89 replies to this topic

[malbecman]

So I saw an article this weekend by an integrative medicine MD talking about the anti-inflammatory/anti-arthritic properties of Boswellia. (its apparently an extract from the tree that frankincense comes from). Anyways, they wrote of a study last year in the Indian Journal of Pharmacology about people with arthritis of the knees taking 300mgs orally 3X per day for 6 months. They saw significant reductions in knee pain and stiffness altho' it took a 2 months to take full effect. Effects lasted for ~1 month after stopping dosage.

Anyone tried this extract or know any more about it?

[krillin]

So I saw an article this weekend by an integrative medicine MD talking about the anti-inflammatory/anti-arthritic properties of Boswellia. (its apparently an extract from the tree that frankincense comes from). Anyways, they wrote of a study last year in the Indian Journal of Pharmacology about people with arthritis of the knees taking 300mgs orally 3X per day for 6 months. They saw significant reductions in knee pain and stiffness altho' it took a 2 months to take full effect. Effects lasted for ~1 month after stopping dosage.

Anyone tried this extract or know any more about it?

I've never noticed anything from it or from 5-Loxin (the more refined version).

[jubai]

I've used boswellin when my rosacea was bad a while ago and it did work for overall inflammation, and I noticed less knee/joint pains too.

[HighDesertWizard]

I recently began to read about Boswellia and have spent probably 40 to 50 hours reading about it. I've begun to write about it at Dr. Davis' TrackYourPlaque.com forum related to my coronary artery disease.

It's an incredible substance. I can't imagine that there is a more significantly beneficial supplement than Boswellia that hasn't been discuss much at ImmInst.org. I had planned to write about what I've found in doing a bit of research in a couple weeks, but TheFirstImmortal's cancer thread has moved up my timeline for that. My making some posts about it in this thread will be less organized than I had planned but hopefully will still make the point that Boswellia is a substance that we should be paying attention to.

Here is a graphic of inflammatory pathways found in a relatively recent LEF article. The 5-LOXIN reference in the 5-Lipoxygenase box is the name of the LEF Boswellia product.

 ArachidonicAcidPathway.jpg   38.41KB   25 downloads

The key point to be clear about is the importance of the 5-Lipoxygenase Inflammatory pathway.

[HighDesertWizard]

There is an ongoing human study at the Cleveland Clinic for use of Boswellia in treatment of Brain Cancer. There are two links to look at.

The first link provides the protocol for the study with a completion target of September 2008. The text associated with the second link which describes the study is pasted in below the second link.


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http://www.cancer.go...s/CASE-CCF-7348


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http://www.cancer.go...t-CASE-CCF-7348

Herbal Therapy for Brain Cancer

Name of the Trial

Phase II Randomized Study of Adjuvant Boswellia serrata and Standard Treatment Versus Standard Treatment Alone in Patients With Newly Diagnosed or Recurrent High-Grade Gliomas (CASE-CCF-7348). See the protocol summary.
Principal Investigator
Dr. Glen Stevens
Dr.Glen Stevens
Principal Investigator

Dr. Glen Stevens, Cleveland Clinic Foundation.
Why This Trial Is Important

High-grade gliomas are among the most common and aggressive forms of adult brain cancer. Swelling of the brain (brain edema) is an often debilitating symptom of glioma and may continue to affect patients even if the tumor is surgically removed.

Resin from the Boswellia serrata tree (frankincense) has been shown in animal and human studies to reduce inflammation, which is a primary cause of brain edema. Additionally, laboratory studies suggest that B. serrata resin may also cause human brain cancer cells to undergo programmed cell death (apoptosis).

In this trial, patients will be randomly assigned to take an herbal preparation of B. serrata orally four times a day in conjunction with standard treatment for six months or to take standard treatment alone for six months. All patients are advised to eat low-fat healthy diet. Diets rich in red meat contain a substance called arachidonic acid, and chemicals in fat can be converted to arachidonic acid. Arachidonic acid is converted in the brain to signaling molecules called eicosanoids that may promote inflammation and tumor growth. Doctors want to see if B. serrata can help reduce brain edema, tumor growth, and levels of 5-lipoxygenase, an enzyme that helps convert arachidonic acid to eicosanoids, in these patients when combined with standard treatment.

"Some small studies have suggested that frankincense extract may help limit brain edema and even have an anti-tumor effect," said Dr. Stevens. "We hope that use of this herbal preparation in conjunction with a healthy diet will help improve patient outcomes and act in a complementary fashion with standard treatments for high-grade gliomas."

[HighDesertWizard]

If/when you think about supplementing Boswellia....

Be sure to use a Boswellin extract" but the product should include one of the two following terms.

* acetyl-11-keto-β-boswellic acid
* AKBA

I thought "AKBA" was the acronym for acetyl-11-keto-β-boswellic acid. But I've also seen a statement to the effect that it is an acronym for "acetyl-keto-beta". So I'm not sure what AKBA actual signifies at the moment.

For the time being, I'm also only going to use Boswellia forumulations that use the PlThomas formulation indicated by the "5-Loxin" trademark. The most significant LEF Boswellia product is based on the 5-Loxin formulation. The rationale for only using the 5-Loxin formulation goes something like this.

* It looks like PlThomas specializes in "branded" supplements. "Branded" supplements looks to be a key business for them. Hence, they have some expertise in what it takes to maintain the brand, quality, testing, government regs, etc.

http://www.plthomas....ingredients.htm

* The business relationship that PlThomas has with the Indian manufacturer is respectable. These guys are in it for the long term "business" and I like that.

http://www.npicenter...w...98&zoneid=2

* There has been a published study of the safety of the 5-Loxin formulation.

http://www.nutraingr...loxin-boswellia

With that kind of product context and without a comparable competitive formulation, I can't see how it makes any sense to use anything other than the 5-Loxin formulation. If you google "5-Loxin" you'll see that there are multiple supplement providers who sell the 5-Loxin formulation.

So then the only question is who has the lowest price for comparabale dosages.

Edited by wccaguy, 28 July 2008 - 01:50 PM.

[HighDesertWizard]

Here's a useful link for information on dosing. The text from that link related to dosing appears below the asterisks. The link has other information about Boswellia too, including what looks to be a recent, streamlined bibliography of studies.

http://www.intelihea...ml?d=dmtContent

It's not clear to me that the "boswellic acids" referenced refers to boswellia in general or to AKBA in particular. My guess would be that it refers to boswellia in general because AKBA appears almost always to be referenced specifically.

Regarding dosing: Be sure to examine the link in the previous post related to the safety study done on 5-Loxin. Here's that link again.

http://www.nutraingr...loxin-boswellia



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Dosing

The doses listed below are based on scientific research, publications or traditional use. Because most herbs and supplements have not been thoroughly studied or monitored, safety and effectiveness may not be proven. Brands may be made differently, with variable ingredients even within the same brand. Combination products often contain small amounts of each ingredient and may not be effective. Appropriate dosing should be discussed with a health care provider before starting therapy; always read the recommendations on a product's label. The dosing for unproven uses should be approached cautiously, because scientific information is limited in these areas.

Safety of use beyond six months has not been studied. Oral doses of 200 to 400 milligrams may be standardized to contain 37.5% boswellic acids per dose. However, gum resins typically contain 30% boswellic acids, ethanol extracts often contain 43% boswellic acids and some sources may contain up to 65% boswellic acids.

Adults (Aged 18 Or Older)

Asthma

Tablets/capsules: A dose of 300 to 400 milligrams three times per day by mouth has been used.

Arthritic Conditions

Tablets/capsules: A dose of 200 to 400 milligrams three times per day by mouth has been used.

Ulcerative Colitis

Tablets/capsules: A dose of 350 to 400 milligrams three times per day by mouth has been used.

Crohn's Disease

Tablets/capsules: A dose of 1,200 milligrams three times daily by mouth for up to eight weeks has been used.

Children (Younger Than 18)

There are not enough scientific data to recommend boswellia for use in children, and this herb is not recommended because of potential side effects.

Summary

Boswellia has been suggested as a treatment for many conditions. There is some research to support the use of boswellia as a treatment for asthma, although it is not clear what dose is safe and effective. There is not enough scientific evidence to support the use of boswellia for any other medical condition. Boswellia may cause stomach discomfort. It should be avoided in pregnant or breast-feeding women and in children. Safety of use beyond six months has not been well studied. Consult your health care provider immediately if you have any side effects.

The information in this monograph was prepared by the professional staff at Natural Standard, based on thorough systematic review of scientific evidence. The material was reviewed by the Faculty of the Harvard Medical School with final editing approved by Natural Standard.

Edited by wccaguy, 28 July 2008 - 01:55 PM.

[HighDesertWizard]

OK... Enough of the introduction... How about some studies...

Here are two studies which link the 5-LO pathway with Coronary Artery Plaque INSTABILITY

Remember... Boswellia is a 5-LO inhibitor...

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Expression of 5-lipoxygenase and leukotriene A4 hydrolase in human atherosclerotic lesions correlates with symptoms of plaque instability

Leukotrienes (LT) are a group of proinflammatory lipid mediators that are implicated in the pathogenesis and progression of atherosclerosis. Here we report that mRNA levels for the three key proteins in LTB4 biosynthesis, namely 5-lipoxygenase (5-LO), 5-LO-activating protein (FLAP), and LTA4 hydrolase (LTA4H), are significantly increased in human atherosclerotic plaque (n = 72) as compared with healthy controls (n = 6). Neither LTC4 synthase nor any of the LT receptors exhibits significantly increased mRNA levels. Immunohistochemical staining revealed abundant expression of 5-LO, FLAP, and LTA4H protein, colocalizing in macrophages of intimal lesions. Human lesion tissue converts arachidonic acid into significant amounts of LTB4, and a selective, tight-binding LTA4H inhibitor can block this activity. Furthermore, expression of 5-LO and LTA4H, but not FLAP, is increased in patients with recent or ongoing symptoms of plaque instability, and medication with warfarin correlates with increased levels of FLAP mRNA. In contrast to human plaques, levels of 5-LO mRNA are not significantly increased in plaque tissues from two atherosclerosis-prone mouse strains, and mouse plaques exhibit segregated cellular expression of LTA4H and 5-LO as well as strong increases of CysLT1 and CysLT2 mRNA. These discrepancies indicate that phenotypic changes in the synthesis and action of LT in specific mouse models of atherosclerosis should be cautiously translated into human pathology. The abundant expression of LTA4H and correlation with plaque instability identify LTA4H as a potential target for pharmacological intervention in treatment of human atherosclerosis.

PMID: 16698924 [PubMed - indexed for MEDLINE]

PMCID: PMC1459628


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Association between 5-lipoxygenase expression and plaque instability in humans.

Note: I fixed one very clear typo in the abstract and my change is bracketed [] and bolded below.


OBJECTIVE: The participation of 5-lipoxygenase (5-LO) in the development of atherosclerosis has been suggested by recent studies. However, a role for 5-LO as a modulator of atherosclerotic plaque instability has not been previously reported in humans. Thus, the aims of this study was to analyze the expression of 5-LO in human carotid plaques and to investigate the mechanism by which this enzyme could lead to plaque instability and rupture. METHODS AND RESULTS: We obtained atherosclerotic plaques from 60 patients undergoing carotid endarterectomy. We divided the plaques into symptomatic and [a]symptomatic according to clinical evidence of plaque instability. Clinical evidence of plaque instability was provided by the assessment of recent ischemic symptoms attributable to the stenosis and by the presence of ipsilateral cerebral lesion(s) determined by computed tomography. Plaques were analyzed for CD68+ macrophages, CD3+ T cells, alpha-actin+ smooth muscle cells, 5-LO, cyclooxygenase 2, matrix metalloproteinase (MMP)-2, and MMP-9 by immunohistochemical, immunoblotting, and densitometric analyses. MMP activity was assessed by zymography. Leukotriene (LT) B4 and collagen were quantified by ELISA and Sirius red polarization, respectively. The percentage of macrophage-rich and T-cell-rich areas was larger in symptomatic compared with asymptomatic patients (25+/-6% versus 8+/-4%, P<0.0001, and 74+/-17 versus 18+/-4 cell/mm2, P<0.003). 5-LO expression was higher in symptomatic compared with asymptomatic plaques (24+/-4% versus 6+/-3%, P<0.0001) and was associated with increased MMP-2 and MMP-9 expression (27+/-4% versus 7+/-3%, P<0.0001, and 29+/-5% versus 8+/-2%, P<0.0001) and activity and with decreased collagen content (6.9+/-2.4% versus 17.8+/-3.1%, P<0.01). Immunofluorescence showed that 5-LO and MMPs colocalize in activated macrophages. Notably, higher 5-LO in symptomatic plaques correlated with increased LTB4 production (18.15+/-3.56 versus 11.27+/-3.04 ng/g tissue, P<0.0001). CONCLUSIONS: The expression of 5-LO is elevated in symptomatic compared with asymptomatic plaques and is associated with acute ischemic syndromes, possibly through the generation of LTB4, subsequent MMP biosynthesis, and plaque rupture.

PMID: 15933245 [PubMed - indexed for MEDLINE]

[HighDesertWizard]

Here are a few abstracts about Boswellia and cancer... There are DOZENS more of these sorts of studies....




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J Neurooncol. 2007 Mar;82(1):91-3. Epub 2006 Sep 26
A lipoxygenase inhibitor in breast cancer brain metastases.
Flavin DF.
Foundation for Collaborative Medicine and Research, Greenwich, CT 06831, USA. Dana_FK@hotmail.com

The complication of multiple brain metastases in breast cancer patients is a life threatening condition with limited success following standard therapies. The arachidonate lipoxygenase pathway appears to play a role in brain tumor growth as well as inhibition of apoptosis in in-vitro studies. The down regulation of these arachidonate lipoxygenase growth stimulating products therefore appeared to be a worthwhile consideration for testing in brain metastases not responding to standard therapy. Boswellia serrata, a lipoxygenase inhibitor was applied for this inhibition. Multiple brain metastases were successfully reversed using this method in a breast cancer patient who had not shown improvement after standard therapy. The results suggest a potential new area of therapy for breast cancer patients with brain metastases that may be useful as an adjuvant to our standard therapy.

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J Immunol. 2006 Mar 1;176(5):3127-40
Acetyl-11-keto-beta-boswellic acid potentiates apoptosis, inhibits invasion, and abolishes osteoclastogenesis by suppressing NF-kappa B and NF-kappa B-regulated gene expression.
Takada Y, Ichikawa H, Badmaev V, Aggarwal BB.
Cytokine Research Section, Department of Experimental Therapeutics, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA.

Acetyl-11-keto-beta-boswellic acid (AKBA), a component of an Ayurvedic therapeutic plant Boswellia serrata, is a pentacyclic terpenoid active against a large number of inflammatory diseases, including cancer, arthritis, chronic colitis, ulcerative colitis, Crohn's disease, and bronchial asthma, but the mechanism is poorly understood. We found that AKBA potentiated the apoptosis induced by TNF and chemotherapeutic agents, suppressed TNF-induced invasion, and inhibited receptor activator of NF-kappaB ligand-induced osteoclastogenesis, all of which are known to require NF-kappaB activation. These observations corresponded with the down-regulation of the expression of NF-kappaB-regulated antiapoptotic, proliferative, and angiogenic gene products. As examined by DNA binding, AKBA suppressed both inducible and constitutive NF-kappaB activation in tumor cells. It also abrogated NF-kappaB activation induced by TNF, IL-1beta, okadaic acid, doxorubicin, LPS, H2O2, PMA, and cigarette smoke. AKBA did not directly affect the binding of NF-kappaB to the DNA but inhibited sequentially the TNF-induced activation of IkappaBalpha kinase (IKK), IkappaBalpha phosphorylation, IkappaBalpha ubiquitination, IkappaBalpha degradation, p65 phosphorylation, and p65 nuclear translocation. AKBA also did not directly modulate IKK activity but suppressed the activation of IKK through inhibition of Akt. Furthermore, AKBA inhibited the NF-kappaB-dependent reporter gene expression activated by TNFR type 1, TNFR-associated death domain protein, TNFR-associated factor 2, NF-kappaB-inducing kinase, and IKK, but not that activated by the p65 subunit of NF-kappaB. Overall, our results indicated that AKBA enhances apoptosis induced by cytokines and chemotherapeutic agents, inhibits invasion, and suppresses osteoclastogenesis through inhibition of NF-kappaB-regulated gene expression.

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Anticancer Res. 2002 Sep-Oct;22(5):2853-62
Cytostatic and apoptosis-inducing activity of boswellic acids toward malignant cell lines in vitro.
Hostanska K, Daum G, Saller R.
Departmment of Internal Medicine, University Hospital Zürich, Rämistrasse 100, 8091 Zürich, Switzerland. katarina.hostanska@access.unizh.ch

Boswellic acids from frankincense were indentified as the active compounds which inhibit leukotriene biosynthesis, 5-lipoxygenase and exert antiproliferative activity toward a variety of malignant cells. Because of the relevance for the clinical application, we tested the ethanolic extract of Boswellia serrata gum resin containing a defined amount of boswellic acids for its cytotoxic, cytostatic and apoptotic activity on five leukemia (HL-60, K 562, U937, MOLT-4, THP-1) and two brain tumor (LN-18, LN-229) cell lines by WST-1 assay and flow cytometry. The Boswellia serrata extract induced dose-dependent antiproliferative effects on all human malignant cells tested with GI50 values (extract concentration producing 50% cell growth inhibition) between 57.0 and 124.1 micrograms/ml. In three haematological cell lines (K562, U937, MOLT-4) the effect of total extract expressed in GI50 was 2.8-, 3.3- and 2.3-times more potent (p < 0.05) than pure 3-O-acetyl-11-keto-beta-boswellic acid (AKBA). Morphological changes after 24-27 hours and the detection of apoptotic cells by AnnexinV-binding and/or by the detection of propidium iodide-labelled DNA with flow cytometry, confirmed the apoptotic cell death. The results of this study suggest the effectiveness of Boswellia serrata extract with defined content of boswellic acids.

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Inhibition of I
B Kinase Activity by Acetyl-boswellic Acids Promotes Apoptosis in Androgen-independent PC-3 Prostate Cancer Cells in Vitro and in Vivo*

Signaling through NF-_B has been implicated in the malignant phenotype as well as the chemoresistance of various cancers. Here we show that the natural compounds acetyl-_-boswellic acid and acetyl-11-keto-_-boswellic acid (AK_BA) inhibit proliferation and elicit cell death in chemoresistant androgen-independent PC-3 prostate cancer cells in vitro and in vivo. Induction of apoptosis was demonstrated in cultured PC-3 cells by several parameters including mitochondrial cytochrome c release and DNA fragmentation. At the molecular level these compounds inhibit constitutively activated NF-_B signaling by intercepting the I_B kinase (IKK) activity; signaling through the interferon-stimulated response element remained unaffected, suggesting specificity for IKK inhibition. The impaired phosphorylation of p65 and the reduced nuclear translocation of NF-_B proteins were associated with down-regulation of the constitutively overexpressed and NF-_B-dependent antiapoptotic proteins Bcl-2 and Bcl-xL. In addition, expression of cyclin D1, a crucial cell cycle regulator, was reduced as well. Down-regulation of IKK by antisense oligodeoxynucleotides confirmed the essential role of IKK inhibition for the proliferation of the PC-3 cells. Both compounds tested were active in vivo, yet AK_BA proved to be far superior. Indeed, topical application of water-soluble AK_BA-_-cyclodextrin on PC-3 tumors xenografted onto chick chorioallantoic membranes induced concentration-dependent inhibition of proliferation as well as apoptosis. Similarly, in nude mice carrying PC-3 tumors, systemic application of AK_BA-_- cyclodextrin inhibited tumor growth and triggered apoptosis in the absence of detectable systemic toxicity. Thus, AK_BA and related compounds acting on IKK might provide a novel approach for the treatment of chemoresistant human tumors such as androgen-independent human prostate cancers.

[HighDesertWizard]

Cancer and Coronary Artery Disease are not even the diseases that Boswellia has been used to treat the most... Here are a few more studies...

It would take DAYS to post all the abstracts about Boswellia and significant diseases including ASTHMA, ARTHRITIS, COLITIS, CROHNES DISEASE, and the list goes on...

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Crohnes Disease

Therapy of active Crohn disease with Boswellia serrata extract H 15

BACKGROUND: The purpose of this clinical trial was to compare efficacy and safety of the Boswellia serrata extract H15 with mesalazine for the treatment of active Crohn's disease. PATIENTS AND METHODS: Randomised, double-blind, verum-controlled, parallel group comparison for which 102 Patients were randomised. The per protocol population included 44 patients treated with H15 and 39 patients treated with mesalazine. As primary outcome measure the change of the Crohn Disease Activity Index (CDAI) between the status of enrolment and end of therapy was chosen. H 15 was tested on non-inferiority compared to standard treatment with mesalazine. RESULTS: The CDAI between the status of enrolment and end of therapy after treatment with H15 was reduced by 90 and after therapy with mesalazine by 53 scores in the mean. In this non-inferiority-trial the test hypothesis was confirmed by the statistical analysis. The difference between both treatments could not be proven to be statistically significant in favor to H15 for the primary outcome measure. The secondary efficacy endpoints confirm the assessment of the comparison of H15 and mesalazine. The proven tolerability of H15 completes the results of the shown clinical efficacy. CONCLUSIONS: The study confirms that therapy with H15 is not inferior to mesalazine. This can be interpreted as evidence for the efficacy of H15 according to the state of art in the treatment of active Crohn's disease with Boswellia serrata extract, since the efficacy of mesalazine for this indication has been approved by the health authorities. Considering both safety and efficacy of Boswellia serrata extract H15 it appears to be superior over mesalazine in terms of a benefit-risk-evaluation.


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Colitis

Effects of gum resin of Boswellia serrata in patients with chronic colitis

Patients studied here suffered from chronic colitis characterized by vague lower abdominal pain, bleeding per rectum with diarrhoea and palpable tender descending and sigmoid colon. The inflammatory process in colitis is associated with increased formation of leukotrienes causing chemotaxis, chemokinesis, synthesis of superoxide radicals and release of lysosomal enzymes by phagocytes. The key enzyme for leukotriene biosynthesis is 5-lipoxygenase. Boswellic acids were found to be non-redox, non-competitive specific inhibitors of the enzyme 5-lipoxygenase. We studied the gum resin of Boswellia serrata for the treatment of this disease. Thirty patients, 17 males and 13 females in the age range of 18 to 48 years with chronic colitis were included in this study. Twenty patients were given a preparation of the gum resin of Boswellia serrata (900 mg daily divided in three doses for 6 weeks) and ten patients were given sulfasalazine (3 gm daily divided in three doses for 6 weeks) and served as controls. Out of 20 patients treated with Boswellia gum resin 18 patients showed an improvement in one or more of the parameters: including stool properties, histopathology as well as scanning electron microscopy, besides haemoglobin, serum iron, calcium, phosphorus, proteins, total leukocytes and eosinophils. In the control group 6 out of 10 patients showed similar results with the same parameters. Out of 20 patients treated with Boswellia gum resin 14 went into remission while in case of sulfasalazine remission rate was 4 out of 10. In conclusion, this study shows that a gum resin preparation from Boswellia serrata could be effective in the treatment of chronic colitis with minimal side effects.


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Arthritis

Efficacy and tolerability of Boswellia serrata extract in treatment of osteoarthritis of knee--a randomized double blind placebo controlled trial

Osteoarthritis is a common, chronic, progressive, skeletal, degenerative disorder, which commonly affects the knee joint. Boswellia serrata tree is commonly found in India. The therapeutic value of its gum (guggulu) has been known. It posses good anti-inflammatory, anti-arthritic and analgesic activity. A randomized double blind placebo controlled crossover study was conducted to assess the efficacy, safety and tolerability of Boswellia serrata Extract (BSE) in 30 patients of osteoarthritis of knee, 15 each receiving active drug or placebo for eight weeks. After the first intervention, washout was given and then the groups were crossed over to receive the opposite intervention for eight weeks. All patients receiving drug treatment reported decrease in knee pain, increased knee flexion and increased walking distance. The frequency of swelling in the knee joint was decreased. Radiologically there was no change. The observed differences between drug treated and placebo being statistically significant, are clinically relevant. BSE was well tolerated by the subjects except for minor gastrointestinal ADRs. BSE is recommended in the patients of osteoarthritis of the knee with possible therapeutic use in other arthritis.

PMID: 12622457 [PubMed - indexed for MEDLINE]


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I don't have time just now to post more of these. There are dozens if not hundreds more HUMAN studies and even more in-vitro and animal studies. It goes on and on and on. Check it out for yourself with google.

[health_nutty]

Thanks wccaguy!

[HighDesertWizard]

Many studies of Boswellia have been done in Germany. Here's one that attempts to take a more detailed and broader view.

Boswellic acids: biological actions and molecular targets

Gum resin extracts of Boswellia species have been traditionally applied in folk medicine for centuries to treat various chronic inflammatory diseases, and experimental data from animal models and studies with human subjects confirmed the potential of B. spec extracts for the treatment of not only inflammation but also of cancer. Analysis of the ingredients of these extracts revealed that the pentacyclic triterpenes boswellic acids (BAs) possess biological activities and appear to be responsible for the respective pharmacological actions. Approaches in order to elucidate the molecular mechanisms underlying the biological effects of BAs identified 5-lipoxygenase, human leukocyte elastase, toposiomerase I and II, as well as IkappaB kinases as molecular targets of BAs. Moreover, it was shown that depending on the cell type and the structure of the BAs, the compounds differentially interfere with signal transduction pathways including Ca(2+/-) and MAPK signaling in various blood cells, related to functional cellular processes important for inflammatory reactions and tumor growth. This review summarizes the biological actions of BAs on the cellular and molecular level and attempts to put the data into perspective of the beneficial effects manifested in animal studies and trials with human subjects related to inflammation and cancer.

PMID: 17168710 [PubMed - indexed for MEDLINE]

[luv2increase]

I was going to start taking boswellia but feared it would have a detrimental set back affect on my bodybuilding/strength training program due to being a strong anti-inflammatory ---> to build muscle you need inflammation...

[Ben]

I believe they use this in L'Oreal's men expert series. Except they call it boswellox for obvious marketing purposes.

I used it. I'm pretty certain it helped with the redness after the shower

Edited by Ben - Aus, 29 July 2008 - 02:00 AM.

[HighDesertWizard]

And I suppose, even if Boswellia isn't helpful for disease prevention and treatment, it still might be fun to smoke....

http://www.fasebj.or...s_Release.shtml

8-)

[krillin]

I was going to start taking boswellia but feared it would have a detrimental set back affect on my bodybuilding/strength training program due to being a strong anti-inflammatory ---> to build muscle you need inflammation...

If this experiment isn't a fluke, then the situation may be more complicated.

Combining pain relievers with weight training may increase muscle strength, mass

[HighDesertWizard]

I've been doing more reading about the 5-LO pathway and boswellia and posting various studies to the TrackYourPlaque forum. At some point, I'll get around to posting them here.

But I found a really great overview article on Leukotrienes and Atherosclerosis.

Seems to me that it is significant support for the notion that there is incredible benefit to thinking alot about the 5-LO pathway.

And it's got pictures.

Here's the overview diagram that is explained in text in the article.

 LeukotrieneSynthesis.gif   20.97KB   100 downloads

[Shepard]

Combining pain relievers with weight training may increase muscle strength, mass

I've wondered how much of this was due to the anti-inflammatories helping the older people workout harder due to less pain.

[luv2increase]

I've wondered how much of this was due to the anti-inflammatories helping the older people workout harder due to less pain.

That is my only logical assumption as well.

[HighDesertWizard]

The following study is so hot off the presses that the ink hasn't dried yet on the abstact... 8-)

Notice that the study used this new 5-LOXIN Boswellia formulation I discussed earlier in this thread. I'm going to post another study later today that also had amazing results related to Coronary Artery Disease that was based on the 5-LOXIN formulation. Looks like this 5-LOXIN formulation is going to be the standard unless and until somebody like Anthony Loera decides that he can put together a competitive formulation too. 8-)


http://arthritis-res...ontent/10/4/R85

A double blind, randomized, placebo controlled study of the efficacy and safety of 5-Loxin for treatment of osteoarthritis of the knee

Abstract (provisional)

Introduction

5-Loxin® is a novel Boswellia serrata extract enriched with 30% 3-O-acetyl-11-keto-beta-boswellic acid (AKBA), which exhibits potential anti-inflammatory properties by inhibiting the 5-lipoxygenase enzyme. A 90-day, double-blind, randomized, placebo-controlled study was conducted to evaluate the efficacy and safety of 5-Loxin® in the treatment of osteoarthritis (OA) of the knee.
Methods

Seventy-five OA patients were included in the study. The patients received either 100 mg (n = 25) or 250 mg (n = 25) of 5-Loxin® daily or a placebo (n = 25) for 90 days. Each patient was evaluated for pain and physical functions by using the standard tools (visual analog scale, Lequesne's Functional Index, and Western Ontario and McMaster Universities Osteoarthritis Index) at the baseline (day 0), and at days 7, 30, 60 and 90. Additionally, the cartilage degrading enzyme matrix metalloproteinase-3 was also evaluated in synovial fluid from OA patients. Measurement of a battery of biochemical parameters in serum and haematological parameters, and urine analysis were performed to evaluate the safety of 5-Loxin® in OA patients.
Results

Seventy patients completed the study. At the end of the study, both doses of 5-Loxin® conferred clinically and statistically significant improvements in pain scores and physical function scores in OA patients. Interestingly, significant improvements in pain score and functional ability were recorded in the treatment group supplemented with 250 mg 5-Loxin® as early as 7 days after the start of treatment. Corroborating the improvements in pain scores in treatment groups, we also noted significant reduction in synovial fluid matrix metalloproteinase-3. In comparison with placebo, the safety parameters were almost unchanged in the treatment groups.
Conclusions

5-Loxin® reduces pain and improves physical functioning significantly in OA patients; and it is safe for human consumption. 5-Loxin® may exert its beneficial effects by controlling inflammatory responses through reducing proinflammatory modulators, and it may improve joint health by reducing the enzymatic degradation of cartilage in OA patients. (Clinical trial registration number: ISRCTN05212803.)

Edited by wccaguy, 31 July 2008 - 12:51 PM.

[Anthony_Loera]

This is interesting....

A

[HighDesertWizard]

I was hoping to get your attention Anthony. I've been thinking for several days now that you have demonstrated, at least to me, that you're the sort of person who could drive a significant effort for an additional, high quality formulation of Boswellia with some significant AKBA component.

If you don't do it Anthony, someone else will.

The science, including A LOT of human studies, both in-vitro and in-vivo, is overwhelming.

I've been posting a great deal about this over at Dr. Davis' TrackYourPlaque.com website for the last couple weeks. I'm just posting the highlights here as I have time. I'm going to post a couple of studies here today and tomorrow that, taken together, carry significant hope for those with atherosclerosis.

Edited by wccaguy, 31 July 2008 - 01:36 PM.

[HighDesertWizard]

I posted 4 studies upthread which described positive impacts of Boswellia on cancers. Two types of trials are listed below....

In the first trial listed, the 5-LOXIN Boswellia formulation I described upthread is specifically shown to prevent expression of a key cancer (and other disease) gene--VCAM-1.

A second partial list of trials have explored the significance and role of VCAM-1 per se in various types of cancer.


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Human Genome Screen to Identify the Genetic Basis of the Anti-inflammatory Effects of Boswellia in Microvascular Endothelial Cells

(Notice that the study below was done using the 5-LOXIN Boswellia formulation.)

Inflammatory disorders represent a substantial health problem. Medicinal plants belonging to the Burseraceae family, including Boswellia, are especially known for their anti-inflammatory properties. The gum resin of Boswellia serrata contains boswellic acids, which inhibit leukotriene biosynthesis. A series of chronic inflammatory diseases are perpetuated by leukotrienes. Although Boswellia extract has proven to be anti-inflammatory in clinical trials, the underlying mechanisms remain to be characterized. TNFα represents one of the most widely recognized mediators of inflammation. One mechanism by which TNFα causes inflammation is by potently inducing the expression of adhesion molecules such as VCAM-1. We sought to test the genetic basis of the antiinflammatory effects of BE (standardized Boswellia extract, 5-Loxin®) in a system of TNFα-induced gene expression in human microvascular endothelial cells. We conducted the first whole genome screen for TNFα- inducible genes in human microvascular cells (HMEC). Acutely, TNFα induced 522 genes and downregulated 141 genes in nine out of nine pairwise comparisons. Of the 522 genes induced by TNFα in HMEC, 113 genes were clearly sensitive to BE treatment. Such genes directly related to inflammation, cell adhesion, and proteolysis. The robust BE-sensitive candidate genes were then subjected to further processing for the identification of BE-sensitive signaling pathways. The use of resources such as GenMAPP, KEGG, and gene ontology led to the recognition of the primary BE-sensitive TNFα-inducible pathways. BE prevented the TNFα-induced expression of matrix metalloproteinases. BE also prevented the inducible expression of mediators of apoptosis. Most strikingly, however, TNFα-inducible expression of VCAM-1 and ICAM-1 were observed to be sensitive to BE. Realtime PCR studies showed that while TNFα potently induced VCAM-1 gene expression, BE completely prevented it. This result confirmed our microarray findings and built a compelling case for the anti-inflammatory property of BE. In an in vivo model of carrageenan-induced rat paw inflammation, we observed a significant antiinflammatory property of BE consistent with our in vitro findings. These findings warrant further research aimed at identifying the signaling mechanisms by which BE exerts its anti-inflammatory effects.
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But how important is VCAM-1 in various types of cancer?

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Soluble VCAM-1 and E-selectin in breast cancer : relationship with staging and with the detection of circulating cancer cells

In breast cancer, the correct evaluation of cancer dissemination is essential to establish prognosis and treatment choices. This study analyses the relationship between circulating levels of soluble VCAM-1 and E-selectin and the presence of circulating cancer cells in breast cancer patients. Plasma levels of VCAM-1 and E-selectin were measured by enzyme-linked immunosorbent assay (ELISA). The presence of circulating cancer cells was diagnosed using a RT nested-PCR assay detecting the cancer specific transcript, epidermal growth factor receptor variant III (EGFRvIII) mRNA. Blood samples were collected from 64 patients divided in three groups: group A of 11 women selected for neoadjuvant chemotherapy; group B of 13 women with metastatic disease and group C, with 40 women having completed their treatment at least one year ago and with no evidence of relapse. The mutant transcript was detected in 45.5% of patients from group A, in 61.5% of patients from group B and in none of the group C patients. For both VCAM-1 and E-selectin, plasma levels increased with disease staging and with the presence of EGFRvIII mRNA in peripheral blood. The differences were statistically significant (p<0.025) when group C was compared with all patients from group B, with patients from group B with EGFRvIII positive results or with all patients with EGFRvIII positive results. Increased plasma levels of VCAM-1 and E-selectin are associated with advanced stage of breast cancer and with the presence of circulating cancer cells. The combined analysis of these parameters may contribute to a more accurate evaluation of cancer dissemination.
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Caveolin-1 Is Associated with VCAM-1 Dependent Adhesion of Gastric Cancer Cells to Endothelial Cells

Background/Aims: Cell adhesion molecules play a critical role in the invasion and metastasis of a variety of human tumors. Abnormal expression of VCAM-1 has been demonstrated to correlate with the malignant progression of gastric tumors, but the molecular mechanism underlying the VCAM-1-dependent metastasis has been rarely investigated. To explore the role for tumor cell-expressing adhesion molecules in the carcinoma-endothelium adhesion, we analyzed expression status of adhesion molecules in gastric cancer cells and its association with tumor cell capability of endothelial adhesion. Methods: Endothelial adhesion ability of gastric tumor cells was tested using calcein AM staining assay. Expression of cell surface proteins was determined by Western blot, flow cytometry, and immunofluorescence assays. RNAi-mediated knockdown of gene expression and neutralization with specific antibodies were utilized for functional analysis. Results: One of three cell lines tested was identified to be adhesive to endothelial cells and express VCAM-1. Adherence ability of the cells was dramatically decreased by neutralization of surface VCAM-1. VCAM-1 was co-localized with Caveolin-1 and siRNA-mediated knockdown of Caveolin-1 expression significantly blocked the VCAM-1-dependent cell adhesion. Conclusions: Our data imply important roles for VCAM-1 and Caveolin- 1 in the regulation of metastatic potential of gastric tumor cells.
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Stromal cells expressing elevated VCAM-1 enhance survival of B lineage tumor cells

In the current study we generated murine bone marrow stromal cells that constitutively express human VCAM-1. These stromal cell lines allow investigation of the contribution of VCAM-1 initiated signaling to tumor cell survival. Co-culture of ALL cell lines with stromal cells engineered to over express VCAM-1 enhanced survival of leukemic cells in a PI-3 kinase-dependent manner, compared to co-culture with parental stromal cells expressing only endogenous VCAM-1. These observations suggest that modulation of stromal cell VCAM-1 by specific chemotherapeutic drugs may have utility in decreasing residual disease. In addition, these novel lines provide an in vitro model in which other tumor types that interact with stromal cells in the bone marrow microenvironment may be evaluated to determine the contribution of VCAM-1 initiated signaling to modulation of treatment response.
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Serum Levels of Soluble ICAM-1 and VCAM-1 Predict Pre-clinical Cancer

To investigate whether serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were related to first stage cancer before diagnosis of cancer, we compared serum levels of these adhesion molecules between preclinical cases and controls using a nested case-control study method. Cancer cases were recruited from a cohort database of 1465 participants who completed a baseline questionnaire and provided blood samples, and were followed up from 1989 to 2003. They consisted of 15 individuals who died of cancer and 31 individuals newly diagnosed with cancer during the follow-up period. Controls were subjects who did not suffer from cancer, cerebral apoplexy, diabetes mellitus, liver disease, or myocardial infarction during the follow-up period. Using commercially available enzyme-linked immunosorbent assay (ELISA) kits, we showed that serum levels of sVCAM-1, but not sICAM-1 were elevated in cases with pre-clinical or early cancer. We suggest that elevated serum levels of sVCAM-1 might serve as a possible marker for detecting pre-clinical or early cancer.
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Celecoxib modulates adhesion of HT29 colon cancer cells to vascular endothelial cells by inhibiting ICAM-1 and VCAM-1 expression.

BACKGROUND AND PURPOSE:
Cyclooxygenase-2 (COX-2) is highly expressed during inflammation and can promote the progression of colorectal cancer. Interactions between cancer cells and vascular endothelial cells are key events in this process. Recently, the selective COX-2 inhibitor, celecoxib, was shown to inhibit expression of the adhesion molecules, ICAM-1 and VCAM-1, in the human colon cancer cell line HT29 and to inhibit adhesion of HT29 cells to FCS-coated plastic wells. Here, we evaluated the effects of celecoxib on adhesion of HT29 cells to human umbilical vein endothelial cells (HUVEC), mediated by ICAM-1 and VCAM-1, to assess further the potential protective effects of celecoxib on cancer development.

EXPERIMENTAL APPROACH:
Celecoxib was incubated for 4 h with HT29 cells and HUVEC and adhesion was quantified by a computerized micro-imaging system. Expression analysis of ICAM-1 and VCAM-1 cell adhesion molecules was performed by western blot.

KEY RESULTS:
Celecoxib (1 nM-10 microM) inhibited, with the same potency, adhesion of HT29 cells to resting HUVEC or to HUVEC stimulated by tumour necrosis factor-alpha (TNF-alpha), mimicking inflammatory conditions. Analysis of ICAM-1 and VCAM-1 expression showed that celecoxib inhibited expression of both molecules in TNF-alpha-stimulated HUVEC, but not in resting HUVEC; inhibition was concentration-dependent and maximal (about 50%) at 10 microM celecoxib.

CONCLUSIONS AND IMPLICATIONS:
In conclusion, our data show that celecoxib inhibits HT29 cell adhesion to HUVEC and expression of ICAM-1 and VCAM-1, in stimulated endothelial cells. These effects may contribute to the chemopreventive activity of celecoxib in the development of colorectal cancer.
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Serum levels of E-selectin, ICAM-1 and VCAM-1 in colorectal cancer patients: correlations with clinicopathological features, patient survival and tumour surgery
The serum concentrations of the cell adhesion molecules E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) were investigated in 63 patients with colorectal cancer and in 51 controls by an enzyme-linked immunosorbent assay (ELISA). Their relationship to clinicopathological variables and patient survival and changes in their levels after surgery were examined. Colorectal cancer patients showed significantly higher serum levels of E-selectin, ICAM-1 and VCAM-1 compared with healthy controls. There was a significant association between the serum levels of these molecules, disease stage and the presence of both lymph node and distant metastases. Both ICAM-1 and VCAM-1 levels correlated with serum E-selectin and carcinoembryonic antigen (CEA) levels. Serum levels of all three molecules decreased significantly after radical resection of the tumour. Elevated pre-operative E-selectin, ICAM-1 and VCAM-1 levels were significant prognostic factors, although not independent of stage, for patient survival. These findings suggest that serum concentrations of E-selectin, ICAM-1 and VCAM-1 may reflect tumour progression and metastasis. Since these markers are linked to CEA levels, it is uncertain whether their measurement will prove cost-effective in colorectal cancer management.
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Over-expression of ICAM-1, VCAM-1 and ELAM-1 might influence tumor progression in colorectal cancer

Adhesion molecules might play a role in tumor progression. We investigated expression of the adhesion molecules ICAM-1, VCAM-1 and ELAM-1 in 24 primary colorectal carcinomas using immuno-histochemistry and Northern blot analysis. Normal colonic tissue from the same patients served as controls. ICAM-1 immunostaining was restricted to the intercellular matrix and vascular endothelial cells. The vast majority of normal tissue samples revealed only faint ICAM-1 immunoreactivity. However, moderate to strong immunostaining was found in 86% of cancerous sections. The ICAM-1 immunoreaction was more intense in well-differentiated carcinomas as well as in the adenomatous parts and transition zones of cancers. Similarly, the cancers exhibited markedly enhanced VCAM-1 and ELAM-1 immunostaining in the endothelial cells of small blood vessels. The intense vascular immunostaining by ICAM-1 and VCAM-1 was associated with a strong presence of CD3-positive T lymphocytes, whereas ELAM-1 immunoreactivity did not correlate with round cell infiltration. On Northern blot analysis, ICAM-1, VCAM-1 and ELAM-1 mRNA levels were increased in 67%, 57% and 63% of carcinomas, respectively, in comparison with normal tissue samples. Densitometric analysis of Northern blots revealed an increase in ICAM-1 by 2.1-fold, an increase in VCAM-1 by 3.4-fold and an increase in ELAM-1 by 2.2-fold in cancerous tissues compared to normal controls. Over-expression of ICAM-1 might prevent cell-cell disruption and, hence, tumor dissemination. Furthermore, over-expression of ICAM-1 and VCAM-1, but not ELAM-1, might favor host anti-tumor defense by trafficking of lymphocytes. Int. J. Cancer (Pred. Oncol.) 79:76-81, 1998.
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Edited by wccaguy, 01 August 2008 - 03:21 PM.

[HighDesertWizard]

My Boswellia Supplement Trial Plan

I've been mulling over how to proceed with a Boswellia trial on myself and here are my current best thoughts about it. Any feedback is much appreciated.

* I was going to switch from the 5-LOXIN formulation to the TrueBotanica formulation because of the preponderance of AKBA in the latter. But then I found the study yesterday that used the 5-LOXIN formulation and found dramatic prevention of VCAM-1. So, for now I'm going to stick with the 5-LOXIN formulation.

I'm certain it will turn out to be useful to try the TrueBotanica product. But to kick this off, I'll stick with the 5-LOXIN brand. The use of the 5-LOXIN product in the study noted upthread was the clincher in making the decision.


* Just to make things simpler, I'm going to stick with the "Pure Encapsulations" 5-LOXIN product. It comes in a larger dosage than does the LEF product so I don't have to take as many capsules. Here's the product page for the Boswellia formulation I'm using.

http://www.purecaps....y00.asp?T1=BWA1


* My plan is to take 1 gram per day of that Boswellia extract in 3 divided doses for two months starting last week. That will be 300mg of the AKBA specific extract. The dose for Crohn's disease is larger than that and there was a safety study done by the 5-LOXIN folks that I referenced upthread showing that toxicity occured at doses that were 100s if not 1000s of times larger than that.

I would anticipate that I could lower the dosage after the two month period. But we'll see.


* I'm primarily interested in Boswellia for its cardiovascular effects. After two months, I will recheck all my lipids and probably get an NMR as well including Lp(a) volume and particle number as well. I'm certain I can talk the health professional I'm working with to prescribe the tests though I'll pay for the NMR out of pocket.

I've got numbers from my HMO for the standard lipid panel going back a few years so there are previous benchmarks to compare to.


If you have any thoughts about the current plan, don't hesitate to let me know.

I started the regmine about 10 days ago. I'm only getting around to posting it today because I think I have a first physiological response to my taking it.

[HighDesertWizard]

Well, I think I may have experienced the first physiological response to taking the 5-Loxin Boswellia.

As you all know, it's hard to trace these things down to a single new change. And it could be that the change I've noticed is due to something else besides my taking Boswellia. With that caveat in mind, here's what I've noticed.

I spend a lot of time at a computer screen and keyboard. I do that both for work and pleasure. For the last 5 or so years, I've had the early stages of carpal tunnel syndrome. No pain, but when I sleep, if I don't consciously position my hands in a certain way, when I wake up one or both of my hands will have fallen asleep. Positioning of the hands has worked pretty well for reducing the frequency of this occuring but it still has regularly occured a few times a week.

The Wikipedia entry on Carpal Tunnel Syndrome clearly describes the symptoms I've had now for a few years.

I woke up in the middle of the night realizing that my hands hadn't fallen asleep at night for a week or so. Also, I can't put my finger on it but there is some different feeling in my wrist joints. I can't really describe it. They just feel "looser" and "better oiled".

So I consciously tried to position my hands in a way that I know makes them fall asleep while I'm sleeping. I haven't yet been able to put them to sleep like I used to be able to.

Is it due to the Boswellia? Well, I googled Carpal Tunnel and Boswellia and got this link among others...

http://www.mamaherb....ConditionId=611

And I just realized after already expressing the caveat above that, if the Boswellia was behind the change in my hands falling asleep that I should expect to find some scientific studies discussing Carpal Tunnel and VCAM-1 and/or MMPs.

I haven't removed the caveat noted above, maybe the absence of the falling asleep symptom is due to something else. But here are some telling studies about what might be behind this change. There are quite a few more that could be posted. It's not clear to me that these are even the best ones.

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MMP-2 expression is associated with rapidly proliferative arteriosclerosis in the flexor tenosynovium and pain severity in carpal tunnel syndrome

Due to the lack of correlation between symptom severity and electrophysiology or nerve function, the 'container hypothesis' has emerged as a new concept in carpal tunnel syndrome (CTS). This proposes that symptoms relate to connective tissue alteration rather than to nerve fibre pathology. This study was conducted to investigate the pathology of the flexor tenosynovium and its relationship with symptomatology. The subjects comprised 40 patients with electrophysiologically proven CTS who underwent open carpal tunnel release (age range: 31-79 years). In all patients, subjective symptom severity was assessed with a Likert scale and symptom duration was recorded preoperatively. Flexor tenosynovium biopsied during surgery was analysed for arterial and connective tissue alteration. Proliferative arteriosclerosis was graded using the modified Banff score. Gelatin zymography and immunohistochemistry were also performed to investigate the role of gelatinase in CTS. Relationships were evaluated using Spearman rank correlation coefficients. Proliferative arteriosclerosis occurred with disease progression in the flexor tenosynovium, in the absence of inflammation. This event did not correlate with patient age but correlated closely with symptom duration. Immunohistochemistry with antibodies against MMP-2 and elastic van Gieson staining revealed that arterioles express high levels of MMP-2 within 3 months of symptom onset and that intimal hyperplasia proceeded rapidly between 4 and 7 months, resulting in severe vascular narrowing. Gelatin zymography showed that MMP-2 activity correlated negatively with symptom duration and positively with pain severity.

PMID: 15685708 [PubMed - indexed for MEDLINE]
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Relationship between Clinical Symptoms and Gelatinase in Carpal Tunnel Syndrome

Recent studies with validated outcome assessment demonstrate that clinical symptoms from carpal tunnel syndrome (CTS) are more severe in earlier phases than in the advanced phases and correlate with function of median nerve. Furthermore, MRI findings demonstrated that tenosynovial swelling within the carpal tunnel was the most common cause of CTS. Accordingly, we analyzed gelatinase in tenosynovium and evaluated the relationship between clinical symptoms and gelatinase (MMP-2/-9) in CTS. The study group consisted of 22 patients (6 males and 16 females) with surgical treatment for CTS. The patients were divided into 3 groups based on duration of disease: early group (n=9; .LEQ.3 months); intermediate group (n=7; 4-6 months); and late group (n=6; 7-12 months). The following symptoms were investigated and classified by their severity into 6 stages: daytime pain, nocturnal pain, daytime pareasthesia, nocturnal paresthesia and wake up frequency due to pain. Gelatinase activities in the tenosynovium were analysed by gelatin zymography and quantitatively analyzed using computer-assisted image analysis. Patients in early and intermediate groups complained of significantly more nocturnal and daytime pain, and woke up more often than those in late group. There were no significant differences in severity of daytime or nocturnal paresthesia among the groups. Analysis with zymography demonstrated that although MMP-9 (92kDa) was not activated in any of the groups, MMP-2 activation level (activated-(62kDa)/total-MMP2 (66kDa+62kDa)) was higher in early and intermediate groups than in late group (not statistically significant). MMP-2 activation level significantly correlated with daytime and nocturnal pain and wake-up frequency due to pain. It has been thought that clinical symptoms of CTS were caused by entrapment disorder of median nerve.... (author abst.)
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Expression of inflammatory cytokines and adhesion molecules in haemodialysis-associated amyloidosis

Background. The occurrence of various arthropathies including carpal-tunnel syndrome (CTS) in dialysis-associated amyloidosis, a condition caused by the deposition of β2 microglobulin (β2MG), has been emphasized for several years. We attempted to analyse the pathogenesis of CTS in haemodialysis-associated amyloidosis (HA). Methods. The expression of cell adhesion molecules and inflammatory cytokines in tenosynovial tissues was determined by using both reverse-transcriptase polymerase chain reaction (RT-PCR) and immunostaining. Results. There was a marked expression of ICAM-1, VCAM-1, E-selectin mRNAs together with increased mRNA expression of inflammatory cytokines (IL-1β, TNFα, IL-6 and MCP-1) in proliferating synovial tissues. ICAM-1 was expressed not only on vascular endothelial cells, but also on synovial cells. In contrast, both VCAM-1 and E-selectin were exclusively expressed on endothelial cells. Mononuclear cells bearing CD13, CD14, CD33 and HLA-DR with macrophage-like morphology were accumulated in the perivascular area and expressed VLA-4, LFA-1 and Mac-1. Moreover, synovial lining cells, vascular endothelial cells and infiltrated mononuclear cells expressed chemokines such as MCP-1 and MIP-1α. Conclusions. These data suggest that upregulated expression of inflammatory cytokines and adhesion molecules promotes activation and infiltration of macrophages causing CTS in haemodialysis-associated amyloidosis patients.
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[bran319]

Great thread wccaguy! As a runner I'm definitely interested in this product for achy knees so I will be following your reports with interest!

[TianZi]

So it falls on me to rain a bit on the parade of positive data posted in this thread about Boswellia (but we should keep in mind that the results of this study may be wrong, or highly dependent on testing methodology).

Per a 2004 U. of Arizona study published in the American Journal of Gastrointestinal and Liver Physiology:

"In summary, boswellia does not ameliorate symptoms of colitis in chemically induced murine models and, in higher doses, may become hepatotoxic."

http://ajpgi.physiol...hort/288/4/G798

(A substance which is hepatotoxic induces liver damage, which can lead to acute liver failure and death.)


"The goal of this study was to evaluate the effectiveness of boswellia extracts in controlled settings of dextran sulfate- or trinitrobenzene sulfonic acid-induced colitis in mice. Our results suggest that boswellia is ineffective in ameliorating colitis in these models. Moreover, individual boswellic acids were demonstrated to increase the basal and IL-1-stimulated NF-B activity in intestinal epithelial cells in vitro as well as reverse proliferative effects of IL-1. We also observed hepatotoxic effect of boswellia with pronounced hepatomegaly and steatosis. Hepatotoxity and increased lipid accumulation in response to boswellia were further confirmed in vitro in HepG2 cells with fluorescent Nile red binding/resazurin reduction assay and by confocal microscopy. Microarray analyses of hepatic gene expression demonstrated dysregulation of a number of genes, including a large group of lipid metabolism-related genes, and detoxifying enzymes, a response consistent with that to hepatotoxic xenobiotics."

The full text of the study is here:

http://ajpgi.physiol...full/288/4/G798

The hepatotoxic effects found here seem consistent with my understanding of the effects of high / long-term doses of NSAID's, and if confirmed in further studies, undermines the attractiveness of taking Boswellia as an alternative to NSAID's.

I will leave it to others to decipher the relevance and appropriateness of the testing methodology; for example, the method by which the Boswellia material used in the study was derived (the researchers didn't simply use an off-the shelf product, but rather, heavily modified an off-the-shelf product), and the dosage used.

Edited by TianZi, 03 August 2008 - 08:45 AM.

[TianZi]

I thought I'd follow up my post above with another based on further research.

Consistent with standard online practice, the webpage featuring the abstract to the U. of Arizona study included links to articles that cited this study. Following a very rough and cursory glance at the more recent studies that cited the 2004 study, I found none that reported in the main summary any negative effect on the experimental subjects (indeed, the title to one indicated that effects in mice are breed / strain dependent).

I just don't have sufficient interest in Boswellia to take this research any further and attempt as a layman to compare and contrast these studies, so someone more motivated will have to do this.

[Anthony_Loera]

An update for wccaguy

It seems like pricing for raw materials on this is all over the map... I believe there are probably quality issues at this time, and decent company sources are unknown. It will take time to investigate why this is...

A

[HighDesertWizard]

An update for wccaguy

It seems like pricing for raw materials on this is all over the map... I believe there are probably quality issues at this time, and decent company sources are unknown. It will take time to investigate why this is...

A

Thanks for the update Anthony.

To my mind, this is confirmation that, at least for the time being, the 5-Loxin formulation makes the most sense and perhaps should be the only Boswellia formulation considered for supplementation.

Meanwhile, I'm now about a week I think into sleeping at night without my hands going numb due to early carpal tunnel syndrome. And by the way, both my sister and my father have had operations for their carpal tunnel syndrome. I guess I'll see if the streak continues.

Edited by wccaguy, 03 August 2008 - 03:32 PM.