Chronic Inflamation

Chronic Inflammation can Cause Many Diseases

The underlying cause of many diseases might be due to chronic inflammation. There is plenty of evidence,
by the medical profession, that correcting a chronic inflammation disorder may help prevent or reverse
many diseases. 

Inflammatory cytokines may contribute to the progression of many degenerative
diseases Rheumatoid arthritis is an auto-immune disease in which
levels of several cytokines are elevated: TNF-a, IL-6, IL-1(b), and interleukin-8 (IL-8) all examples of
cytokines that can cause or contribute to inflammation.

 
A large nuber of Diseases can be related to Chronic Inflammation, among these one are:

Allergy Inflammatory cytokines induce autoimmune reactions of the immune defence system

Mutiple Sclerosis inflammatory cytokines destroyes the myelin sheat of the axons from neurons
 
Alzheimer's Chronic inflammation destroys brain cells through myeloid plack
 
Anemia Inflammatory cytokines attack erythropoietin production

Aortic valve stenosis Chronic inflammation damages heart valves
 
Arthritis Chronic inflammation causes many cancers
 
Congestive heart failure Chronic inflammation contributes to heart muscle wasting
 
Fibromyalgia Inflammatory cytokines are elevated
 
Fibrosis Inflammatory cytokines attack traumatized tissue
 
Heart Attack Chronic inflammation contributes to coronary atherosclerosis
 
Kidney failure Inflammatory cytokines restrict circulation and damage nephrons
 
Lupus Inflammatory cytokines induce an autoimmune attack
 
Pancreatitis Inflammatory cytokines induce pancreatic cell injury
 
Stroke Chronic inflammation promoted thromboembolic events
 
Surgical complications Inflammatory cytokines prevent healing

 
Reducing inflammation without resorting to drugs may involve two monosaccharides (simple sugars)
called Mannose and N-acetyl-glucosamine. Both Mannose and N-acetyl-glucosamine have been shown to
reduce inflammation (Brink U et al 1998).The Worlds first clinical human study on Medox® and its effect on Chronic InflammationThe Worlds first clinical human study on Medox® and its effect on Chronic Inflammation

The Worlds first clinical human study on Medox® and its effect on Chronic Inflammation

The study concludes: ” These data suggest that anthocyanin supplementation (Medox®) may have a role in prevention or treatment of chronic inflammatory diseases by inhibition of NF-KappaB transactivation and deceased plasma concentration of pro-inflammatory chemokines, cytokines, and inflammatory mediators. R. Blomhoff et al, Journal of Nutrition, August 2007, USA.

Anthocyanins Inhibit Nuclear Factor-kB Activation in Monocytes and Reduce Plasma Concentrations of Pro-Inflammatory
Mediators in Healthy Adults

Anette Karlsen,4 Lars Retterstøl,6 Petter Laake,5 Ingvild Paur,4 Siv Kjølsrud-Bøhn,4 Leiv Sandvik,7
and Rune Blomhoff4*

4Department of Nutrition, and 5Department of Biostatistics, Institute of Basic Medical Sciences, University of
Oslo, Oslo,Norway N-0316 and 6Department of Medical Genetics and 7Research Centre, Ullevaal University Hospital, Oslo,
Norway N-0407

Abstract

The transcription factor nuclear factor-kB (NF-kB) is activated by oxidative stress and pro-inflammatory stimuli
and controls the expression of numerous genes involved in the inflammatory response. Dampening NF-kB activation
and thereby limiting the inflammatory response have been suggested as a potential strategy to prevent chronic
inflammatory diseases. In cultured monocytes, anthocyanins isolated from bilberries and black currants (Medox)
efficiently suppressed LPS-induced activation of NF-kB. Furthermore, we studied the effect of anthocyanin
supplementation (Medox, 300 mg/d for 3 wk) in a parallel-designed, placebo-controlled clinical trial (n ¼ 120
men and women aged 40–74 y). Differences were observed in several NF-kB related inflammatory mediators in the
Medox group compared to placebo. The changes in the NF-kBcontrolled pro-inflammatory chemokines IL-8, ‘‘regulated
upon activation, normal T cell expressed and secreted,’’ (RANTES) and IFNa (an inducer of NF-kB activation) in
the Medox group (45, 15, and 40% decreases from baseline, respectively) differed from those in the placebo group
(20, 0, and 15% decreases from baseline, respectively) (P , 0.050). Similarly, changes in IL-4 and IL-13, 2
cytokines that mediate pro-inflammatory responses and induce NF-kB activation, in the Medox group (60 and 38%
decreases from baseline, respectively) tended to differ from those in the placebo group (4 and 6% decreases)
(P ¼ 0.056 and, P ¼ 0.089, respectively).These data suggest that anthocyanin supplementation may have a role
in the prevention or treatment of chronic inflammatory diseases by inhibition of NF-kB transactivation and
deceased plasma concentrations of pro-inflammatory chemokines, cytokines, and inflammatory mediators. J. Nutr.
137: 1951–1954, 2007.

4Department of Nutrition, and 5Department of Biostatistics, Institute of Basic Medical Sciences, University of
Oslo, Oslo,Norway N-0316 and 6Department of Medical Genetics and 7Research Centre, Ullevaal University Hospital,
Oslo, Norway N-0407

Anthocyanins prevent CD40-Activated Proinflammatory Signaling in Endothelial Cells by Regulating cholesterol Distribution

In a study based on Biolink Group anthocyanins, medical researchers at the Sun Yat-sen University in Guangzhou, Peoples Republic of China, found that anthocyanins inhibits NF-KappaB .The conclusions on the study was; “ Our findings suggest that anthocyanin protects from CD-40-induced proinflammatory signaling by preventing TRAF-2 translocation to lipid rafts through regulation of cholesterol distribution, which thereby may represent a mechanism that would explain the anti-inflammatory response of anthocyanin. Wenhua Ling et al,  “Arteriosclerosis, Thrombosis and Vascular Biology” April, 2007, USA.