, @katabasis?

I take Source Natural's and that does seem to help with brain inflammation.

Also how often and at what dose are you taking it?

Thank you.

I take SuperiorLabs Boswellia Extract. One serving contains 500 mg extract standardized to 65% boswellic acid, 100 mg L-leucine, and 7.5 mg BioPerine, and I have been taking two servings per day.

 

[Pyrrhus]

5-LOX inhibition is not the only way by which Boswellia extract exerts its anti-inflammatory properties. AKBA also inhibits NF-kappa B, a cellular receptor regulating inflammatory and immune responses. Activators of NF-kappa B include TNF-alpha, reactive oxygen species, IL-1 beta, and bacterial LPS - all factors which have significant notoriety in ME/CFS discourse. AKBA also may actually bind directly with LPS. And finally, it turns out that incensole acetate, one of Boswellia’s terpenoids, inhibits the expression of TNF-alpha, IL-1 beta, and other cytokines, though most supplements do not appear to standardize for this compound.

Thanks for this very helpful information!

I have heard Boswellia mentioned multiple times here on Phoenix Rising, but I wasn't sure of its mechanism of action.

 

[Learner1]

Thanks @katabasis for highlighting this great supplement. This is another article that describes it's various benefits.

https://www.sciencedirect.com/science/article/pii/S2225411016301961

I use Thorne Boswellia for brain inflammation from IVIG, up to 4g daily.

 

[Oberon]

@katabasis

You may very well still have Crohn's even if your Colonoscopies and Endoscopies have all come back normal. I saw multiple GI doctors and had 3 colonoscopies and over the years and they all came back normal. I also had abdominal CT scans which came back clear.

I also never had any bleeding which is one of the first signs they look for, but I had enough G.I. symptoms and my Fecal Calprotectin test came back elevated multiple times. One doctor finally said let's try a capsule endoscopy. Well wouldn't you know it they found ulceration/Crohn's in an area that can only be properly seen with a capsule endoscopy.

I would consider asking your doctor for a fecal calprotectin test to see if you have elevated inflammatory markers. It's usually about $100.00 and is very specific for IBD. If you do have an elevated fecal calprotectin I would also consider a pill cam in case you're more of a rare case like me.
__________________
Since this is a CFS forum to those who are curious Crohn's treatments, i.e. TNF-A blockers did not help my CFS although I was never able to achieve full remission only somewhat a reduction of g.i. symptoms with treatment.

 

[Learner1]

@katabasis

You may very well still have Crohn's even if your Colonoscopies and Endoscopies have all come back normal. I saw multiple GI doctors and had 3 colonoscopies and over the years and they all came back normal. I also had abdominal CT scans which came back clear.

I also never had any bleeding which is one of the first signs they look for, but I had enough G.I. symptoms and my Fecal Calprotectin test came back elevated multiple times. One doctor finally said let's try a capsule endoscopy. Well wouldn't you know it they found ulceration/Crohn's in an area that can only be properly seen with a capsule endoscopy.

I would consider asking your doctor for a fecal calprotectin test to see if you have elevated inflammatory markers. It's usually about $100.00 and is very specific for IBD. If you do have an elevated fecal calprotectin I would also consider a pill cam in case you're more of a rare case like me.
__________________
Since this is a CFS forum to those who are curious Crohn's treatments, i.e. TNF-A blockers did not help my CFS although I was never able to achieve full remission only somewhat a reduction of g.i. symptoms with treatment.

Just curious... What did your stool test say? Any abnormal or missing bacteria? Any fungi, parasites or viruses? And nutrient deficiencies due to gut malabsorption?

If so, what did the doctor do then?

 

[katabasis]

@katabasis

You may very well still have Crohn's even if your Colonoscopies and Endoscopies have all come back normal. I saw multiple GI doctors and had 3 colonoscopies and over the years and they all came back normal. I also had abdominal CT scans which came back clear.

I also never had any bleeding which is one of the first signs they look for, but I had enough G.I. symptoms and my Fecal Calprotectin test came back elevated multiple times. One doctor finally said let's try a capsule endoscopy. Well wouldn't you know it they found ulceration/Crohn's in an area that can only be properly seen with a capsule endoscopy.

I would consider asking your doctor for a fecal calprotectin test to see if you have elevated inflammatory markers. It's usually about $100.00 and is very specific for IBD. If you do have an elevated fecal calprotectin I would also consider a pill cam in case you're more of a rare case like me.
__________________
Since this is a CFS forum to those who are curious Crohn's treatments, i.e. TNF-A blockers did not help my CFS although I was never able to achieve full remission only somewhat a reduction of g.i. symptoms with treatment.

I've actually had fecal calprotectin run a bunch of times, and it's always been below detection limits. You bring up a good point with capsule endoscopy though - I've had upper endoscopy, colonoscopy, and even MR enterography done, but I was talking with the consulting gastroenterologist when I was in the hopsital with C. Diff, and he mentioned that even MR enterography will sometimes miss mild inflammation, and that pill endoscopy is the only way to know for sure. I should probably ask my regular gastroenterologist about that, but the ME/CFS and more recently the C. Diff have taken higher priority.

I strongly suspect that there is something like a 'Crohn's disease variant' that results in little visible mucosal inflammation but lots of microbiome dysregulation and low-grade, systemic inflammation. Doctors are too quick to force things into discrete categories - most of them would say I have IBS, but there's such an obvious connection between my gut symptoms and my systemic symptoms (stuff like joint pain and fever which doctors usually wouldn't attribute to IBS).

 

[LINE]

Boswellia (frankincense) has broad spectrum microbe killing power.

 

[Learner1]

You bring up a good point with capsule endoscopy though - I've had upper endoscopy, colonoscopy, and even MR enterography done, but I was talking with the consulting gastroenterologist when I was in the hopsital with C. Diff, and he mentioned that even MR enterography will sometimes miss mild inflammation, and that pill endoscopy is the only way to know for sure. I should probably ask my regular gastroenterologist about that, but the ME/CFS and more recently the C. Diff have taken higher priority.

I strongly suspect that there is something like a 'Crohn's disease variant' that results in little visible mucosal inflammation but lots of microbiome dysregulation and low-grade, systemic inflammation.

None of the tests you mention look at microbiome composition. Regular gastroenterologists seem to look at intestinal issues as plumbing problems and totally miss the huge number of non-human cells that live inside our intestines that do essential tasks in our biochemistry as well as creating lots of mischief.

It might be quite interesting to run a Diagnostic Solutions GI Map, a Genova Diagnostics GI Effects or a Viome test, or all three to figure out what your microbiome might be doing to cause inflammation and symptoms. A functional medicine doctor could help you with this, though Viome is consumer-purchased.

Or, if you do have clostridium difficile, you might qualify for a fecal transplant which may help. This seems to be one of the only microbiome irregularities conventional GI docs recognize and will treat.

 

[katabasis]

one of the tests you mention look at microbiome composition. Regular gastroenterologists seem to look at intestinal issues as plumbing problems and totally miss the huge number of non-human cells that live inside our intestines that do essential tasks in our biochemistry as well as creating lots of mischief.

It might be quite interesting to run a Diagnostic Solutions GI Map, a Genova Diagnostics GI Effects or a Viome test, or all three to figure out what your microbiome might be doing to cause inflammation and symptoms. A functional medicine doctor could help you with this, though Viome is consumer-purchased.

Or, if you do have clostridium difficile, you might qualify for a fecal transplant which may help. This seems to be one of the only microbiome irregularities conventional GI docs recognize and will treat.

Sorry, I was a bit less than thorough in listing the scope of my tests and treatment. I've done a GI MAP and 3 different Thryve microbiome PCRs. There's definitely been evidence of dysbiosis, though no serious pathogens so much as opportunistic ones.

My most recent C. Diff recurrence was pretty severe, and was not totally responsive to vancomycin or fidaxomicin, so I ended up getting into an open label clinical trial for FMT. By all appearances, the FMT completely cured the C. Diff - no more watery diarrhea, no more colitic (i.e. constant, burning etc.) abdominal pain, negative toxin EIA. My post-FMT Thryve PCR shows a strikingly normal gut flora status - virtually no opportunistic pathogens out of range, and the strains in which I was severely deficient are all restored to normal or close to normal levels.

However, the FMT did not improve my ME/CFS symptoms. In fact, I feel like it may have actually worsened them. It is hard to fully disentangle the effects of the FMT from the after-effects of the C. Diff - the stress of the infection, the starvation diet, the exertion that frequent bowel movements entail - but two new symptoms occurred right after the FMT that weren't present even during the C. Diff. First, I started getting hives on a daily basis, and second, I was only able to sleep 90 minutes at a time. I started taking ketotifen for the hives, and more recently Boswellia has really helped all my symptoms. But despite resolving the C. Diff, I still seem to have a lot of GI issues that fixing my microbiome didn't seem to help.

 

[Learner1]

Thanks for explaining further. That must be frustrating to go through so much and be where you are. FMTs are Not perfect and when you're adding someone else's bacteria to your own, unpredictable things can happen even though they are carefully screened and only given in certain situations.

I have found Viome to be helpful once ruling out parasites and fungi. It gave specific actionable information on foods to focus on, foods to avoid, and gut supplements to take, that have helped me improve my microbiome. I found a German herbal supplement this way that helped instantaneously, as well as lactobacillus plantarum which I wouldn't have paid attention to otherwise. The test goes on sale every once in awhile for around $149, so it might be worth a try.

I found curcumin, quercetin, and Neuroprotek to be helpful mast cell stabilizers.

Best wishes...

 

[Oberon]

Just curious... What did your stool test say? Any abnormal or missing bacteria? Any fungi, parasites or viruses? And nutrient deficiencies due to gut malabsorption?

If so, what did the doctor do then?

@Learner1

All stool tests came back clear for the most part except for Fecal Calprotectin. If I remember correctly I did GI Effects which was completely clear. My Mycotox test had elevated Ochratoxin A and Gilotoxin. One parasite test showed Blastocystis Hominis but it never showed up again on any other test.

Note that I have tried very extensive antibiotic, anti fungals, and anti parasitics most with no success in improving my CFS or Crohn's. (This was largely due to trialing lyme treatments.)

So far the things that have helped me the most with digestive issues are really Crohn's treatments and surprisingly metronidazole seemed to help when I was taking it.

 

[Oberon]

I've actually had fecal calprotectin run a bunch of times, and it's always been below detection limits. You bring up a good point with capsule endoscopy though - I've had upper endoscopy, colonoscopy, and even MR enterography done, but I was talking with the consulting gastroenterologist when I was in the hopsital with C. Diff, and he mentioned that even MR enterography will sometimes miss mild inflammation, and that pill endoscopy is the only way to know for sure. I should probably ask my regular gastroenterologist about that, but the ME/CFS and more recently the C. Diff have taken higher priority.

I strongly suspect that there is something like a 'Crohn's disease variant' that results in little visible mucosal inflammation but lots of microbiome dysregulation and low-grade, systemic inflammation. Doctors are too quick to force things into discrete categories - most of them would say I have IBS, but there's such an obvious connection between my gut symptoms and my systemic symptoms (stuff like joint pain and fever which doctors usually wouldn't attribute to IBS).

@katabasis

I'd agree that sounds very potentially autoimmune. When my Crohn's is flaring there is a large increase in joint pain, hip pain along with the abdominal pain. Have you ever trialed any of the first line Crohn's/Colitis treatments, i.e. mesalamine, methotrexate or immuran to see if they help? Maybe your doctor would consider giving you a trial?

Without the elevated fecal calprotectin it's less likely you have Crohn's if you can get a pill cam it may still be worth a shot.

 

[katabasis]

@katabasis

I'd agree that sounds very potentially autoimmune. When my Crohn's is flaring there is a large increase in joint pain, hip pain along with the abdominal pain. Have you ever trialed any of the first line Crohn's/Colitis treatments, i.e. mesalamine, methotrexate or immuran to see if they help? Maybe your doctor would consider giving you a trial?

Without the elevated fecal calprotectin it's less likely you have Crohn's if you can get a pill cam it may still be worth a shot.

Even though there hadn't been clear evidence of Crohn's, I was seeing a rheumatologist who agreed that it might be instructive to try a DMARD/immunosuppressant. I tried sulfasalazine, but ended up being allergic. I was to try methotrexate next, but this was when the C. Diff came up and I thought it better to avoid an immunosuppressant for the time being. I'm hoping to get IVIG in the near future for SFN, so I figured I'd wait to get that before trialing methotrexate, since IVIG is also known to be effective for Crohn's among many other autoimmune diseases.

 

[lenora]

Boswellia (frankincense) has broad spectrum microbe killing power.

Hello Everyone....I've taken boswellia with many other components in capsules for years. Right now, it's boswellia/quercetin b/c allergies have been very difficult this year...get worse each year it seems.

I heard where we're getting dust in TX from sandstorms in the Sahara Desert, so I'm assuming that's the reason as July, August and Sept. are usually our only allergy free months here in n. Texas. We used to get duststorms from other parts of TX but building has created a barrier for us...at least. But yes, boswellia is very good for inflammation and is definitely one of the vitamins/supplements that I have stuck with over the years. I hope all of you will find relief for your ills. Yours, Lenora.

 

[splusholia]

and her rationale for why it may benefit ME/CFS sufferers is that by increasing the availability of fatty acids, the synthesis of anti-inflammatory compounds like resolvins and HEPE will be increased.

What do you think of resolvin supplements? There are a few on the market now.

 

[Violeta]

I just started taking Boswellia yesterday, we'll see how it goes.

Modulation of the immune system by Boswellia serrata extracts and boswellic acids​

https://pubmed.ncbi.nlm.nih.gov/20696559/

Extracts from the gum resin of Boswellia serrata and some of is constituents including boswellic acids affect the immune system in different ways.

In the humoral defence system a mixture of boswellic acis at higher doses reduced primary antibody titres; on the other hand lower doses enhanced secondary antibody titres following treatment with sheep erythrocytes.

In the cellular defence boswellic acides appear to increase lymphocyte proliferation whereas higher concentrations are even inhibitory.

Moreover, BAs increase phagocytosis of macrophages. BAs affect the cellular defence system by interaction with production/release of cytokines.

Thus, BAs inhibit activation of NFkappaB which is a product of neutrophile granulocytes. Consequently a down regulation of TNF-alpha and decrease of IL-1, IL-2, IL-4, IL-6 and IFN-gamma, which are proinflammatory cytokines by BEs and BAs has been reported.

Suppressions of the classic way of the complement system was found to be due to inhibition of the conversion of C3 into C3a and C3b.

Among the mediators of inflammatory reaction, mast cell stabilisation has been described by a BE.

...leading to a decreased production of leukotrienes.

At the end of the cascade of events in the cellular immune system as far as it directs to various tissues of the body - i.e. autoimmune diseases - formation of oxygen radicals and proteases (for example elastase) play an important destructive role. Here, BEs as well as BAs have been found to be inhibitory.

From the pharmacological properties of BEs and BAs it is not surprising that positive effects of BEs in some chronic inflammatory diseases including rheumatoid arthritis, bronchial asthma, osteoarthritis, ulcerative colitis and Crohn's disease have been reported.