Approximately 80% of Americans will develop back pain at some point in life.
As many as 9% of Americans are suffering with back or neck pain at any given time.
1% of the working age population is disabled because of lower back pain.
Neck pain accounts for 15% of all chronic pain.
Pain results from inflammation.
Let’s get better.
Back pain is the leading cause of chronic pain in the U.S. and a major cause of disability in those under 45.
55 million Americans suffer with frequent back pain - 26 million of them under 64 years of age.
Americans spend at least $50 billion each year on treatments for back pain.
Neck pain most commonly results from injury, poor posture or as a symptom of arthritis.
Neck pain may originate with muscles, ligaments, and nerves—as well as the bones and joints of the cervical spine. Pain originating in the neck frequently radiates to (can also be felt in) the shoulder, arm or upper back.
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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NF-kB over-activation was found to account for exaggerated pain states such as are common in conditions such as back pain, especially neuropathic pain. In this case sciatic nerve pain in particular was studied.
The publication:
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Eur J Neurosci. 2005 Oct;22(8):1977-86.
Ledeboer A, Gamanos M, Lai W, Martin D, Maier SF, Watkins LR, Quan N.
Department of Psychology & Center for Neuroscience, University of Colorado at Boulder, Boulder, CO 80309-0345, USA.
Proinflammatory cytokines, such as interleukin-1beta and tumour necrosis factor-alpha, are released by activated glial cells in the spinal cord and play a major role in pain facilitation.
These cytokines exert their actions, at least partially, through the activation of the transcription factor, nuclear factor kappaB (NF-kB). In turn, NF-kappaB regulates the transcription of many inflammatory mediators, including cytokines.
This study investigated whether NF-kB is involved in neuropathic pain induced by sciatic nerve inflammation.
The results obtained demonstrated that spinal cord NF-kB activation is involved, at least in part, in exaggerated pain states.
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The publication:
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Spine (Phila Pa 1976). 2009 May 15;34(11):1127-33.
OBJECTIVE: To investigate the oxidative/nitrosative effects of peroxynitrite on human nucleus pulposus (NP) cells.
SUMMARY OF BACKGROUND DATA: Peroxynitrite is an important tissue-damaging species generated at sites of inflammation and degeneration. The aim of this study was to examine the effects of oxidative/nitrosative stress caused by peroxynitrite and the peroxynitrite donor SIN-1 in human NP cells.
METHODS: Degenerated human intervertebral disc (IVD) tissue was analyzed for nitrosylation by immunofluorescence. Nitrosylation, accumulation of intracellular reactive oxygen species, NF-kappaB nuclear translocation, and cell viability were analyzed. Gene expression of TNF-alpha, IL-1beta, IL-6, IL-8, and IL-10 was quantified.
RESULTS: Degenerated IVD tissue showed strong nitrosylation, especially in the NP. NF-kappaB/p65 sustained nuclear translocation of NF-kappaB/p65 and stimulation of IL-1beta, IL-6, and IL-8 expression was noted.
CONCLUSION: This study provides evidence that peroxynitrite may play a role in disc degeneration and discogenic back pain development by an increased synthesis of proinflammatory cytokines. Nuclear translocation of NF-kappaB was identified as the potential underlying pathway. Therefore, neutralizing peroxynitrite and its derivatives (e.g., via the use of antioxidants) may be a novel treatment option for discogenic back pain.
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Comments:
Stopping inflammation is the key to eliminating discogenic back pain
In this study the effects of peroxynitrite are reviewed. We’re told that it’s an important tissue damaging compound that is generated at sites of inflammation and disc degeneration.
We’re not told to what extent the peroxynitrite results from inflammation vs. to what extent it causes the inflammation. It could both cause and result from inflammation, as is often the case with mediators of inflammation. The ’species’ causes damage/inflammation AND stimulates further inflammation. A vicious cycle. Sometimes, for no obvious reason, inflammation cannot ‘turn off.” The result is chronic inflammation and pain that continues to worsen over time.
We are told they observed “sustained NF-kB translocation” which means NF-kB was chronically turned on. That is exactly what we would expect in chronic inflammation. The Master Switch remains stuck in the “on” position.
We are also told that high levels were observed for various mediators of inflammation – IL-1, IL-6 and IL-8. This is also what would be expected to observe when NF-kB is chronically turned on.
The researchers conclude by observing that NF-kB is the “potential” underlying pathway and suggest that back pain might be effectively treated with anti-oxidants.
It seems clear, however, that NF-kB is more than just the “potential” underlying pathway – it is clearly the reason for the inflammation. Rather than attempting to neutralize peroxynitrite with anti-oxidants, a better solution, it seems, would be to go “upstream” to the source. Inhibition of the source, NF-kB, would be a more effective anti-inflammation strategy than trying to limit one of the many pro-inflammatory species observed in this study of discogenic back pain.
It might be difficult to believe that a single agent could effectively treat a large number of inflammatory conditions, including:
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.
Takada Y, Ichikawa H, Badmaev V, Aggarwal BB.
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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