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Simple question - is there any epidemiological evidence that indicates reduction in disease in populations that eat lots of curry?Second question - nothing is without cost - what is the trade off - what are the risks with chronic overdosing on Curcumin ?
Quote from: another_someone on 21/02/2007 23:52:29Simple question - is there any epidemiological evidence that indicates reduction in disease in populations that eat lots of curry?Second question - nothing is without cost - what is the trade off - what are the risks with chronic overdosing on Curcumin ?Hi George,I think there are suggestions, more than real evidence.It seems almost impossible to demonstrate something like that just epidemiologically: there are too many differences in diet and lifestyle between populations eating lots of curry and the rest of the world.On the other hand, "significant preventive and/or curative effects have been observed in experimental animal models of a number of diseases, including arteriosclerosis, cancer, diabetes, respiratory, hepatic, pancreatic, intestinal and gastric diseases, neurodegenerative and eye diseases" (see below). Experimental toxicity of curcumin has probably been defined as LD50 in animals and should be far higher than usual 'doses' (sorry I can't find any reference).No idea about chronic overdosing.ikod
Curcumin is a nutrient, not a drug.Modified synthetic analogues are faraway to come: these discoveries arequite recent for western science.As with vitamin D in cod liver oil,eventually a low dose should be goodfor us, too much......exactly the opposite.ikodP.S.I'm not trying to sell either curcumin or cod liver oil.I am trying to communicate my enthusiasm about simplenutrients that could help in human disease.I have this feeling that they are neglected, a bit.
The old Ayurvedal/Chinese medicine is finally joining western orthodox medicine and is already giving very promising results, perhaps thanks to the immigrants from Asia to the USA/UK who are now leading big research labs.
http://www.brown.edu/Courses/Bio_160/Projects1999/malaria/images/Image7.gif Sequestration of parasites and obstruction of brain vessels (RPH) The cause of cerebral malaria is not well understood. Currently, there are two major hypotheses explaining its etiology. They are the mechanical and the humoral hypotheses. The mechanical hypothesis asserts that a specific interaction between a P. falciparum erythrocyte membrane protein (PfEMP-1) and ligands on endothelial cells, such as ICAM-1 or E-selectin, reduces microvascular blood flow and induces hypoxia. This selective cytoadherence of PRBCs and non-PRBCs, also known as rosetting, can apparently better account for CM’s histopathological hallmark and its characteristic coma condition. However, this hypothesis is inadequate in explaining the relative absence of neurological deficit even after days of unconsciousness. The humoral hypothesis suggests that a malarial toxin may be released that stimulates macrophages to release TNF-a and other cytokines such as IL-1. The cytokines themselves are not harmful, but they may induce additional and uncontrolled production of nitric oxide. Nitric oxide would diffuse through the blood-brain barrier and impose similar changes on synaptic function as do general anesthetics and high concentrations of ethanol, leading to a state of reduced consciousness. The biochemical nature of this interaction would explain the reversibility of coma.click here to read more: http://www.brown.edu/Courses/Bio_160/Projects1999/malaria/cermal.html