Natural Back Pain Relief | Neck Pain Relief

What is back (or neck) pain?

Back or neck pain is (by definition) a symptom (pain.) It appears difficult to treat because it may result from:

  • Muscle, tendon, nerve or bone issues (e.g. arthritis)
  • Disc inflammation/herniation
  • Fibromyalgia, lupus, or other conditions that cause back pain.

But whatever the cause, pain is pain.

Banjo addresses the root cause of pain and inflammation - the root cause of back pain and neck pain.

Back & Neck Pain Notes

Perspective on back pain and neck pain

Back and neck pain are the most common chronic pain conditions.

Back and neck pain can arise from any part of the back or neck, including joints, ligaments, muscles, bones and connective tissue. Not infrequently, a specific cause for the pain cannot be identified.

Common causes of back and neck pain include:

  • Degenerative disc disease
  • Nerve compression
  • Nerve compression within the spine itself
  • Back strain or sprain
  • Pain that persists for more than 3 months is considered chronic.

Back and neck pain result from 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.

Given that neck and back pain may result from any number of causes, it is not possible to examine the theory on a case by case basis relative to each possible cause. Nonetheless, what is known in general supports the following observations:

  • Back and neck pain are associated with inflammation.
  • Back and neck pain are associated with excess NF-kB activation.
  • There is evidence that inhibiting NF-kB is beneficial in the treatment of back and neck pain.
  • There is evidence that natural NF-kB inhibitors are beneficial in treating back and neck pain.

Experience trumps theory.

Banjo has been found to provide excellent relief from back and neck pain.

Incidence and impact of back pain & neck pain

Back pain is the second most common complaint for which individuals see a physician, and Americans spend at least $50 billion each year on back pain.

When asked about common types of chronic pain, respondents of a National Institute of Health Statistics survey indicated that back pain was the most common (27%), followed by  neck pain (15%).

Back pain is the leading cause of disability in Americans under 45 years old. More than 26 million Americans between the ages of 20-64 experience frequent back pain.

Some common causes of back and neck pain include:

  • sprain and strain of the back or neck;
  • pain arising from the discs of the spine themselves, called “discogenic pain”;
  • pain that results when bulging discs compress nerves, called “radicular pain”;
  • pain from arthritis (any type) of the facet joints – the joints that hold the spine in alignment (“facet joint syndrome”); and
  • pain from bony compression of the nerves of the spine, which is called spinal stenosis.

Acute or short-term neck pain or back pain generally lasts from a few days to a few weeks. Most acute back pain is mechanical, the result of physical stress or strain.  Symptoms may primarily resemble muscle ache, or may be characterized as shooting or stabbing pain. Limited flexibility and range of motion is common.

Chronic back pain or neck pain is defined by its duration. Back or neck pain that persists for more than 3 months is considered chronic. It is frequently progressive and the cause is often difficult to determine.

NF-kappaB inhibition reduces inflammation & pain, increases GABA after spinal cord injury

Spinal cord injury is often followed by increased pain perception. There is both immediate gross inflammation and chronic micro-inflammation.

Treatment with an NF-kB ‘decoy’ effectively blocks (inhibits) NF-kB activation, and was shown to improve outcome after spinal cord injury. Inflammation and pain were reduced, and an increase in GABA neurotransmitter was evidenced.

The publication:

February, 2008

Nuclear factor-kappaB decoy amelioration of spinal cord injury-induced inflammation and behavior outcomes.

Summary of the abstract

Spinal cord injury (SCI) results in a pathophysiology that includes altered nociception (pain perception) and hyperalgesia (lower pain threshold and increased pain sensation). SCI triggers an early and prolonged inflammatory response, with increased interleukin-1beta levels.

Transient changes are observed in NF-kappaB.

There were significant early increases in COX-2 and inducible nitric oxide synthase after SCI.

We used synthetic double-stranded “decoy” deoxyoligonucleotides containing selective NF-kB protein dimer binding consensus sequences. Decoys targeting the p65/p50 binding site on the COX-2 promoter decreased SCI-induced cell losses, NF-kappaB p65/p50 DNA-binding activity, and COX-2 and iNOS protein levels. NF-kappaB p65/p50 targeted decoys improved early locomotor recovery after moderate but not severe SCI, yet ameliorated SCI-induced hypersensitization after both moderate and severe SCI.

To determine whether changes in GABA activity played a role in decreased hypersensitivity after SCI and p65/p50 targeted decoy, we counted gamma-aminobutyric acid (GABA)-containing neurons in laminae 1-3. There were significantly more GABAergic neurons in the p65/p50 targeted decoy-treated group at the level of injury.

Back pain, disc damage & NF-kappaB

Degenerating discs cause back pain as a result of inflammation resulting from NF-kappaB activation

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.

The publication:

May, 2009

Peroxynitrite induces gene expression in intervertebral disc cells

Summary of the abstract

Peroxynitrite is an important tissue-damaging species generated at sites of inflammation and degeneration. The aim of this study was to examine the effects resulting from peroxynitrite.

Degenerated human intervertebral disc (IVD) tissue was analyzed for nitrosylation. 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.

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.

This study provides evidence that peroxynitrite may play a role in disc degeneration and discogenic back pain development by the increased synthesis of proinflammatory cytokines that results from the activation of NF-kB. Neutralizing peroxynitrite and its derivatives (e.g., via the use of antioxidants) may be a novel treatment option for discogenic back pain.