Tag Archive: Inflammation

Overview of peppermint’s 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.

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The citrus flavonoid hesperidin is an effective anti-inflammatory agent

Endotoxin shock represents an extreme in whole body inflammation. The ability of the citrus flavonoid hesperidin to suppress endotoxin induced shock suggests that it is a powerful anti-inflammatory agent.

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Lemon peel inhibits NF-kB, reduces inflammation

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.

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Dandelion reduces pain and inflammation

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.

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Sunflower seeds alleviate asthma symptoms

Asthma is a serious and sometimes life threatening condition. It is also extremely common. Good treatments exist, but standard treatments are sometimes unable to offer adequate control. As a result, asthma is one of the most common reason for an emergency room visit, the most common reason for absence among school aged children and a leading overall cause of diminished quality of life. The incidence of asthma is increasing globally.

A simple, inexpensive, effective treatment for asthma would be welcome – especially one relatively free from side effects and perhaps entirely free from serious side effects. Sunflower seeds appear attractive from many perspectives, not least of all because the reduction in inflammation observed is unlikely restricted to lungs and asthma. It’s likely that sunflower seeds reduce inflammation generally.

The researchers whose publication is cited below conclude that further work is required to identify the specific factors responsible for the reduction in inflammation – and reduction in asthma symptoms – they observed. Or perhaps we could simply use an aqueous extract of sunflower seeds – since that appears to be both safe and effective.

Banjo contains an aqueous extract of sunflower seeds.

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Ginger – multiple effects reduce pain & inflammation

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.

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Ginger inhibits inflammation – affects macrophages & T-cells

Activated macrophages are present in high concentrations in a number of inflammatory lesions. The most common inflammatory cell identified in active central nervous system lesions of multiple sclerosis is, for example, the macrophage.

The study briefly summarized below may have implications on the possible use of ginger extract in the treatment of multiple sclerosis, especially to the extent that ginger extract was associated with a significant reduction in T cell proliferation in response to allostimulation – thought to be important in the pathology of multiple sclerosis.

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Theory of inflammation

Inflammation can be good or bad – appropriate or excessive. Unless otherwise indicated, when used here the word “inflammation” means bad or excess inflammation – the kind that results in disease – not the kind that protects us from infections and assists in healing.
Good and bad inflammation are different but not unrelated. In fact all [...]

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NF-kB 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.

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Natural NF-kB inhibitors in migraine

Migraine is a disease of inflammation – and NF-kB is the Master Switch for inflammation.

Emerging consensus recognizes the importance, in migraine, of the over-production of:

* TNF – NF-kB controls it.

* iNOS (NO) – NF-kB controls it.

* CGRP – NF-kB at least affects it, perhaps critically, perhaps entirely.

Therefore, by inhibiting NF-kB, a reduction in each of the above mediators of migraine inflammation might be achieved.

Inhibition of NF-kB might be achieved most effectively, and certainly most safely, with the use of natural NF-kB inhibitors.

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Migraine mix: CGRP, TNF, NF-kB, TMJ

In both TMJ and migraine, high levels of CGRP are found in the trigeminal ganglion. CGRP is a neuropeptide and its release is associated with neuroinflammation. That inflammation is associated with an increase in other pro-inflammatory cytokines.

In the study briefly summarized below, administration of TNF led to an increase in CGRP. While the authors postulate that the MAPK pathway is of greatest importance, NF-kB was also shown to be activated. NF-kB activation both results from, and results in, higher levels of TNF. That is, TNF activates NF-kB and activated NF-kB turns on the production of more TNF.

As with most inflammation events, the interaction of the various components is complex and not completely understood. What is clear is that inflammation happens, that it’s important, and that CGRP, NF-kB, TNF and the trigeminal ganglion are each involved – both in migraine and in TMJ.

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Inflammation and excitotoxicity in migraine pathogenesis

Migraine involves inflammation and neurons that are over-excited. The two are probably linked.

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Neuronal inflammation of trigeminal ganglion in migraine

Brainstem dysfunction is favored in consideration of the diverse symptoms associated with the pain of migraine. Specifically, symptoms such as extreme sensitivity to lights and sounds most are most likely to originate in the brainstem.

The publication briefly summarized below suggests spreading inflammation of the trigeminal ganglion and associated structures as one possible means by which to account for both the pain and associated symptoms of migraine.

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Migraine: Inflammation of the trigemino-vascular system

Inflammation is a key component of migraine, and can be observed in the trigeminal nerve and associated vasculature.

As the theory of what causes migraine has evolved, it is easy to neglect the fact that inflammation has always been seen as a key component of migraine pathology, regardless of whether the emphasis was on the blood vessels or the nerves.

The theory on the mechanism of action by which triptans work has also changed over the years. At first they were believed to work (and were in fact designed to work) primarily by constricting the vessels – as vessel dialtion was believed to be the source of pain in migraine.

More recently the triptans have been deemed to work by inhibiting the release of CGRP, and a new generation of CGRP inhibitors have been under development for some time. CGRP is a pro-inflammatory neuropeptide. To that extent, understanding of migraine pathology has again returned to inflammation.

In any case, ‘leaky’ blood vessels (plasma protein extravasation) are associated with migraine. Both the ergots and the triptans reduce extravasation.

While the publication briefly summarized below is somewhat dated, it nonetheless suggests inflammation, affecting the vessels, mediated through the trigeminal nerve – all of which is consistent with present day understanding of migraine, despite any change in ‘emphasis’ – past or present.

Migraine always has been and always will be a disease closely associated with inflammation.

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Ginger extract reduces inflammation in arthritis

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.

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Ginger an effective anti-inflammatory agent in arthritis

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.

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Synergy of multiple NF-kB inhibitors

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.

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Ginger: ancient remedy, modern miracle

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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Neurotransmitters and inflammation

Acetylcholine, a neurotransmitter, exerts an anti-inflammatory effect, probably by inhibiting NF-kB.

This may, at least in part, explain certain neurotransmitter imbalances and other central nervous system abnormalities associated with inflammatory conditions.

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Type 2 diabetes risk and inflammation

Type 2 diabetes onset results from chronic low-grade inflammation.

Type 2 diabetes is characterized by insulin resistance. The body is producing enough insulin, but that insulin is less effective than it should be. It is poorly absorbed by the cells – which are said to ‘resist’ the effects of insulin.

In type 2 diabetes the body tries to compensate for this insulin resistance by producing more insulin. So while it may appear as if there is too little insulin (the symptoms of insulin deficiency are present) there may in fact be an actual excess of insulin – especially in the early stages of type 2 diabetes.

Insulin resistance is associated with, or caused by, chronic low-grade inflammation.

There is evidence that insulin resistance in the liver specifically results from over activation of NF-kB. It is likely that insulin resistance in general results from over-activation, though the mechanism remains unclear.

What is clear is that insulin resistance – and therefore diabetes type 2 – results from chronic inflammation.

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