katabasis
Senior Member
- Messages
- 164
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.
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.
Last edited: