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I've been involved with research through the NIH and various other research institutes into defects in innate immunity and auto-inflammation for 15 yrs. I am pretty sure I know a lot more about this than you do.
Just one article with a good overview of inflammation in the Abstract:
Nutr Rev. 2007 Dec;65(12 Pt 2):S140-6.Click here to read Links Inflammatory mechanisms: the molecular basis of inflammation and disease. Libby P.
Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115, USA. plibby@rics.bwh.harvard.edu
Inflammation participates importantly in host defenses against infectious agents and injury, but it also contributes to the pathophysiology of many chronic diseases. Interactions of cells in the innate immune system, adaptive immune system, and inflammatory mediators orchestrate aspects of the acute and chronic inflammation that underlie diseases of many organs. A coordinated series of common effector mechanisms of inflammation contribute to tissue injury, oxidative stress, remodeling of the extracellular matrix, angiogenesis, and fibrosis in diverse target tissues. Atherosclerosis provides an example of a chronic disease that involves inflammatory mechanisms. Recruitment of blood leukocytes characterizes the initiation of this disease. Its progression involves many inflammatory mediators, modulated by cells of both innate and adaptive immunity. The complications of established atheroma, including plaque disruption and thrombosis, also intimately involve inflammation. Mastery of the inflammatory response should aid the development of novel strategies to predict disease susceptibility, target and monitor therapies, and ultimately develop new approaches to the prevention and treatment of chronic diseases associated with aging, such as atherosclerosis.
No b.s. there.
Type II Diabetes is an end-stage result. I'm saying we should be going after the causes. Your parents and grandparents would all have been subjected to the same underlying causation. And that is dietary and environmental as well as a genetic predisposition. Another family with the same exposure to pro-inflammatory substances could end up with cardiac disease and strokes because of a different set of DNA.
I obviously have hit a nerve by stating that I believe that your disease may have been preventable. I'm sorry but I think you are a victim of the current dogma.
These diseases of chronic inflammation overlap and are both simple and complicated. The simple common factor is inflammation - the complicated part are the interactions that lead to the plethora of visible signs and symptoms: diabetes, obesity, alzheimer's, nephropathies, arthritis, atherosclerosis and vasculitis, etc.
Another Abstract illustrating two examples of overlapping pathogenesis:
Biochim Biophys Acta. 2008 Nov 5. Insulin resistance and amyloidogenesis as common molecular foundation for type 2 diabetes and Alzheimer's disease. Zhao WQ, Townsend M.
Alzheimer's Research, Merck Research Laboratories, 770 Sumneytown Pike, 26A-2000 West Point, PA 19486, USA.
Characterized as a peripheral metabolic disorder and a degenerative disease of the central nervous system respectively, it is now widely recognized that type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) share several common abnormalities including impaired glucose metabolism, increased oxidative stress, insulin resistance and amyloidogenesis. Several recent studies suggest that this is not an epiphenomenon, but rather these two diseases disrupt common molecular pathways and each disease compounds the progression of the other. For instance, in AD the accumulation of the amyloid-beta peptide (Abeta), which characterizes the disease and is thought to participate in the neurodegenerative process, may also induce neuronal insulin resistance. Conversely, disrupting normal glucose metabolism in transgenic animal models of AD that over-express the human amyloid precursor protein (hAPP) promotes amyloid-peptide aggregation and accelerates the disease progression. Studying these processes at a cellular level suggests that insulin resistance and Abeta aggregation may not only be the consequence of excitotoxicity, aberrant Ca(2+) signals, and proinflammatory cytokines such as TNF-alpha, but may also promote these pathological effectors. At the molecular level, insulin resistance and Abeta disrupt common signal transduction cascades including the insulin receptor family/PI3 kinase/Akt/GSK3 pathway. Thus both disease processes contribute to overlapping pathology, thereby compounding disease symptoms and progression.
Keep it simple.
We can do far more to prevent the inciting inflammation. But there's money to be made in the causation and in the treating and much less in prevention.
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