Osteoarthritis

27 million Americans have osteoarthritis (OA).

Direct medical costs resulting from OA total $185 billion a year in the U.S.

  • insurers pay $149.4 billion
  • patients pay $36.1 billion out-of-pocket
    • Avg. woman: $1,400 a year
    • Avg. man: $700 a year

Osteoarthritis affects:

  • 25-30% of persons aged 45-64 years
  • 60% of persons older than 65 years
  • Over 80% of persons older than 75 years

Chance you will develop OA in at least one knee: 46%

Between 1996 and 2006:

  • cost of arthritis meds rose from $4.2 to  $13.2 billion
  • number of prescriptions for OA rose from 164 to 231 million

In 2030 the last baby boomer turns 65

In 2030 an estimated 25% of Americans will have osteoarthritis.

Osteoarthritis is chronic joint inflammation.

Let’s get better.

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Related pages:
Joint Pain
Inflammation
Other Arthritis
Banjo - Let's get better

Osteoarthritis results from inflammation that's been smoldering for years.

Pain is your first indication that inflammation and joint damage are accelerating.

Banjo eliminates the inflammation that's causing pain and destroying joints. Once inflammation is eliminated, your body can heal.

Let's get better.

Introduction to Banjo

Banjo provides fast, effective relief from pain and inflammation because it enables your body’s immune system to function properly. It works just like the fruits and vegetables you eat every day – by naturally inhibiting NF-kB, the inflammation Master Switch.

Banjo works better because it combines the most effective natural extracts and delivers them in a form that ensures maximum bio-availability. You get the full spectrum of phytonutrients your body needs to turn off excess inflammation.

Perspective on Osteoarthritis

Overview

Osteoarthritis is a chronic, progressive disease characterized by inflammation in and around the joint space. Inflammation eventually results in damage to joint structures, especially the cartilage covering the end of each bone at the joint space.

Because osteoarthritis commonly makes its appearance late in life, it has often been called “wear and tear” arthritis. That term, however, is generally misleading. An actual tear or other damage to a joint component will increase the likelihood of later developing osteoarthritis and will speed the progression of osteoarthritis. But in the absence of such physical damage, moderate exercise is beneficial to the joint, as it reduces inflammation. If osteoarthritis was simply the result of normal use (e.g. “wear and tear”) then additional wear and tear would not be expected to have a beneficial effect.

Osteoarthritis is not a normal part of aging. It is not many years of use that results in osteoarthritis, but many years of low-grade inflammation. According to the theory advanced on this site, that low-grade inflammation is caused by chronic over-activation of NF-kB. Chronic over-activation of NF-kB results from a combination of too few NF-kB inhibitors and too many NF-kB activators. Aging is associated with an increase in NF-kB activators, which is one reason for the greater prevalence of osteoarthritis with advancing age.

Chronic low-grade inflammation is sometimes referred to as “silent inflammation” – and that term is especially appropriate in osteoarthritis. Because there are no nerves in cartilage, the initial onset and early progression of the disease is usually a pain free process. Eventually, however, increasing levels of inflammation and accumulating damage results in pain.

Unfortunately, there may already be substantial cartilage loss and other joint damage by the time arthritis becomes painful. Nonetheless, once inflammation is alleviated the body is often able to heal itself. Even damaged cartilage is capable of regeneration.

Osteoarthritis is a disease of inflammation.

According to the theory advanced on this site (in brief) every ‘disease of inflammation’:

  1. Is caused by inflammation;
  2. That results from over-activation of NF-kB;
  3. Which can be treated by administering NF-kB inhibitors – especially natural (plant derived) NF-kB inhibitors.

The following – if true – would support (not ‘prove’) the theory in regard to osteoarthritis:

  • Osteoarthritis is associated with inflammation.
  • Osteoarthritis is associated with excess NF-kB activation.
  • There is evidence that osteoarthritis is associated with a defect (especially genetic) or vulnerability that results in excess activation of NF-kB.
  • There is evidence that inhibiting NF-kB is beneficial in the treatment of osteoarthritis.
  • There is evidence that natural NF-kB inhibitors are beneficial in treating or preventing osteoarthritis.
  • There is an explanation for the cause and progression of osteoarthritis that is consistent with the theory.

Osteoarthritis is associated with inflammation – true.

Even the most cursory review of osteoarthritis is sufficient to show that it is closely associated with inflammation. The evidence is so overwhelming that it will not be addressed in any further detail.

Osteoarthritis is associated with excess NF-kB activation – true.

There is evidence that inhibiting NF-kB is beneficial in the treatment of osteoarthritis – true.

  • Chondroitin sulfate is known to relieve certain symptoms of osteoarthritis by inhibiting NF-kB.
  • A molecule isolated from a seahorse has been shown to beneficially reduce collagen breakdown in osteoarthritis by inhibiting NF-kB.
  • Moderate exercise has been shown to reduce inflammation in osteoarthritis by inhibiting NF-kB.
  • In addition, many standard therapeutic agents that can be used in the treatment of osteoarthritis (such as aspirin and the glucocorticoids) act at least in part by inhibiting NF-kB.

There is evidence that natural NF-kB inhibitors are beneficial in treating or preventing osteoarthritis – true.

  • A raw, vegan diet was shown in one study to provide symptomatic relief for arthritis. Such a diet would be high in natural NF-kB inhibitors.
  • An extract of garlic has been shown to inhibit NF-kB, and to be of benefit in the treatment of osteoarthritis.
  • Frankincense has been shown to help with symptoms of osteoarthritis, and to act via inhibition of NF-kB.
  • A great many other natural inhibitors of NF-kB have also been clinically proven to relieve osteoarthritis symptoms – only a few being referenced here.

A defect or vulnerability (especially genetic) specific to this disease results in excess NF-kB activation – true, but the case is not extremely compelling – in part because genetics seems to play a minor role in the development of osteoarthritis.

There is an explanation for the cause and progression of osteoarthritis that is consistent with the theory. Yes.

The basic theory is sufficient to explain both the cause and progression of osteoarthritis – and to suggest what should be the most effective treatment for osteoarthritis.

There is overwhelming support for the theory that osteoarthritis is associated with excess activation of NF-kB, that inhibitors of NF-kB are of benefit in its treatment, that natural NF-kB inhibitors are effective – even that combining multiple agents may enhance the benefits of natural NF-kB inhibitors for the treatment of osteoarthritis – which supports, in part, the rationale behind the development of Banjo.

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ALL OSTEOARTHRITIS POSTS

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January 16, 2010

Overview of peppermint’s beneficial effects

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Peppermint has a many thousand year history of safe use, is noteworthy as an anti-inflammatory, and demonstrates a number of other beneficial effects.

Peppermint is one of the most commonly consumed herbs. That said, unless you drink peppermint tea, you might seldom encounter real peppermint, as the use of real peppermint in diverse products has been largely replaced by the use of less expensive, more easily obtained synthetic flavorings.

Of interest, rosemary is often mentioned as an herb useful in the treatment of inflammation. Peppermint is seldom mentioned in that regard, except in the treatment of irritable bowel syndrome.  However, the primary active ingredient thought responsible for the anti-inflammatory activity of rosemary is rosmarinic acid. Rosemary contains, on average, 38,000 ppm of rosmarinic acid. Peppermint contains, on average, 30,000 ppm of rosmarinic acid. As such, the general anti-inflammatory effects of rosemary might also be manifest by peppermint. Peppermint excels (and is included in Banjo) on account of both its flavor and the additional benefits it provides.

Peppermint is believed to be especially useful in bowel disease, arthritis, and for the treatment of allergies & asthma.

Peppermint is noteworthy as an anti-inflammatory and has been shown to be:

  • Anti-microbial
  • Anti-viral
  • A potent anti-oxidant
  • Anti-tumor
  • Anti-allergic
  • Anti-pain

Adverse reactions to peppermint have not been reported, as per the study below. Caution should be exercised if using peppermint oil. Note that Banjo contains only a pure water extract of peppermint leaf.

The publication:

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Phytother Res. 2006 Aug;20(8):619-33.

A review of the bioactivity and potential health benefits of peppermint tea (Mentha piperita L.).

McKay DL, Blumberg JB.

USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111, USA.

Summary of the abstract

Peppermint (Mentha piperita L.) is widely consumed. Peppermint tea, brewed from the plant leaves, and the essential oil of peppermint are used in traditional medicines. Evidence-based research regarding the bioactivity of this herb is reviewed.

The phenolic constituents of the leaves include rosmarinic acid and several flavonoids, primarily eriocitrin, luteolin and hesperidin. The main volatile components of the essential oil are menthol and menthone.

In vitro, peppermint has significant antimicrobial and antiviral activities, strong antioxidant and antitumor actions, and some antiallergenic potential.

Animal model studies demonstrate a relaxation effect on gastrointestinal (GI) tissue, analgesic and anesthetic effects in the central and peripheral nervous system, immunomodulating actions and chemopreventive potential.

Human studies of peppermint leaf are limited and clinical trials of peppermint tea are absent. Adverse reactions to peppermint tea have not been reported, although caution has been urged for peppermint oil therapy in patients with GI reflux, hiatal hernia or kidney stones.

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January 15, 2010

Lemon peel inhibits NF-kB, reduces inflammation

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Lemon peel is a rich source of nobiletin, found in this study to inhibit NF-kB. Inhibition of NF-kB was associated with a decrease in: NO production,  PGE-2, and COX-2, each of which is an important mediator of pain and inflammation in arthritis.

The publication:

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J Ethnopharmacol. 2007 Aug 15;113(1):149-55. Epub 2007 May 31.

Nobiletin from citrus fruit peel inhibits the DNA-binding activity of NF-kappaB and ROS production in LPS-activated RAW 264.7 cells.

Choi SY, Hwang JH, Ko HC, Park JG, Kim SJ.

Department of Life Science, Cheju National University, 66 Jejudahakno, Jejusi, Jeju 690-756, Republic of Korea.

Summary of the abstract

Post-treatment with nobiletin, which was purified from the fruit peel of citrus was shown to significantly suppress NF-kB, NO and PGE(2) production, and iNOS and COX-2 protein expression in an animal model of arthritis.

Nobiletin interrupted the DNA-binding activity of activated NF-kappaB.

As reactive oxygen species (ROS) are known to regulate the activation of NF-kB, the effect of nobiletin on LPS-induced ROS generation was tested. Nobiletin significantly inhibited LPS-induced intracellular ROS production.

These results suggest that nobiletin may exert an anti-inflammatory effect through the interruption of NF-kB DNA-binding activity and the suppression of ROS generation.

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January 15, 2010

Dandelion reduces pain and inflammation

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Dandelion (Taraxacum officinale) has a long history of use as a natural medicine for the relief of pain and inflammation. On investigating dandelion the researchers whose publication is summarized below demonstrated a diversity of effects attributable to an extract of dandelion, including a reduction in numerous markers of inflammation. The historic use of dandelion is thereby confirmed by modern research.

The publication:

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J Ethnopharmacol. 2008 Jan 4;115(1):82-8. Epub 2007 Sep 15.

Anti-inflammatory activity of Taraxacum officinale.

Jeon HJ, Kang HJ, Jung HJ, Kang YS, Lim CJ, Kim YM, Park EH.

College of Pharmacy, Sookmyung Women’s University, Cheongpa-dong, Yongsan-ku, Seoul 140-742, Republic of Korea.

Summary of the abstract

Taraxacum officinale (dandelion) has been widely used as a folkloric medicine for the treatment of diverse diseases.

In this study, the dried plant was extracted with 70% ethanol to generate its ethanol extract (TEE).

TEE showed radical scavenging activity, decreased the reactive oxygen species (ROS) level, and had anti-angiogenic activity (significant in the prevention or treatment of cancer.)

In a model of asthma and pneumonia, TEE inhibited production of exudate, and significantly diminished nitric oxide (NO) and leukocyte levels in the exudate. It acted to reduce inflammation. TEE was also analgesic – it decreased pain.

The anti-inflammatory effects of TEE included a reduction in vascular permeability, decreased production of NO, decreased expression of inducible nitric oxide synthase (iNOS) and decreased cyclooxygenase-2 (COX-2) in lipopolysaccharide (LPS)-stimulated macrophages.

Collectively, Taraxacum officinale contains anti-angiogenic, anti-inflammatory and anti-nociceptive (anti-pain) activities through its inhibition of NO production and COX-2 expression and/or its antioxidative activity.

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January 15, 2010

Sunflower seeds may be effective for arthritis

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Sunflower seeds, rich in alpha-amyrin palmitate, may be an effective treatment for arthritis.

Sunflower seeds are a rich source of alpha-amyrin palmitate. In the study briefly summarized below, administration of alpha-amyrin palmitate was shown to substantially improve arthritis in the animal model. This might account, in part, for the fact that sunflower seeds have long been used in traditional medicines – they reduce inflammation.

The publication:

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Drugs Exp Clin Res. 1994;20(1):1-5.

Effect of alpha-amyrin palmitate on adjuvant arthritis.

Kweifio-Okai G, Bird D, Eu P, Carroll AR, Ambrose R, Field B.

Department of Anatomy and Physiology, Royal Melbourne Institute of Technology, Bundoora, Australia.

Summary of the abstract

Alpha-amyrin palmitate was synthesized and tested on adult male Wistar rats with arthritis.

When administered orally at 66 mg/kg BW every 48 h for 5 days from days 32 to 40 post-adjuvant and assessed on day 50, alpha-amyrin palmitate returned the increases in serum hyaluronate and blood granulocytes toward non-arthritic levels and corrected the moderate anaemia of adjuvant arthritis.

Tissue examinations of the joints showed reduced synovial proliferation and invasion of joints and reduced leucocyte infiltration of bone marrow in alpha-amyrin palmitate-treated rats. In addition, the drug prevented or reduced bone (subchondral or cortical) and cartilage (articular) destruction in arthritic rats.

The results suggest that alpha-amyrin palmitate is antiarthritic in the adjuvant model of arthritis in rats.

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January 14, 2010

Ginger – multiple effects reduce pain & inflammation

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Relief from pain and inflammation without significant side effects.

When properly administered, ginger offers greater potential for relief of pain and inflammation than non-steroidal anti-inflammatory drugs (NSAIDs) – but with fewer side effects – for several reasons.

Ginger directly inhibits prostaglandin synthesis and thereby acts as both a COX-I and COX-II inhibitor.

Ginger also inhibits 5-lipoxygenase by direct action – thereby inhibiting the production of leukotrienes. Leukotrienes are key regulators (promoters) of inflammation. They may be of particular importance in allergy and asthma, but are probably involved in promoting and sustaining inflammation generally. Recent studies suggest a role for leukotrienes in cancer, arthritis, pain perception, cardiovascular disease and neurological disease.

Ginger further exerts its anti-inflammatory and anti-pain effect by inhibiting expression of pro-inflammatory genes that encode cytokines, chemokines, and the inducible enzyme cyclooxygenase-2. Chief among these effects is its inhibition of NF-kB – the inflammation Master Switch.

Banjo delivers a combination of herbal extracts, including ginger extract, by means of a lozenge. By allowing the lozenge to dissolve in your mouth, active components (actives) are absorbed trans-mucosally (through the lining of the mouth.) This results in faster delivery of a higher concentration of actives to the bloodstream. Of perhaps greater significance, actives are not first subject to the harsh, destructive environment of the stomach, neither are they immediately destroyed by the liver (the “first pass” effect.)

The traditional means of administering ginger – as well as other medicinal herbs – was by chewing or eating. Of course both chewing and eating require that the product spend a substantial time in direct contact with the mucous membranes of the mouth. That might be important.

Most such products are now delivered by means of a gelatin capsule that is immediately swallowed, which may be one reason for the limited efficacy of such products. Banjo provides effective relief from pain and inflammation by employing an effective combination of agents, delivered so as to ensure maximum bio-availability.

The publication:

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J Med Food. 2005 Summer;8(2):125-32.

Ginger–an herbal medicinal product with broad anti-inflammatory actions.

Grzanna R, Lindmark L, Frondoza CG.

RMG Biosciences, Inc.

Summary of the abstract

The anti-inflammatory properties of ginger have been known and valued for centuries.

Ginger inhibits prostaglandin biosynthesis and as such is an herbal medicinal product that shares pharmacological properties with non-steroidal anti-inflammatory drugs.

Ginger suppresses prostaglandin synthesis through inhibition of cyclooxygenase-1 and cyclooxygenase-2. Ginger also inhibits 5-lipoxygenase. This pharmacological property distinguishes ginger from nonsteroidal anti-inflammatory drugs, and might explain why ginger has a better therapeutic profile and fewer side effects than non-steroidal anti-inflammatory drugs.

The characterization of the pharmacological properties of ginger entered a new phase with the discovery that ginger extract inhibits the induction of several genes involved in the inflammatory response. These include genes encoding cytokines, chemokines, and the inducible enzyme cyclooxygenase-2.

This discovery provided the first evidence that ginger modulates biochemical pathways activated in chronic inflammation.

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December 7, 2009

NF-kB activation in joint leads to cartilage destruction

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Cartilage destruction is a hallmark feature of osteoarthritis. It is associated with elevated production of basic fibroblast growth factor (bFGF) and matrix metalloproteinase-13 (MMP-13). In addition, it is reported in the study briefly summarized below that the ability of cartilage to heal is severely limited in the presence of bFGF.

MMP-13 was found to be elevated in large part due to over-activation of NF-kB. This may in part account for the observation that cartilage healing is severely limited when joints are inflamed, but may progress rapidly once joint inflammation is relieved.

The publication:

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J Biol Chem. 2007 Oct 26;282(43):31409-21. Epub 2007 Aug 27.

Basic fibroblast growth factor activates the MAPK and NFkappaB pathways that converge on Elk-1 to control production of matrix metalloproteinase-13 by human adult articular chondrocytes.

Muddasani P, Norman JC, Ellman M, van Wijnen AJ, Im HJ.

Department of Biochemistry, Rush University Medical Center, Chicago, Illinois 60612, USA.

Summary of the abstract

The pathology of joint destruction is associated with elevated production of basic fibroblast growth factor (bFGF) and matrix metalloproteinase-13 (MMP-13).

In osteoarthritic joint disease, expression of bFGF and MMP-13 in chondrocytes and their release into the synovial fluid are significantly increased.

We have previously found that the capacity for cartilage repair in human adult articular chondrocytes is severely compromised by minimal exposure to bFGF.

This study provides evidence that elevated expression of MMP-13 occurs through a pathway that includes activation of NF-kB, resulting in degradation of the cartilage matrix in degenerative joint diseases such as osteoarthritis.

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December 7, 2009

Ginger extract reduces inflammation in arthritis

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Ginger root extract was found to reduce inflammation in this study of cartilage cells in a pig model of arthritis.

Nitric oxide (NO) and prostaglandin-E2 (PGE2) were both reduced within 24 hours after application of ginger root extract. Both are key pro-inflammatory agents thought to be important in the pain and inflammation of arthritis.

It is suggested that ginger root extract may play an important role in the future treatment of arthritis.

The publication:

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J Med Food. 2005 Summer;8(2):149-53.

Comparative effects of ginger root (Zingiber officinale Rosc.) on the production of inflammatory mediators in normal and osteoarthrotic sow chondrocytes.

Shen CL, Hong KJ, Kim SW.

Department of Pathology, Texas Tech University, Lubbock, Texas 79409-2141, USA.

Summary of the abstract

Ginger root was previously demonstrated to exert anti-arthritic effects in sow cartilage explants.

This study further investigated the comparative effects of ginger root extract (GRE) on the production of inflammatory mediators, including nitric oxide (NO) and prostaglandin E2 (PGE2), in normal chondrocytes (NC) and osteoarthrotic chondrocytes (OC) isolated from pigs.

Collectively, OC produce more inflammatory mediators than do NC, and the production of inflammatory mediators was reduced when GRE was added to both the OC and the NC. The inhibitory effects of GRE on NO and PGE2 production by sow OC observed in this study suggest an important role for GRE as an anti-arthritic agent.

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December 7, 2009

Ginger an effective anti-inflammatory agent in arthritis

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Ginger shown to reduce COX2 and tumor necrosis factor-alpha (TNF-alpha) – probably via inhibition of NF-kB.

Arthritis is characterized by joint inflammation that causes pain and results in cartilage destruction.

TNF-alpha plays a key role in the course and progression of arthritis. It is both a product and an activator of NF-kB. It is probably by means of this NF-kB activating effect that it leads to an increase in other pro-inflammatory cytokines as well as destructive enzymes – all of which means that TNF-alpha plays a central role in arthritis.

In the study summarized below, ginger was found to decrease the level of TNF-alpha while also reducing the level of pro-inflammatory cytokines and destructive enzymes.

A decrease in the level of activated NF-kB was also observed, which is the most likely mechanism by which ginger exerts its beneficial effects in arthritis.

The publication:

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In Vitro Cell Dev Biol Anim. 2004 Mar-Apr;40(3-4):95-101.

An in vitro screening assay for inhibitors of proinflammatory mediators in herbal extracts using human synoviocyte cultures.

Frondoza CG, Sohrabi A, Polotsky A, Phan PV, Hungerford DS, Lindmark L.

Division of Arthritis Surgery, Department of Orthopaedic Surgery, Johns Hopkins University, Baltimore, Maryland 21205, USA.

Summary of the abstract

Tumor necrosis factor-alpha (TNF-alpha), cyclooxygenase-2 (COX2), and prostaglandins (PGs) such as PGE-2 play a critical role in the pathophysiology of arthritis.

TNF-alpha mediates induction of other cytokines, COX-2, PGs, and metalloproteinases, which leads to cartilage degradation.

An assay system was developed for screening inhibitors of proinflammatory mediators in herbal extracts.

Ginger extract significantly inhibited the activation of TNF-alpha and COX-2 expression and also suppressed production of TNF-alpha and PGE-2. Inhibition of TNF-alpha and COX-2 activation was accompanied by inhibition of NF-kB and IkappaB-alpha induction.

These observations indicate that ginger extract offers a complementary and alternative approach to modulate the inflammatory process involved in arthritis.

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December 7, 2009

Synergy of multiple NF-kB inhibitors

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Turmeric (curcumin) and resveratrol found to act synergistically in the treatment of arthritis.

This is an essential publication because it demonstrates that by combining different natural inhibitors of NF-kB, a greater anti-inflammatory effect may be achieved than is possible with either agent alone. The study further suggests that this might be especially true when the different agents act to inhibit NF-kB through different mechanisms.

By implication, the observed synergy will not be limited to the specific combination studied (curcumin + resveratrol.)

Banjo combines a number of different natural NF-kB inhibitors, each of which may act through a slightly different mechanism in the inhibition of NF-kB. While many of the individual agents might provide some benefit, Banjo is expected to provide a substantially greater benefit than any single agent. That possibility is confirmed by the study briefly summarized below.

The publication:

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Arthritis Res Ther. 2009 Nov 4;11(6):R165.

Synergistic chondroprotective effects of curcumin and resveratrol in human articular chondrocytes: inhibition of IL-1beta-induced NF-kappaB-mediated inflammation and apoptosis.

Csaki C, Mobasheri A, Shakibaei M.

Musculoskeletal Research Group, Institute of Anatomy, Ludwig-Maximilians-University Munich, Pettenkoferstrasse 11, 80336 Munich, Germany.

Summary of the abstract

Currently available treatments for osteoarthritis (OA) are restricted to nonsteroidal anti-inflammatory drugs, which exhibit numerous side effects and are only temporarily effective. Novel, safe and more efficacious anti-inflammatory agents are needed for OA.

Naturally occurring polyphenolic compounds, such as curcumin and resveratrol, are potent agents for modulating inflammation. Both compounds mediate their effects by inhibiting NF-kB.

In chondrocytes (cartilage) resveratrol modulates the NF-kB pathway by inhibiting the proteasome, while curcumin modulates the activation of NF-kB by inhibiting upstream kinases (Akt). However, the combinational effects of these compounds in chondrocytes has not been studied and/or compared with their individual effects.

This study investigated the potential synergistic effects of curcumin and resveratrol.

Treatment with curcumin or resveratrol was found to inhibit NF-kB.  It is suggested that each works through a distinct mechanism and that combining these two agents in the treatment of arthritis might be of more value than the use of either agent separately.

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December 6, 2009

Ginger: ancient remedy, modern miracle

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This publication speaks for itself. Ginger may have many applications and its mechanism(s) of action are being investigated.

The publication:

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Hawaii Med J. 2007 Dec;66(12):326-7.

Ginger: an ancient remedy and modern miracle drug.

Hoffman T.

Department of Complementary and Alternative Medicine, John A. Burns School of Medicine, University of Hawaii, USA.

Summary of the abstract

Ginger has been used safely for thousands of years in traditional and folk medicine. Advanced technology enables the validation of these traditional experiences.

The National Center for Complementary and Alternative Medicine (NCCAM) has evaluated the results of the available studies, rating the reports from “suggestive” (for short-term use of Ginger for safe relief from pregnancy related nausea and vomiting), to “mixed” (when used for nausea caused by motion sickness, chemotherapy, or surgery), and to “unclear” for treating rheumatoid arthritis, osteoarthritis, or joint and muscle pain).

The scope of ginger’s use will soon be clearly identified and incorporated into mainstream therapeutic options, thereby integrating east and west, old with new, to render ginger as a true “Universal Remedy”.

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December 5, 2009

Moderate exercise reduces joint inflammation

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NF-kB is the master switch controlling response to exercise.

This is really quite interesting. Somehow, moderate exercise – through the transmission of physical forces in your joints – leads to the inhibition of NF-kB. The result is a decrease in inflammation.

However, if instead of being subject to the mechanical stress of moderate exercise, your joints are instead subject to a higher magnitude of physical forces – those physical forces transmitted to the joint (e.g. knee) activate NF-kB.

NF-kB is truly the Master switch of inflammation. It’s even mediating inflammation or anti-inflammation effects in response to physical forces on the knee.

The publication:

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Curr Opin Clin Nutr Metab Care. 2003 May;6(3):289-93.

Signal transduction by mechanical strain in chondrocytes.

Deschner J, Hofman CR, Piesco NP, Agarwal S.

Department of Oral Medicine and Pathology, University of Pittsburgh School of Dental Medicine, Pittsburgh, Philadelphia 15261-1964, USA.

Summary of the abstract

PURPOSE OF REVIEW: Exercise and passive motion are beneficial for inflamed joints, whereas excessive mechanical forces initiate cartilage destruction as observed in osteoarthritis.

However, the intracellular mechanisms that convert mechanical signals into biochemical events responsible for cartilage destruction and repair remain paradoxical.

RECENT FINDINGS: Mechanical strain of low magnitude inhibits inflammation by suppressing IL-1beta and TNF-alpha-induced transcription of multiple proinflammatory mediators involved in cartilage degradation.

This also results in the upregulation of proteoglycan and collagen synthesis that is drastically inhibited in inflamed joints.

On the contrary, mechanical strain of high magnitude is proinflammatory and initiates cartilage destruction while inhibiting matrix synthesis. Investigations reveal that mechanical signals exploit nuclear factor-kappa B (NF-kB) for the activation of inflammation and cartilage destruction.

Mechanical strain of low magnitude inhibits NF-kB whereas mechanical strain of high magnitude activates NF-kB.

SUMMARY: The beneficial effects of exercise result from the inhibition of NF-kB.

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December 5, 2009

Subchondral bone inflamed in OA

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Active inflammatory processes were found to be ongoing in the subchondral bone (the bone underneath the collagen) of those with osteoarthritis.

The suggestion is offered that this ‘deeper’ inflammation may be responsible for some substantial portion of cartilage damage witnessed in osteoarthritis.

The publication:

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J Orthop Sci. 2008 May;13(3):202-10. Epub 2008 Jun 6.

Enhanced expression of interleukin-6, matrix metalloproteinase-13, and receptor activator of NF-kappaB ligand in cells derived from osteoarthritic subchondral bone.

Sakao K, Takahashi KA, Mazda O, Arai Y, Tonomura H, Inoue A, Saito M, Fujioka M, Takamiya H, Imanishi J, Kubo T.

Department of Orthopaedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, Japan.

Summary of the abstract

BACKGROUND: The aim of this study was to clarify the significance of subchondral bone in the pathology of osteoarthritis (OA) by investigating the expression of inflammatory cytokines, proteases, and receptor activator of NF-kappaB ligand (RANKL)/receptor activator of NF-kappaB (RANK)/osteoprotegerin (OPG) involved in cartilage degeneration.

RESULTS: Higher levels of interleukin-6 (IL-6), matrix metalloproteinase-13 (MMP-13), and RANKL were found in OA SBOs compared to SBOs without OA. The expressions of these genes was greater in patients with severe cartilage damage than in those with mild cartilage damage.

CONCLUSION: The increases in IL-6, MMP-13, and RANKL expression in OA SBOs suggest that in subchondral bone OA progression involves abnormal osseous tissue remodeling, which induces mechanical property changes. Cartilage degeneration in OA may also be due, at least in part, to IL-6 and MMP-13 produced by SBOs. Comprehensive research on these pathological features may lead to the development of more effective therapies for OA by administration of molecules that affect bone remodeling and metabolism.

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December 5, 2009

Genetics in osteoarthritis

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In general, genetics play a weak role in the development of osteoarthritis.

The strongest genetic association is with FRZB – also known as “frizzled-related-protein-3″  – which is associated with hip osteoarthritis in women. Why might that be?

FRZB is an antagonist to (counter balances) the effects of the WNT pathway.

When there is a slight mutation at the gene coding for FRZB, the FRZB that the body produces is slightly defective – it does not do quite so good a job at inhibiting or counter-balancing WNT. Therefore, whatever WNT does – when FRZB is defective, WNT will do more of it. Got that?

What does WNT do? One thing it does is activate NF-kB.

So defective FRZB => more WNT activity => more NF-kB activity => hip osteoarthritis in women.

I have no idea why the hip – or why women.

If you’re reading this, please send me an email – I’ll send you a prize of some sort – no one should have to read (let alone write) things like this – but I did commit myself to finding connections between the genetic defects of each condition and excess activation of NF-kB.

OK, I’ve done it – I’m moving on…

As per usual the publications are summarized below.

The first publication:

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Proc Natl Acad Sci U S A. 2004 Jun 29;101(26):9757-62. Epub 2004 Jun 21.

Functional variants within the secreted frizzled-related protein 3 gene are associated with hip osteoarthritis in females.

Loughlin J, Dowling B, Chapman K, Marcelline L, Mustafa Z, Southam L, Ferreira A, Ciesielski C, Carson DA, Corr M.

Institute of Musculoskeletal Sciences, Botnar Research Centre, Nuffield Orthopaedic Centre, University of Oxford, Oxford OX1 7LD, United Kingdom.

Very brief summary of the abstract

Osteoarthritis (OA) is a leading cause of disability in Western society with multiple risk factors, including a complex genetic pattern. Identifying loci involved in the heredity of OA might lead to insights into the molecular pathogenesis of this common disorder.

[Long discussion of gene mapping and statistical associations.]

Hence, functional polymorphisms within FRZB confer susceptibility for hip OA in females and implicate the wnt signaling pathway in the pathogenesis of this disease.

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The second publication:

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Invest Ophthalmol Vis Sci. 2009 Oct 29.

The pathogenic role of the canonical Wnt pathway in age-related macular degeneration.

Zhou T, Hu Y, Chen Y, Zhou K, Zhang B, Gao G, Ma JX.

Biochemistry, Zhongshan University, Guangzhou, China.

Summary of the abstract

PURPOSE. Our previous studies showed that the Wnt signaling pathway is activated in the retina and retinal pigment epithelium of animal models of age-related macular degeneration (AMD) and diabetic retinopathy (DR). The purpose of this study is to investigate the role of the canonical Wnt pathway in pathogenesis of these diseases.

The activation of the Wnt pathway significantly up-regulated expression of VEGF, NF-kB and TNF-alpha. Further, Ad-S37A induced ROS generation in a dose-dependent manner. Wnt3a also induced a 2-fold increase of ROS generation. Intravitreal injection of Ad-S37A up-regulated expression of VEGF, ICAM-1, NF-kappaB, TNF-alpha and increased protein nitrotyrosine levels in the retina of normal rats.

CONCLUSION. Activation of the canonical Wnt pathway is sufficient to induce retinal inflammation and oxidative stress and plays a pathogenic role in AMD and DR

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December 5, 2009

Garlic for inflammation

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Garlic extract reduces inflammation via inhibition of NF-kB.

As is the case with many plant extracts, especially those with a history of medicinal use (such as garlic), the extract is found to be at least somewhat effective in the treatment of inflammation because it inhibits NF-kB.

I sincerely believe it would be difficult to find a fruit or vegetable that on close study would not be found to inhibit NF-kB. Nonetheless, this is presented as yet another example of NF-kB inhibition as both common and effective – efficacy being relative, of course (meaning it’s effective, but almost certainly quite weak.)

The publication:

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Osteoarthritis Cartilage. 2009 Jan;17(1):91-9.

Inhibition of cyclooxygenase 2 expression by diallyl sulfide on joint inflammation induced by urate crystal and IL-1beta.

Lee HS, Lee CH, Tsai HC, Salter DM.

Department of Pathology, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan, ROC.

Summary of the abstract

OBJECTIVE: Investigation of the effects of diallyl sulfide (DAS), a garlic sulfur compound, on joint tissue inflammation.

RESULTS: DAS inhibited IL-1beta induced elevation of COX-2 expression in primary synovial cells and chondrocytes.

NF-kB activation was blocked by DAS.

CONCLUSIONS: DAS prevents IL-1beta and COX-2 increases, effectively blocking inflammation in synovial cells and chondrocytes by inhibiting NF-kB. DAS may be of value in treatment of joint inflammation.

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December 5, 2009

Everything you need to know about osteoarthritis

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NF-kB inhibition as the Holy Grail of osteoarthritis treatment.

This is an essential publication because it really does tell us (nearly) everything we need to know in order to effectively treat osteoarthritis.

The publication referenced below lays it out – it’s very simple:

  • Osteoarthritis is characterized by cartilage destruction and inflammation of the membrane that surrounds the joint (the synovium.)
  • Cartilage destruction is the result of inflammation.
  • The inflammation results from excess activation of NF-kB.
  • Chondroitin sulfate works because it inhibits NF-kB.

The cause of osteoarthritis.

In chronological order:

Excess NF-kB activation => inflammation => joint destruction & pain

The root of the problem is obvious: Excess NF-kB activation.

The ideal treatment is obvious: Prevent excess NF-kB activation.

Disputing with the publication

The authors’ statement that chondroitin sulfate (CS) “prevents joint space narrowing and reduces joint swelling and effusion” implies a degree of efficacy that is not consistent with real-world results.

  • CS may be effective or somewhat effective at providing symptomatic relief for up to around 30% of patients by the end of 90 to 180 days of use.
  • CS has not been convincingly shown to prevent joint space narrowing (which is taken to mean it prevents further cartilage destruction.) CS might do this for some patients, but clinical trial results have been mixed at best.

But since all that really matters is patient safety and satisfaction, the above ‘disputes’ are trivial. CS is very safe – certainly much safer than NSAIDs (e.g. aspirin, Motrin, etc.)

Many patients obtain adequate and satisfactory relief from CS, and for some this class of product has proved to be life changing. CS is a great product.

Further discussion

It is this author’s opinion that CS is a relatively weak inhibitor of NF-kB.

The reason for pointing this out is not to disparage CS – which is a great product for some. Rather, it is important to make a distinction between mechanism (NF-kB inhibition) and efficacy (e.g. strength.)

Those who have been unsuccessful with CS and glucosamine products should not conclude that NF-kB inhibitors are ineffective.

Evidence that CS is generally a weak inhibitor of NF-kB includes the following:

  • Patients are instructed to take the product for 90 days, as it may take that long before any beneficial effects are noticed.
  • A minority of patients respond adequately to the product, and few obtain complete relief.
  • The product has not been shown to be effective (even subjectively, or anecdotally) in the treatment of other conditions associated with inflammation.

Banjo is a faster acting, more effective NF-kB inhibitor.

  • Nearly all those with osteoarthritis will experience a substantial improvement within 7 days.
  • Most of those with osteoarthritis will notice a significant improvement in symptoms within 30 minutes to 48 hours.
  • Most of those with osteoarthritis will have achieved complete or nearly complete relief from all symptoms within the first 30 days of use.
  • Banjo effectively treats a diversity of conditions – not just osteoarthritis but also related conditions (joint pain, neck pain, back pain, muscle & tendon pain, degenerative disc pain, etc.) as well as relatively unrelated conditions such as migraine.

The publication:

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Osteoarthritis Cartilage. 2008;16 Suppl 3:S14-8. Epub 2008 Jul 29.

Anti-inflammatory activity of chondroitin sulfate.

Iovu M, Dumais G, du Souich P.

Department of Pharmacology, Faculty of Medicine, University of Montréal, Montréal, Québec, Canada.

Summary of the abstract

Osteoarthritis is primarily characterized by areas of destruction of articular cartilage and by synovitis.

Articular damage and synovitis are secondary to local increase of pro-inflammatory cytokines, enzymes with proteolytic activity (matrix metalloproteinases), and enzymes with pro-inflammatory activity (cyclooxygenase-2 and nitric oxide synthase-2).

Enhanced expression of these proteins in chondrocytes and in synovial membrane appears associated to the activation and nuclear translocation of nuclear factor-kappaB (NF-kB).

Chondroitin sulfate (CS) prevents joint space narrowing and reduces joint swelling and effusion. To produce these effects, CS inhibits NF-kB.

This review discusses the evidence supporting that CS pleiotropic effects in chondrocytes and synoviocytes are primarily due to a common mechanism, e.g., the inhibition of NF-kappaB nuclear translocation.

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December 5, 2009

Nitric oxide & NF-kB in osteoarthritis

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Nitric oxide (NO) inhibits NF-kB in osteoarthritis joints.

As such, it is acting as an anti-inflammatory agent.

The role of NO as either beneficial or detrimental in the arthritic joint has long been debated. NO appears to act in a very complex manner. However, the fact that it inhibits NF-kB and therefore serves an anti-inflammatoey roles suggests that NO inhibition may have detrimental effects in osteoarthritis.

The publication:

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Nitric Oxide. 2008 Nov;19(3):276-83. Epub 2008 Jul 17.

Nitric oxide synthase isoforms and NF-kappaB activity in normal and osteoarthritic human chondrocytes: regulation by inducible nitric oxide.

Rosa SC, Judas F, Lopes MC, Mendes AF.

Center for Neurosciences and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal.

Summary of the abstract

The goal of this study was to elucidate the role of inducible nitric oxide (NO) on the regulation of NF-kB activity in human chondrocytes (cartilage cells.)

Normal and osteoarthritis cells were examined.

NF-kB activation in osteoarthritis cells was found to be twice as high as in normal cells.

Endogenous inducible NO was found to inhibit NF-kB activation. NF-kB activity appears to be regulated, at least in part, by the balanced production of NO resulting from a dynamic process.

NO inhibition in the therapy of osteoarthritis should be approached with caution, since it plays a role in NF-kB inhibition.

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December 5, 2009

New glucosamine derivative acts by inhibiting NF-kB

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Glucosamine is a weak inhibitor of NF-kB, and thus an anti-inflammatory agent with potential therapeutic use in the treatment of inflammation, such as in osteoarthritis.

A new derivative of glucosamine was examined it was likewise found to be an inhibitor of NF-kB.

The publication:

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Bioorg Med Chem. 2008 Sep 15;16(18):8390-6. Epub 2008 Aug 22.

Suppression of cytokine production in lipopolysaccharide-stimulated mouse macrophages by novel cationic glucosamine derivative involves down-regulation of NF-kappaB and MAPK expressions.

Mendis E, Kim MM, Rajapakse N, Kim SK.

Department of Food Science and Technology, Faculty of Agriculture, University of Peradeniya, Peradeniya, Sri Lanka.

Summary of the abstract

Exposure of macrophages to bacterial lipopolysaccharide (LPS) induces release of proinflammatory cytokines that play crucial roles in chronic inflammation.

Glucosamine has reported to possess anti-inflammatory properties and currently is the oral supplement of choice for the management of inflammation related complications including osteoarthritis.

In this study, QAGlc, a newly synthesized glucosamine derivative was found to inhibit production of pro-inflammatory cytokines.

Since production of cytokines is regulated mainly via activation of NF-kB this study examined if QAGlc is acting via inhibition of NF-kB and found that it was.

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December 5, 2009

NF-kB controls harmful bone resorption in OA

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Excess activation of NF-kB leads to osteoclast over-activation and increased bone destruction in arthritis.

Healthy bone metabolism requires a balance between osteoclasts (break down and re-absorb bone) and osteoblasts (make new bone.)

Osteoclasts – the bone destroying cells – are over-active in many disease conditions that include bone destruction (such as osteoarthritis.)

In the study summarized below, it was found that excess NF-kB activation led to osteoclast over-activity.

The authors note that the NF-kB inhibitor parthenolide (a major active component in the herb feverfew) has shown a beneficial therapeutic effect in reducing inflammation induced bone destruction in a mouse model.

It is noted that NF-kB over-activation and associated osteoclast over-activity is also seen in Paget’s disease of bone, and periodontitis.

The publication:

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Cytokine Growth Factor Rev. 2009 Feb;20(1):7-17. Epub 2008 Nov 28.

NF-kappaB modulators in osteolytic bone diseases.

Xu J, Wu HF, Ang ES, Yip K, Woloszyn M, Zheng MH, Tan RX.

Centre for Orthopaedic Research, School of Surgery, University of Western Australia, Nedlands, Australia.

Summary of the abstract

Osteoclasts are responsible for bone resorption and play a pivotal role in the pathogenesis of osteolytic disorders.

NF-kB is a set of nuclear factors that bind to consensus DNA sequences called kappaB sites, and is essential for osteoclast formation and survival.

NF-kappaB signalling pathways are strictly regulated to maintain bone homeostasis by cytokines such as RANKL, TNF-alpha and IL-1, which differentially regulate classical and/or alternative NF-kappaB pathways in osteoclastic cells.

Abnormal activation of NF-kappaB signalling in osteoclasts has been associated with excessive osteoclastic activity, and frequently observed in osteolytic conditions, including periprosthetic osteolysis, arthritis, Paget’s disease of bone, and periodontitis.

NF-kappaB modulators such as parthenolide and NEMO-binding domain peptide demonstrate therapeutic effects on inflammation-induced bone destruction in mouse models.

Unravelling the structure and function of NF-kappaB pathways in osteoclasts and other cell types will be important in developing new strategies for treatments of bone diseases

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November 19, 2009

Arthritis relief by Christmas (with frankincense)

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Frankincense inhibits NF-kB, which accounts for its efficacy against cancer, arthritis, chronic colitis, ulcerative colitis, Crohn’s disease, and bronchial asthma

It might be difficult to believe that a single agent could effectively treat a large number of inflammatory conditions, including:

  • cancer (prevention actually, not treatment)
  • arthritis
  • chronic colitis
  • ulcerative colitis
  • Crohn’s disease
  • asthma, and
  • many other ailments

But that’s what natural NF-kB inhibitors do. Some do it (much) better than others. But they all do it – because they fight inflammation.

So at first it’s hard to believe, but since NF-kB inhibitors fight inflammation, it makes sense. If inflammation contributes to the cause of many conditions (and it does) then whatever relieves inflammation (actually treating the cause, not just masking the symptoms) should be effective in treating many ailments.

So you might want to consider using natural NF-kB inhibitors.

Except that you’re already using them. Every fresh fruit and vegetable is a natural NF-kB inhibitor.

The problem is – you’re probably not using enough of them. That’s because our modern world is filled with so many things that cause inflammation. It might not be enough to ‘only’ eat the recommended 9 portions of fruits and vegetable each day. And if you have an autoimmune disease – or if conditions related to inflammation run in your family – then you probably have a genetic vulnerability to inflammation. If so, you’ll need even more of these NF-kB inhibitors.

Frankincense is a very effective NF-kB inhibitor. Banjo is a combination of many very effective NF-kB inhibitors. And because Banjo uses a unique “trans-mucosal” delivery system, it’s very fast acting and even more effective.

So take your pick. With additional NF-kB inhibitors from fruits and vegetables (a lot for a long time) or frankincense, or Banjo – you can get better. That’s my theory. And it’s consistent with the results from thousands of studies, a few of which are referenced on this site – one of which is briefly summarized below.

The publication:

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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.

Summary of the absrtract

Acetyl-11-keto-beta-boswellic acid (AKBA), a component of an Ayurvedic therapeutic plant Boswellia serrata (frankincense) is 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.

AKBA was found to inhibit NF-kB. AKBA suppressed NF-kB activation in tumor cells. It also countered inflammation and NF-kB activation induced by cigarette smoke.

Overall, 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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November 16, 2009

How fat cells cause arthritis

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Fat cells secrete leptin, which activates NF-kB, resulting in inflammation

Osteoarthritis has been called “wear and tear” arthritis. But that’s somewhat misleading. Osteoarthritis results not from years of use, but from years of chronic, low grade inflammation.

Yes, mechanical stress (the pounding your knee joint takes every time you walk or run) does cause mild inflammation. But that inflammation would normally resolve quickly and entirely. When it doesn’t – when your body can’t entirely turn off the inflammation – chronic inflammation results.

Chronic, mild inflammation eventually progresses to chronic severe inflammation. Osteoarthritis results when that inflammation begins causing pain.

One reason your body might have trouble turning off the inflammation is “leptin.”

Leptin is produced by fat cells. It stimulates NF-kB, resulting in inflammation. And, with high levels of leptin constantly in circulation, it keeps NF-kB, and inflammation, from ever fully turning off.

That’s why excess weight results in a higher incidence of osteoarthritis not only in the knees, but in the hands, shoulders, and every other joint in your body.

Basically, the inflammation stimulants (leptin is only one of many) have overwhelmed the inflammation inhibitors – which is why most of us are walking around with chronic, low grade inflammation – leading to a higher incidence of osteoarthritis, Alzheimer’s, cancer, autoimmune disease, and a nearly endless list of inflammation related ailments.

The solution is simple. Reduce inflammation stimulants (through weight loss and lifestyle changes) and add inflammation inhibitors (e.g. eat more fruits and vegetables.)

The publication:

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Mediators Inflamm. 2009;2009:345838. Epub 2009 Aug 13.

Leptin enhances synthesis of proinflammatory mediators in human osteoarthritic cartilage–mediator role of NO in leptin-induced PGE2, IL-6, and IL-8 production.

Vuolteenaho K, Koskinen A, Kukkonen M, Nieminen R, Päivärinta U, Moilanen T, Moilanen E.

Summary of the abstract

Obesity is an important risk factor for osteoarthritis in weight-bearing joints, but also in hand joints, pointing to an obesity-related metabolic factor that influences on the pathogenesis of OA.

Leptin is an adipokine regulating energy balance, and it has recently been related also to arthritis and inflammation as a proinflammatory factor. In the present paper, the effects of leptin on human osteoarthritis cartilage were studied.

Leptin resulted in the production of pro-inflammatory mediators.

The effects of leptin are mediated through activation of transcription factor nuclear factor kappaB (NF-kB.)

These findings support the idea of leptin as a factor enhancing the production of proinflammatory factors in osteoarthritis and as an agent contributing to the obesity-associated increased risk for osteoarthritis.

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November 16, 2009

Glucosamine and chondroitin for arthritis

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Americans spend approximately $1 billion each year on various forms of glucosamine supplements, primarily for the treatment of osteoarthritis. Is that money well spent, or wasted?

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November 16, 2009

Turmeric as wonder drug

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Curcumin, or turmeric, is believed to have many beneficial effects relative to inflammation and disease. It is an inhibitor of NF-kB, but also affects other pathways and mediators of inflammation.

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November 14, 2009

Puree of seahorse for arthritis

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You don’t really need to grind up a seahorse to get relief from arthritis pain. Though it might be one way, it’s probably not the best way and definitely not the easiest way. NF-kB inhibitors are all around us.

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