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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Category Archives: Other Ailments
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.
Ginger improves lipid (cholesterol) profile
Ginger lowers ‘bad’ cholesterol, raises ‘good’ cholesterol.
Daily ginger decreased levels of triglycerides, total cholesterol, low density lipoprotein (LDL), and very low density lipoprotein (VLDL), while increasing high-density lipoprotein (HDL – ‘good’ cholesterol.)
Ginger for periodontal disease – gingivitis
Ginger effectively inhibits the growth of, or kills, bacteria associated with periodontitis.
So in addition to treating pain and inflammation, Banjo may also improve the health of your gums, preserve your teeth – even freshen your breath. How nice!
Ginger extract may delay onset and progression of Alzheimer’s
Alzheimer’s disease is associated with the formation, in the brain, of amyloid plaques. While the existence of these plaques in Alzheimer’s has long been known, their role in the disease has remained somewhat uncertain. There is however increasing recognition of the very significant role played by inflammation in the onset and progression of Alzheimer’s. Indeed, the plaques of Alzheimer’s are found to be surrounded by cells (microglia) that cause inflammation through the release of pro-inflammatory chemicals (cytokines.)
In the study briefly summarized below, ginger extract was found to reduce microglia inflammation and the release of cytokines by microglia. As such, the authors conclude that ginger extract might be useful in preventing, or at least delaying, both the onset and progression of Alzheimer’s disease.
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.
Glucocorticoid therapy in MS inhibits NF-kB
Methylprednisolone administration in multiple sclerosis patients (pulsed therapy) resulted in clinical improvement that showed a correlation to NF-kB inhibition.
The publication:
Blessed milk thistle may bless those with MS
Silibinin is a mixture of flavonolignans extracted from blessed milk thistle. It has for some time been recognized for its beneficial effects in protecting the liver against toxins. More recently it has been demonstrated that silibinin inhibits NF-kB.
The researchers whose publication is briefly summarized below hypothesized that, as a natural NF-kB inhibitor, silibinin might be useful in the treatment of multiple sclerosis.
Employing the mouse model of MS, experimental autoimmune encephalomyelitis (EAE), they looked at the effects of silibinin on spinal cord demyelination and inflammation. The results of their investigation indicated that silibinin is both immunosuppressive and immunomodulatory and that it might be useful in the treatment of MS.
Fumaric acid inhibits NF-kB, treats psoriasis and perhaps MS
Fumaric acid is widely used in Germany (where it is known as Fumaderm®) in the treatment of psoriasis. It’s mechanism of action is uncertain, but it is believed to act primarily via the inhibition of NF-kB through by increasing the levels of reduced glutathione.
A total of 13 studies have confirmed that 50-70% of psoriasis patients show an approximate 75% reduction in their “psoriasis area and servitiy index” (PASI) after 4 months of treatment. However, side effects can be significant, and include nausea, vomiting and diarrhea in up to 30% of patients. These side effects limit the duration of treatment to 6 weeks, which of course limits the usefulness of this product in the treatment of chronic disease.
Fumarate is known to be an immunomodulator, which is one reason for its present consideration as a possible new drug for the treatment of multiple sclerosis.
In a recent phase II study involving 257 patients, fumarate reduced by 69% the average number of lesions on MRI between weeks 12 and 24, reduced newly enlarging lesions by about 50% and reduced the annualized relapse rate by 32%. Adverse events included headache, infections, GI symptoms and slightly increased liver enzymes, all of which were reversible.
Natural inhibitor of NF-kB as potential new treatment for multiple sclerosis
Triptolide, the presumed active component of T. wilfordii, is known to be an inhibitor of NF-kB.In the study briefly summarized below, oral administration of triptolide was shown to be therapeutic in a mouse model of multiple sclerosis, both when used as an acute treatment (after development of disease) and when used in the prevention of disease onset.
Experimental autoimmune encephalomyelitis (EAE) is a well accepted animal model of human demyelinating disease such as multiple sclerosis. However, it should be noted that the condition studied is not multiple sclerosis, and that the ‘patient’ is a mouse, not a human.
Nonetheless, the results of oral administration of the natural NF-kB inhibitor triptolide were encouraging:
* Disease onset was delayed.
* Clinical symptoms were reduced.
* Relapse rate decreased.
* Inflammation and demyelination in CNS tissue were both diminished.
Triptolide was shown to inhibit NF-kB.
Progressive MS might be effectively treated via NF-kB inhibition.
Inhibition of NF-kB was found to be effective in preventing relapse in a mouse model of multiple sclerosis.
The publication:
Pregnancy lowers relapse in MS via NF-kB inhibition
Lower relapse rates in multiple sclerosis patients during pregnancy result from higher levels of estrogen leading to NF-kB inhibition.
Women with multiple sclerosis have been reported to suffer fewer relapses (attacks or disease exacerbations) during the time of pregnancy. While there has been some controversy on this issue, the PRIMS study (pregnancy and MS study) documented a modest but significant decrease in the rate of relapse in 227 women with MS during pregnancy, especially during the third trimester. Those same women then experienced a higher than normal (pre-pregnancy) rate of relapse following childbirth, especially in the first three months after childbirth.
Increased estrogen (or estriol) levels during pregnancy have been postulated as the source of this ‘protective effect’.
In the study summarized below, the researchers note the effects of estriol on various mediators of inflammation and on the inhibition of NF-kB.
Genetic study points to NF-kB dysregulation in MS
Variation in genes controlling inhibitors of NF-kB strongly influences susceptibility to multiple sclerosis.
Multiple sclerosis (MS) is known to be associated with both excess, chronic inflammation and with immune dysfunction. Since NF-kB is central to the control of inflammation, the researchers whose publication is summarized below investigated genetic variations associated with NF-kB in multiple sclerosis patients.
That is, rather than looking at the entire genome (all the genes in an individual) they only investigated those genes related to NF-kB. By focusing on and more closely examining NF-kB, more subtle differences can be investigated, especially the combination of slight differences between individuals with and without MS. Specifically, they looked for mutations, polymorphisms and sequence variations (MPSV) in NF-kB related genes.
Parthenolide for migraine and MS
Parthenolide, though previously shown to inhibit NF-kB, was shown in the study summarized below to inhibit NO production through an alternate pathway. It is likely that parthenolide (the presumptive active component of feverfew) acts by various mechanisms in the body.
The investigators conclude that parthenolide might be useful in the treatment of those conditions where excess NO is believed to play a significant role, such as multiple sclerosis and migraine.
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.
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.
NF-kB, atherosclerosis and aging
Excess NF-kB activation underlies vascular damage associated with aging.
A number of risk factors are associated with the onset of clinically significant atherosclerosis. Among those risk factors are high blood pressure, metabolic disease and a number of lifestyle related risks such as obesity and smoking.
Aging itself has come to be seen as an independent risk factor in the development of atherosclerosis, as vascular inflammation and atherosclerosis is observed with increasing frequency at greater age, even in the absence of other risk factors. Age-related oxidative stress is believed responsible for this effect on aging vessels.
The review briefly summarized below suggests that oxidative stress is mediated through multiple pro-inflammatory pathways, all of which converge on NF-kB, resulting in excess activation of NF-kB in the aged vasculature.
The implication of this publication is that by preventing or reducing excess NF-kB activation the effects of aging on blood vessels can be countered.
Ancient problem – ancient cure
The risk of cancer is reduced as excess NF-kB activation is reduced.
This is an essential publication because it so effectively and efficiently summarizes both the mechanism underlying well-known cancer risks and the means by which we can protect ourselves from those risks.
* Things which put us at risk are those which activate NF-kB – because cancer is a disease of inflammation.
* So the things that protect us are NF-kB inhibitors – fruits and vegetables.
Noteworthy is that the publication originates with M.D. Anderson cancer Center, one of the most well-known and well-respected cancer research and treatment facilities in the world.
I would only add that, according to the theory advocated on this site, an initial deficit in NF-kB inhibitors (as is prevalent in those eating a ‘Western’ diet) is sufficient in and of itself to increase the risk of cancer – because it means that NF-kB is chronically over-activated. Additional exposure to carcinogens increases that risk.
The weak NF-kB inhibitor glucosamine may be useful in IBD.
Essentially all NF-kB inhibitors, even the relatively ineffective NF-kB inhibitor glucosamine, may be of benefit in the treatment of diverse conditions associated with inflammation – including inflammatory bowel disease.
Glucosamine, which was originally combined with chondroitin sulfate in preparations for the treatment of osteoarthritis, was originally believed to act primarily by “re-building cartilage” and “providing nutrition” to the joint.
It is now recognized, however, that glucosamine is an anti-inflammatory agent – a weak NF-kB inhibitor.
As such, glucosamine will do what NF-kB inhibitors do – it will treat inflammation and may therefore find application in any number of inflammation related conditions.
In the study summarized here, the effects of glucosamine in the treatment of a rat model of inflammatory bowel disease are investigated and found to be promising.
However, it is this author’s opinion that glucosamine will never find practical application in the treatment of inflammatory bowel disease (ulcerative colitis and Crohn’s.) It is simply not a potent enough inhibitor of NF-kB and would require administration in amounts far too great to be practical.
Furthermore, there are much more effective, faster-acting NF-kB inhibitors readily available.
Nonetheless, this study serves as a useful demonstration of the safety and efficacy of NF-kB inhibitors – in this case when used for the treatment of inflammatory bowel disease.
Natural NF-kB inhibitor acts synergistically to stop inflammation in IBD
Curcumin effectively inhibits NF-kB only in combination with IL-10.
This is a key publication because it:
* Demonstrates one likely reason you can’t overdose on curcumin or any other natural NF-kB inhibitor;
* Suggests ‘cooperation’ between these natural NF-kB inhibitors and the immune system – a ‘vitamin like’ action; and,
* Provides one example of the importance of natural NF-kB inhibitors in shutting down inflammation.
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