Turmeric is being extensively researched for its effects on pain, inflammation, aging and a great many ailments.
Banjo contains a pure water extract of turmeric root.
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.
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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.
Csaki C, Mobasheri A, Shakibaei M.
Musculoskeletal Research Group, Institute of Anatomy, Ludwig-Maximilians-University Munich, Pettenkoferstrasse 11, 80336 Munich, Germany.
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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This is a essential publication because it:
Each of the above is consistent with the theory of inflammation advanced on this site.
Curcumin (a major active component of turmeric) has been shown to exert substantial anti-inflammatory effects. Many studies suggest that it acts primarily by inhibiting NF-kB.
IL-10 is an important chemical messenger in the immune system and a regulator of inflammation. Like most such immune regulating molecules, it interacts with many other components of the immune system in a complex manner resulting in diverse effects. However, IL-10 acts primarily to inhibit/reduce inflammation, largely by inhibiting NF-kB.
IL-10 is especially important in the digestive tract and may play a role in the onset and progression of inflammatory bowel disease: Crohn’s and ulcerative colitis patients may suffer from a deficiency of IL-10.
Inflammatory bowel disease is strongly associated with excess activation of NF-kB.
Ulcerative colitis patients and, to a lesser extent Crohn’s patients, have been found to benefit from administration of curcumin – presumably because of its ability to inhibit NF-kB.
Drugs frequently used as first-line therapy for inflammatory bowel disease, such as glucocorticoids or aminosalicylates (e.g. sulfasalazine) are also inhibitors of NF-kB.
NF-kB inhibition, at least in the treatment of inflammatory bowel disease, seems to be a good thing.
The study briefly summarized below demonstrates a synergistic effect between IL-10 and curcumin. In other words, IL-10 was much more effective as an NF-kB inhibitor when curcumin was present.
That’s significant because a difficulty in shutting down inflammation is common to many of the inflammation related conditions. Much of autoimmune disease is, I believe, not so much a primary attack on the body by one’s own immune system as it is an immune system that can’t turn inflammation off, and so ends up attacking all sorts of things (organs, joints, skin, nerves, etc.)
Also, curcumin was unable to inhibit NF-kB when IL-10 was absent.
The latter fact is quite surprising. Curcumin is ’supposed’ to inhibit NF-kB – but in this study it stopped doing so when IL-10 was absent.
So it seems that when your body is trying to shut down inflammation – when IL-10 is present – curcumin comes alongside and joins in the battle. Then, once that excess inflammation is relieved (IL-10 no longer present) curcumin simply stops acting.
Something unexpected is going on. Curcumin seems as if it is ‘cooperating’ with the immune system, or perhaps being actively and selectively used by the immune system as a ‘tool’ of assistance in shutting down inflammation. To some extent, curcumin seems to be acting like a vitamin.
When the body requires a vitamin it grabs one from the circulation. When that same vitamin is not needed it simply washes away (the water soluble vitamins at least.) But the vitamin has to have been taken in (eaten.) If not – if there is no vitamin to grab – then a deficiency disease will soon develop. The body cannot function properly without the vitamin.
Perhaps the body requires some minimum level of these natural NF-kB inhibitors in order to function properly. Perhaps a shortage of natural NF-kB inhibitors results in a deficiency disease that we recognize as various forms of inflammation. No, I don’t think we need curcumin per se, but I do think we need a steady supply of natural NF-kB inhibitors. I think we need this ‘class’ of molecule – call it a “vita-class.”
While it’s fair to note the above description of curcumin and IL-10 (or everything on this site) as a gross oversimplification – I think it’s also fair to say that everything written on the immune system is grossly simplified – because we still know so very little of what really goes on ‘in there.’
No one could have guessed that curcumin would be found powerless in the absence of IL-10. And tomorrow something new will be discovered, and the day after, and the day after….
Curcumin just happens to be one of the better studied molecules – so at least we know a little. But curcumin certainly isn’t the only molecule that will be found to act in surprising ways. The interaction of curcumin and IL-10 is no doubt only one of a great many yet undiscovered examples of such synergistic cooperation.
The publication:
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Am J Physiol Gastrointest Liver Physiol. 2008 Nov;295(5):G1079-91.
Larmonier CB, Uno JK, Lee KM, Karrasch T, Laubitz D, Thurston R, Midura-Kiela MT, Ghishan FK, Sartor RB, Jobin C, Kiela PR.
Curcumin (a major active ingredient in turmeric) demonstrates profound anti-inflammatory effects in intestinal epithelial cells (IEC) and in immune cells in vitro (“vitro” refers to glass – so in vitro refers to experiments in a ‘test tube’ – outside of a living organism.)
Curcumin also exhibits a protective role in rodent models of chemically induced colitis, with its presumed primary mechanism of action via inhibition of NF-kappaB.
Although it has been demonstrated effective in reducing relapse rate in ulcerative colitis patients, curcumin’s effectiveness in Crohn’s disease (CD) has not been evaluated.
Therefore, the effects of dietary curcumin were investigated in respect to the development of colitis, immune activation, and NF-kB activity in a mouse model of colitis.
Curcumin showed a mild protective effect on the colon.
Surprisingly, activation of NF-kB in mice without IL-10 was not noticeably inhibited by curcumin.
Furthermore, it was demonstrated that IL-10 and curcumin act synergistically to inhibit NF-kB activity. This study in the mouse model suggests that the protective effects of curcumin are IL-10 dependent.
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The study briefly summarized below was undertaken to study the potential benefit of combining curcumin with paclitaxel in the treatment of breast cancer.
Paclitaxel, like most chemotherapeutic agents, increases the activation of NF-kB.Curcumin was found to reduce that NF-kB activation. In a mouse model of breast cancer, curcumin plus paclitaxel was found to be more effective than either agent used alone.
The publication:
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Breast J. 2009 May-Jun;15(3):223-9.
Kang HJ, Lee SH, Price JE, Kim LS.
Division of Breast & Endocrine Surgery, Hallym Sacred Heart Hospital, College of Medicine, Hallym University, Dongan-Gu, Anyang, Korea.
Most anticancer agents activate nuclear factor kappa B (NF-kB), which can increase cell survival, proliferation, and metastasis.
Curcumin has been shown to inhibit the growth of various cancer cells, without toxicity to normal cells.
The antitumor effects of curcumin could be due in part to the inactivation of NF-kB.
Inhibiting NF-kB activity may increase the efficacy of paclitaxel in cancer treatment. This study investigated whether the inactivation of NF-kB by curcumin would enhance the efficacy of paclitaxel for inhibiting breast cancer growth in vitro (in the ‘test tube) and in vivo (in an actual living organism.)
Curcumin inhibition of paclitaxel-induced activation of NF-kB was confirmed. The combination of curcumin with paclitaxel elicited significantly greater inhibition of cell growth and increased death of cancer cells, compared with either agent alone.
In a mouse model of breast cancer, combination therapy with paclitaxel and curcumin significantly reduced tumor size and decreased tumor cell proliferation and increased cancer cell death.
These results clearly suggest that a curcumin-paclitaxel combination could be a novel strategy for the treatment of breast cancer.
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Curcumin cannot, it seems, inhibit NF-kB in the muscle of patients (or at least mice) with muscular dystrophy.
While unfortunate, it suggests (along with other research) that curcumin is only effective when acting in concert with other agents. Those ‘other agents’ may be lacking in the muscle of patients with muscular dystrophy.
The publication:
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Muscle Nerve. 2006 Sep;34(3):298-303.
Durham WJ, Arbogast S, Gerken E, Li YP, Reid MB.
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030, USA.
Skeletal muscle of patients with Duchenne-type muscular dystrophy and mdx mice exhibits elevated activity of NF-kB, which may play a role in muscle catabolism (muscle breakdown.)
Skeletal muscle NF-kB activity in mdx mice was measured at three ages (10 days, 4 weeks, and 8 weeks) to test the hypothesis that NF-kB activity increases with increasing age in these mice.
In addition, the hypothesis that NF-kB activity could be reduced in mdx skeletal muscle by dietary supplementation with curcumin was tested.
NF-kB activity was found to be elevated at 4 and 8 weeks of age but not at 10 days. It was resistant to inhibition by dietary curcumin.
The conclusion is that NF-kB activity is elevated in dystrophic skeletal muscle in an age-related manner, but that it cannot be lowered by curcumin.
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Curcumin (the primary active agent in turmeric) protected dopamine producing cells, at least in part by inhibiting NF-kB.
The destruction of dopamine producing cells in Parkinson’s disease, and the consequent shortage of dopamine in the brain, is what results results in most of the symptoms commonly associated with Parkinson’s.
Curcumen is a natural inhibitor of NF-kB. As such, it has been found effective in the treatment of many other ailments.
This is consistent with the theory that NF-kB is the Master Switch and that the fundamental problem in most inflammation-related conditions is over activation of NF-kB.
On close examination, that excessive activation will generally be found to result from a genetic defect or vulnerability in NF-kB inhibition. In other words, it’s not that NF-kB is too frequently or too excessively turned on – it’s that NF-kB cannot turn off (at least not soon enough and/or not often enough.)
Specific to Parkinson’s disease, consider for example the role of “Nurr1.” Rare mutations in Nurr1 are associated with familial Parkinson’s disease. While the relation of Nurr1 to Parkinson’s was previously unknown, a recent study has established that “Nurr1 functions to inhibit expression of pro-inflammatory neurotoxic mediators in both microglia and astrocytes…. by docking to NF-kappaB-p65 … (ultimately) resulting in clearance of NF-kappaB-p65 and transcriptional repression.”
In simple terms, Nurr1 turns off NF-kB. Hence, when it’s ‘broken’ the result is sustained, excess NF-kB activation leading to neurotoxicity: the dopamine producing cells die.
Of course defective Nurr1 accounts for only a small subset of Parkinson’s cases. But there are no doubt many other such mechanisms, some of which have yet to be discovered.
In any case, if the problem is excess activation of NF-kB, the solution may be to supplement NF-kB inhibitors (e.g. curcumin.) The disease might not be ‘cured’, but at least the severity of symptoms and speed of progression might be favorably impacted.
Natural NF-kB inhibitors such as curcumin have the advantage of being widely available and inexpensive. They come with a 1,000+ year history of safe use and no significant drug interactions have been reportedst. Curcumin and other natural NF-kB inhibitors might therefore be used to augment or ‘complement’ standard therapy (check with your doctor.)
Curcumin has only one ‘problem’, which is its limited bioavailability when administered orally.
Therefore, rather than administering curcumin orally (e.g. as a tablet,) one possibility is to administer it trans-mucosally (e.g. via a lozenge which is held in the mouth until dissolved.) And since curcumin is but one of many natural NF-kB inhibitors, better effect might be obtained by combining several natural NF-kB inhibitors in a single lozenge. That, in simple terms, is the rationale behind Banjo.
Banjo is not intended as a treatment for Parkinson’s. It is a natural anti-inflammatory medication that is proposed to work by inhibiting NF-kB. While that might be of special value in certain other conditions, the intention is to treat migraine and osteoarthritis, both of which respond remarkably well to Banjo.
The publication:
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Neurochem Res. 2008 Oct;33(10):2044-53. Epub 2008 Mar 27.
Yang S, Zhang D, Yang Z, Hu X, Qian S, Liu J, Wilson B, Block M, Hong JS.
Laboratory of Pharmacology and Chemistry, National Institute of Environmental, Health Sciences, National Institutes of Health, PO Box 12233, Research Triangle Park, NC 27709, USA.
Using a rat model of Parkinson’s disease (PD), the effects of curcumin were tested.
Curcumin has well-known anti-inflammation effects, the effect of curcumin on dopamine producing neurons was tested.
Curcumin pretreatment reduced neurotoxicity in this model. Curcumin post-treatment also showed protective effect.
Results revealed that curcumin treatment decreased the activation of NF-kB and activator protein-1 (AP-1).
Taken together, our study implicated that curcumin might be a potential preventive and therapeutic strategy for inflammation-related neurodegenerative diseases.
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Curcumin (a major active ingredient in turmeric) has been reported to possess radical scavenger, iron chelating, and anti-inflammatory properties in different tissues.
In this study, curcumin was shown to protect against chemical neurotoxicity through multiple mechanisms. Curcumin is noteworthy as an antioxidant and inhibitor of NF-kB.
The publication:
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Biochem Pharmacol. 2009 Jul 15;78(2):178-83. Epub 2009 Apr 8.
Wang J, Du XX, Jiang H, Xie JX.
National Key Disciplines: Physiology (in incubation), Department of Physiology, Medical College of Qingdao University, No. 308 Ningxia Road, Qingdao, 266071, China.
Oxidative stress has been implicated in the degeneration of dopaminergic neurons in the substantia nigra of Parkinson’s disease patients, and several anti-oxidants have been shown to be effective on the treatment of Parkinson’s disease.
Curcumin has been previously reported to possess radical scavenger, iron chelating, anti-inflammatory properties in different tissues. The aim of present study is to explore the cytoprotection of curcumin against chemical-induced neuronal death, as well as the underlying mechanism.
Our results showed that curcumin protected cells against chemical neurotoxicity by partially restoring the mitochondrial membrane potential, increasing the level of Cu-Zn superoxide dismutase and suppressing an increase in intracellular reactive oxygen species. Furthermore, curcumin pretreatment significantly inhibited the excess NF-kB activation that resulted from the chemical.
These results suggest that the neuroprotective effects of curcumin are attributed to the antioxidative properties and inhibition of NF-kB.
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The publication:
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Neuro Endocrinol Lett. 2007 Aug;28(4):456-62.
Maes M, Mihaylova I, Bosmans E.
MCare4U Outpatient Clinics, Olmenlaan 9, 2610 Wilrijk, Belgium.
There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress.
Nuclear factor kappa beta (NF-kB) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators.
In order to examine the role of NF-kB in the pathophysiology of CFS, this study examined the production of NFkappabeta p50 in peripheral blood lymphocytes of 18 unmedicated patients with CFS and 18 controls.
NF-kB activation was significantly higher in CFS patients than in controls.
There were significant and positive correlations between NF-kB activation and the severity of illness, as measured by symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and the subjective feeling of infection.
The results show that an intracellular inflammatory response in the white blood cells plays an important role in the pathophysiology of CFS, and that previous findings on increased oxidative stress and inflammation in CFS may be attributed to an increased production of NF-kB.
The results suggest that the symptoms of CFS, such as fatigue, muscular tension, depressive symptoms and the feeling of infection reflect a genuine inflammatory response in those patients.
It is suggested that CFS patients should be treated with antioxidants, which inhibit the production of NFkappabeta, such as curcumin, N-Acetyl-Cysteine, quercitin, silimarin, lipoic acid and omega-3 fatty acids.
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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.
The publication:
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Adv Exp Med Biol. 2007;595:127-48.
Shishodia S, Singh T, Chaturvedi MM.
Curcumin is the active ingredient of turmeric that has been consumed as a dietary spice for ages.
Turmeric is widely used in traditional Indian medicine to cure biliary disorders, anorexia, cough, diabetic wounds, hepatic disorders, rheumatism, and sinusitis.
Extensive investigation over the last five decades has indicated that curcumin:
And that it suppresses symptoms associated with:
And that it:
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Comments:
The only ‘problem’ with curcumin seems to be its low level of bio-availability. That is, not enough curcumin gets into the blood, and to the cells where it can exert its beneficial effects.
Banjo delivers turmeric (and curcumin, its major active ingredient) trans-mucosaly. That is, the active ingredients are absorbed through the mucous membranes of the mouth. This is believed to substantially increase the bio-availability of all active agents, resulting in a much more effective product.
That’s why Banjo is provided as a lozenge that is held in your mouth until dissolved. Active ingredients coat the mucous membrane lining your mouth, and are absorbed through that mucous membrane while the lozenge dissolves.
If you prefer, the Banjo lozenge can instead be dissolved in water to make a great tasting ‘tea.’ By slowly sipping the tea you achieve the same effect, as the tea coats the membranes of your mouth, allowing active ingredients to be absorbed.
This method of administration bypasses the harsh environment of the stomach and avoids immediate destruction of active ingredients by the liver.
Active ingredients are very rapidly absorbed – directly into the bloodstream. That’s one reason why banjo acts so quickly. Significant relief from pain and inflammation often results within minutes.
Patients taking up to 8 grams of pure curcumin daily for 4 months reported no significant side effects.
The publication:
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Adv Exp Med Biol. 2007;595:471-80.
Hsu CH, Cheng AL.
Summary of the abstract
Curcumin has long been expected to be a therapeutic or preventive agent for several major human diseases because of its antioxidative, anti-inflammatory, and anticancerous effects.
In phase I clinical studies, curcumin with doses up to 3600-8000 mg daily for 4 months did not result in discernible toxicities except mild nausea and diarrhea.
The pharmacokinetic studies of curcumin indicated in general a low bioavailability of curcumin.
The effect of curcumin was studied in patients with rheumatoid arthritis, inflammatory eye diseases, inflammatory bowel disease, chronic pancreatitis, psoriasis, hyperlipidemia, and cancers.
Although the preliminary results did support the efficacy of curcumin in these diseases, the data to date are all preliminary and not conclusive. It is imperative that well-designed clinical trials, supported by better formulations of curcumin or novel routes of administration, be conducted in the near future.
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Comments:
The only ‘problem’ with curcumin seems to be its low level of bio-availability. That is, not enough curcumin gets into the blood, and to the cells where it can exert its beneficial effects.
Banjo delivers turmeric (and curcumin, its major active ingredient) trans-mucosaly. That is, the active ingredients are absorbed through the mucous membranes of the mouth. This is believed to substantially increase the bio-availability of all active agents, resulting in a much more effective product.
That’s why Banjo is provided as a lozenge that is held in your mouth until dissolved. Active ingredients coat the mucous membrane lining your mouth, and are absorbed through that mucous membrane while the lozenge dissolves.
If you prefer, the Banjo lozenge can instead be dissolved in water to make a great tasting ‘tea.’ By slowly sipping the tea you achieve the same effect, as the tea coats the membranes of your mouth, allowing active ingredients to be absorbed.
This method of administration bypasses the harsh environment of the stomach and avoids immediate destruction of active ingredients by the liver.
Active ingredients are very rapidly absorbed – directly into the bloodstream. That’s one reason why Banjo acts so quickly. Significant relief from pain and inflammation often results within minutes.
The synovium is normally a very thin, smooth layer of cells that is closely attached to the membrane that encloses the joint and its synovial (lubricating) fluid.
In rheumatoid arthritis the synovium becomes thickened and develops finger-like projections extending out into the joint space. This thickening process is called “hyperplasia,”and typically leads to pannus formation. Pannus means “flap” – and the pannus in rhuematoid arthritis contributes to the joint destruction characteristic of that disease.
One reason the synovium may thicken is that old cells do not die as they are supposed to. So as new cells continue to be made, cells accumulate.
While it might seem strange that cell death is required to maintain health, such is often the case. This “programmed cell death” is called “apoptosis.”
The classic example of cells that do not die as they are supposed to is cancer. In cancer cells, the gene that programs for cell death (apoptosis) has somehow been turned off. So cancer cells live, and proliferate, forever.
The synovial cells in rheumatoid arthritis act like cancer cells in certain ways. They continue to reproduce and live ‘forever.’ They invade and destroy nearby tissue. And what’s ‘nearby’ is the cartilage of the joint capsule.
This, in brief, is how synovial hyperplasia leads to joint destruction. Of course preventing this hyperplasia would be a very good thing.
The publication:
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nt J Mol Med. 2007 Sep;20(3):365-72.
Summary of the abstract
Rheumatoid arthritis (RA) is a chronic inflammatory disease that is characterized by hyperplasia of the synovial fibroblasts, which is partly the result of decreased apoptosis.
This study investigated the mechanisms through which curcumin, a polyphenolic compound from the rhizome of Curcuma longa, exerts its anti-proliferative action in the synovial fibroblasts obtained from patients with RA.
Exposure of the synovial fibroblasts to curcumin resulted in growth inhibition and the induction of apoptosis.
Curcumin decreased the expression levels of the cyclooxygenase (COX)-2 mRNA and protein without causing significant changes in the COX-1 levels, which was correlated with the inhibition of prostaglandin E(2) synthesis.
These results show that curcumin might help identify a new therapeutic pathway against hyperplasia of the synovial fibroblasts in RA.
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Comments:
Curcumin was found to stimulate apoptosis – the programmed cell death that is required if synovial cells are to remain as a nice smooth layer and not build up into a joint-destroying pannus.That is, it seemed to make the synovial cells behave properly.
As something of a ’side benefit’ – curcumin was found to inhibit COX-2 without affecting levels of COX-1. COX-1 is required for stomach protection. By inhibiting only COX-2 one would obtain the analgesic and anti-inflammatory benefits without the stomach-related (and kidney related) side effects common to aspirin and other NSAIDs.
Bone undergoes continuous remodeling through bone formation and resorption, and maintaining the balance for skeletal rigidity. Bone resorption and loss are generally attributed to osteoclasts. Osteoclast activity is inhibited by turmeric and dandelion, probably by means of NF-kB.
This study suggests that a combination of turmeric (curcumin) and ginger extract might provide a novel approach to improving structure and function in skin and, concomitantly, reducing formation of non-healing wounds.
Aging Alzheimer's Arthritis Asthma Atherosclerosis Back Pain Banjo Cancer Chronic Pain Cluster Headache Crohn's Diabetes Fatigue Fibromyalgia Gout Headache Heart Disease IBD Inflammation Joint Pain Lupus Migraine Multiple Sclerosis Muscular Dystrophy Neck Pain Neuropathic Pain NF-kB Osteoarthritis Pain Parkinson's Psoriasis Rheumatoid Arthritis Sjogren's Stroke TMJ Ulcerative Colitis
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