Hallmarks of Alzheimer’s Are Stimulated by Mercury

STORY AT-A-GLANCE

  • Using nucleotide photoaffinity labeling technology, Boyd Haley, Ph.D., showed mercury is the only heavy metal capable of causing a normal brain to develop the same biochemical abnormalities found in Alzheimer’s disease
  • The enzyme creatine kinase is 98 percent inhibited in Alzheimer’s patients, and tubulin is inhibited by more than 80 percent
  • Mercury causes the synaptic clefts to disappear and triggers the formation of neurofibrillary tangles, a major diagnostic hallmark of Alzheimer’s, by causing abnormal hyperphosphorylation of tau
  • The chelating compound Haley developed, called emeramide or NBMI, tightly binds to mercury and expels it through your stool
  • Phase I and Phase II drug trials has shown emeramide significantly lowers mercury burden in animals and humans; the drug is still going through the approval process; it is designated as an orphan drug for use as a mercury chelator in both the U.S. and the European Union

Dr. Mercola Interviews the Experts

This article is part of a weekly series in which Dr. Mercola interviews various experts on a variety of health issues. To see more expert interviews, click here.

Boyd Haley, Ph.D., is a chemist specializing in the development of chemicals to chelate toxic metals, both from the environment and the human body. I had the opportunity to interview Haley (above) at the 2018 Academy of Comprehensive Integrative Medicine (ACIM) conference in Orlando.

Haley has a Ph.D. in chemistry and biochemistry and conducted research funded by the National Institutes of Health (NIH) for 25 years at the University of Wyoming and at the University of Kentucky. Early in his career, he developed a biochemical detection system called nucleotide photoaffinity labeling and has published studies on its usage.1 Haley explains:

“I took ATP and made it radioactive, which isn’t a big feat. But then I attached to that a molecule that would explode when it hit a photon of light. When it exploded, it made a very reactive intermediate that had a half-life of something like 10-12 or 10-13 seconds.

If ATP was bound to a protein, such as sodium potassium ATP [and] … you hit it with light, it would form a covalent bond at the binding site of ATP on the enzyme it was interacting with …

You could use these kinds of probes to see the difference between the ATP, guanosine diphosphate (GDP), cyclic adenosine monophosphate (AMP) and nicotinamide adenine dinucleotide (NADH) — all these binding proteins, to see how the energetics of the cell was changing.”

Haley’s Alzheimer’s Research

He later took a position with the Alzheimer’s Center, a research center for Alzheimer’s disease, where he collaborated with a former graduate student of his. The NIH funded their research for five years, which used Haley’s technology to assess the differences of ATP, GDP and cyclic AMP binding proteins in normal brains versus those with Alzheimer’s disease.

“There were dramatic differences,” he says. For example, the enzyme creatine kinase, which is a fundamental enzyme, is 98 percent inhibited in Alzheimer’s patients. They also discovered that tubulin — a major brain protein that holds an axon in its extended form and controls the growth direction of axons and dendrites — is inhibited by more than 80 percent.

In 1989, he published the paper2 “Aberrant guanosine triphosphate-beta-tubulin interaction in Alzheimer’s disease” in the Annals of Neurology, stating that “These results support the hypothesis that microtubule formation is abnormal in brains affected by Alzheimer’s disease.”

Haley goes on to recount the story of how he got into trouble with the NIH when he decided to investigate the influence of heavy metals on Alzheimer’s susceptibility. A popular theory at the time was that Alzheimer’s was caused by aluminum toxicity.

Using his technology, he was able to show that mercury was the only heavy metal capable of causing a normal brain to develop the same biochemical abnormalities — including abnormal tubulin — that you find in Alzheimer’s disease.

Haley claims his research has since been replicated and confirmed. According to Haley, mercury causes the synaptic clefts to disappear and triggers the formation of neurofibrillary tangles, a major diagnostic hallmark of Alzheimer’s, by causing abnormal hyperphosphorylation of tau.

He also published a paper3 in the respected medical journal Proceedings of the National Academy of Sciences in 1992, detailing how the presence of glutamine synthetase in the cerebrospinal fluid may be a potential diagnostic biochemical marker of Alzheimer’s disease, as well as more than 100 other studies,4 including a review of the relationship between mercury and autism,5 and research showing how the chelating agent he developed, emeramide (NBMI), protects against the cytotoxicity of mercury.6

All Biochemical Abnormalities and Hallmarks of Alzheimer’s Are Stimulated by Mercury

Beta-amyloid, which many associate with Alzheimer’s, is not the actual cause of the disease. It’s just a marker; it’s a result of the disease. However, you can cause beta-amyloid buildup in the brain by treating neurons with mercury.

“What happens is mercury inhibits the expression of neprilysin, which is the main protease in the brain used to chew up beta-amyloid. Mercury doesn’t affect beta-amyloid, but what it does do is it keeps the protease, the cleanup enzyme, from being expressed,” he explains.

“If you give mercury at low levels, very low levels, to tissues that are going to live for a while, you’ll see a buildup of beta-amyloid protein. The bottom line is: 6 out of 6 of the major biochemical abnormalities and pathological hallmarks of Alzheimer’s disease can be stimulated by adding mercury.

I can tell you that was something that NIH, or the people who run NIH at the very top, did not want to hear … They said beta-amyloid is the cause of Alzheimer’s disease. That made them heroes — they found the cause, so now they would find the cure …

But they don’t want to look at it being something simple. There’s no money to be made if you tell people, ‘If you don’t want to get Alzheimer’s disease, don’t expose yourself to mercury.’

Mercury is not the only cause. I would never say that, and I never did say that. I said, ‘Mercury is the major exacerbating factor7 because we put dental amalgams in our mouth, and the major exposure, the source of mercury in our body, comes from them [sic] amalgams, according to the World Health Organization (WHO).'”

The Transformation of a Skeptic

It’s interesting to note that Haley was in fact highly skeptical of the idea that dental amalgam released mercury before he started studying the matter. Like so many others, he assumed the U.S. Food and Drug Administration (FDA) and the American Dental Association would never allow something truly toxic to be placed in people’s mouths.

His scientific investigations eventually convinced him that amalgams are a major source of mercury exposure that can indeed exacerbate and trigger chronic illness — something he details in his 2014 paper,8 “Evidence Supporting a Link Between Dental Amalgams and Chronic Illness, Fatigue, Depression, Anxiety and Suicide.”

Haley also recounts the twists and turns in his life that brought him to investigate the links between mercury toxicity and autism, and how vaccines can be a source of toxic mercury exposure. While thimerosal (mercury-based preservative) has been removed from many childhood vaccines, it’s still used in some….

https://articles.mercola.com/sites/articles/archive/2020/01/12/treating-mercury-toxicity-with-emeramide.aspx

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