%0 Journal Article
%T Zinc Deficiency and Zinc Therapy Efficacy with Reduction of Serum Free Copper in Alzheimer¡¯s Disease
%A George J. Brewer
%A Sukhvir Kaur
%J International Journal of Alzheimer's Disease
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/586365
%X We are in the midst of an epidemic of Alzheimer¡¯s disease (AD) in developed countries. We have postulated that ingestion of inorganic copper from drinking water and taking supplement pills and a high fat diet are major causative factors. Ingestion of inorganic copper can directly raise the blood free copper level. Blood free copper has been shown by the Squitti group to be elevated in AD, to correlate with cognition, and to predict cognition loss. Secondly, we have shown that AD patients are zinc deficient compared to age matched controls. Zinc is important in neuronal protection. We carried out a 6-month small double blind trial of a new zinc formulation on AD patients. We found that in patients 70 years and older, zinc therapy protected against cognition decline compared to placebo controls. We also found that zinc therapy significantly lowered blood free copper levels. So zinc efficacy could be due to restoring neuronal zinc levels, to lowering blood free copper levels, or to both. 1. Introduction We are in the midst of an epidemic of Alzheimer¡¯s disease (AD), particularly in developed countries [1]. We have previously hypothesized that ingestion of inorganic copper from drinking water and supplement pills and a high fat diet are main causal factors in AD [2¨C5]. These two factors interact synergistically because copper oxidizes fats to molecules that are toxic, particularly to neurons. The epidemic correlates temporally with the use of copper plumbing in developed countries, and there is a great amount of additional data that draws the net tighter around a causative role for inorganic copper. Inorganic copper must not be confused with organic copper, the copper in food that is safely bound to protein. Inorganic copper is a simple salt of copper, not bound to anything, and is in part handled differently by the intestinal absorption mechanism, such that some of it contributes immediately to the serum free copper pool [6]. This pool has been shown by Squitti and her group to be expanded in AD [7], to correlate negatively with cognition [8], and to predict deterioration in cognition [9]. So, our inorganic copper hypothesis fits well with the work of the Squitti et al. group. While we believe ingestion of inorganic copper and a high fat diet are major causal factors, there are a number of other known risk factors in AD. These include having an apolipoprotein E4 allele [10], having elevated homocysteine levels [11], or having certain alleles of the iron management genes, hemochromatosis [12] and transferrin [13]. These latter fit with the copper hypothesis
%U http://www.hindawi.com/journals/ijad/2013/586365/