A Link to Alzheimer's

It could be argued that the rise in the prevalence of Alzheimer’s rates, which really is a 20th century phenomenon, loosely corresponds with the rise in rates of copper toxicity.   Even though correlation alone does not prove causation, given the body of evidence surrounding copper’s effects on specific body processes, dismissing any exploration or mention of copper seems to be a willing avoidance to actually find answers.  Dr. George J. Brewer, MD, offers the following comment: 

“Scientists these days like to talk about the complexity of AD. They formulate drugs or agents designed to lessen the amyloid-beta burden in the brain or to attack biochemical aspects of the neurofibrillary tangles. [I have] long suggested there is a simpler line of attack: prevent AD by eliminating ingestion of inorganic copper.  This concept, however, has yet to enter the conversation of the scientific community…It is our belief that the leaching of copper from copper plumbing into the drinking water is a major causal factor in the AD epidemic.” [8]

It could be argued that the copper level rises as a result of the condition rather than as a cause.  However, if copper levels indeed increased as a result and not the cause, then we would need to ask why symptoms improve when copper levels are reduced.  If the copper level rose as a natural response to help heal the symptom, in this case AD, then reducing copper should logically impair the healing process.  However, that is not the case.  For example:

“Clinical trials with copper chelators (either D- penicillamine or clioquinol) resulted in the reduction of the extent of serum peroxides and decreased the rate of cognitive decline in AD patients.”[9]  

Consider further the role that microglial dysfunction plays in Alzheimer’s disease (of which research is beginning to recognize).  

“Our findings highlight the risk of chronic Cu exposure on cognitive decline and altered microglia activation towards degenerative phenotypes. These changes may represent one of the key mechanisms linking Cu exposure or its dyshomeostasis to an increased risk for AD.” [10]

The latest research is “discovering” that brain microglia in AD patients are more frequently in a pre-inflammatory state and may be causing inflammation leading to the death of brain cells.  Have these “latest discoveries” even looked at what potential role the copper toxicity epidemic might be playing?  In the earlier chapter on Mental Health, we looked at how copper (and other toxic metals) can trigger microglial activation resulting in brain inflammation!

Alzheimer’s Disease, just as with depression, schizophrenia, anxiety and other emotional and mental health issues, could surely become better understood if we started looking at the connections they share with  mineral imbalances  such as copper,  along with exposures to other toxic metals/ neurotoxins. Like with other symptoms, it is typically not just about copper alone.  However, given the very clear connection that copper toxicity plays in all of these mental health symptoms, it seems ludicrous how quickly pharmaceuticals are prescribed without even giving consideration that a simple mineral imbalance might be part of the cause.  Rather, the copper toxicity connection, especially when it comes to public messaging, is swept under the rug and dismissed altogether, regardless of what the actual science shows.