{"id":130433,"date":"2023-06-24T17:07:40","date_gmt":"2023-06-24T17:07:40","guid":{"rendered":"https:\/\/organicconsumers.org\/?p=130433"},"modified":"2023-06-28T17:12:46","modified_gmt":"2023-06-28T17:12:46","slug":"hallmarks-of-alzheimers-are-stimulated-by-this-substance","status":"publish","type":"post","link":"https:\/\/organicconsumers.org\/hallmarks-of-alzheimers-are-stimulated-by-this-substance\/","title":{"rendered":"Hallmarks of Alzheimer’s Are Stimulated by This Substance"},"content":{"rendered":"
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Hallmarks of Alzheimer’s Are Stimulated by This Substance<\/h1><\/span>
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If you don’t want Alzheimer’s, avoid this. It’s not the only cause, but it is a major exacerbating factor.<\/em><\/p>\n<\/div>

June 24, 2023 | Source: Mercola.com<\/a> | by Dr. Joseph Mercola<\/p>\n<\/div>

Editor’s Note: This article is a reprint. It was originally published March 10, 2019.<\/strong><\/em><\/p>\n

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.<\/p>\n

Haley\u2019s Ph.D. is in chemistry and biochemistry. He 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<\/a><\/p>\n

Haley explains:<\/p>\n

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“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.<\/em><\/p>\n

If ATP was bound to a protein, such as sodium potassium ATP [and] \u2026 you hit it with light, it would form a covalent bond at the binding site of ATP on the enzyme it was interacting with \u2026<\/em><\/p>\n

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) \u2014 all these binding proteins, to see how the energetics of the cell was changing.”<\/em><\/p>\n<\/blockquote>\n

Haley’s Alzheimer’s Research<\/strong><\/h2>\n
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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.<\/div>\n<\/div>\n<\/div>\n

“There were dramatic differences,” he says. For example, the enzyme creatine kinase, which is a fundamental enzyme, is 98% inhibited in Alzheimer’s patients. They also discovered that tubulin \u2014 a major brain protein that holds an axon in its extended form and controls the growth direction of axons and dendrites \u2014 is inhibited by more than 80%.<\/p>\n

In 1989, he published the paper2<\/a>\u00a0“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.”<\/p>\n

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.<\/p>\n

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 \u2014 including abnormal tubulin \u2014 that you find in Alzheimer’s disease.<\/p>\n

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.<\/p>\n

He also published a paper3<\/a>\u00a0in 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<\/a>\u00a0including a review of the relationship between mercury and autism,5<\/a>\u00a0and research showing how the chelating agent he developed, emeramide (NBMI), protects against the cytotoxicity of mercury.6<\/a><\/p>\n

Biochemical Abnormalities Are Stimulated by Mercury<\/strong><\/h2>\n
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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.<\/div>\n<\/div>\n<\/div>\n
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“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,”<\/em>\u00a0he explains.<\/p>\n

“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.<\/em><\/p>\n

I can tell you that was something that NIH, or the people who run NIH at the very top, did not want to hear \u2026 They said beta-amyloid is the cause of Alzheimer’s disease. That made them heroes \u2014 they found the cause, so now they would find the cure \u2026<\/em><\/p>\n

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.’<\/em><\/p>\n

Mercury is not the only cause. I would never say that, and I never did say that. I said, ‘Mercury is the major exacerbating factor<\/em>7<\/a>\u00a0because 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).'”<\/em><\/p>\n<\/blockquote>\n

The Transformation of a Skeptic<\/strong><\/h2>\n
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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 and the American Dental Association would never allow something truly toxic to be placed in people’s mouths.<\/div>\n<\/div>\n<\/div>\n

His scientific investigations eventually convinced him that\u00a0amalgams<\/a><\/strong>\u00a0are a major source of mercury exposure that can indeed exacerbate and trigger chronic illness \u2014 something he details in his 2014 paper,8<\/a>\u00a0“Evidence Supporting a Link Between Dental Amalgams and Chronic Illness, Fatigue, Depression, Anxiety and Suicide.”<\/p>\n

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.<\/p>\n

One tipoff that thimerosal was bad news came from a 1977 report from Toronto Hospital, where 10 of 13 infants died after having their umbilical region treated with merthiolate (thimerosal) to kill bacterial infection. Merthiolate is no longer in use, as it was discovered that these infants died from mercury toxicity.<\/p>\n

This report revealed that thimerosal turned into ethyl mercury, which the infant body cannot eliminate. Despite that, a mere decade later, in 1988, the U.S. Centers for Disease Control and Prevention decided thimerosal was an appropriate preservative for use in vaccines given to newborn babies and infants.<\/p>\n

How Genetics Influence Your Mercury-Elimination Capacity<\/strong><\/h2>\n
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Haley completed his Alzheimer’s research in 1988, just over 30 years ago, yet he’s never been invited to an Alzheimer’s conference to present his work. He has also published a book in which he proposed a mechanism for why having two copies of the ApoE2 gene renders you more or less immune to Alzheimer’s.<\/div>\n<\/div>\n<\/div>\n

The ApoE2 gene has two cysteine molecules on the surface, whereas ApoE4 \u2014 which is a major risk factor for Alzheimer’s \u2014 has two tyrosine molecules. These are amino acids on the structure. The cysteine amino acid on E2 binds effectively to mercury, whereas the tyrosine on E4 cannot bind to mercury at all.<\/p>\n

As a result, having two copies of the ApoE4 gene places you at a significant disadvantage, as your brain cannot eliminate mercury naturally, whereas having two copies of ApoE2 is highly protective because your brain has the ability to clear out mercury.<\/p>\n

It is also helpful to note that Dr. Dale Bredesen who wrote the book “The End of Alzheimer’s,” believes the ApoE4 allele may actually protect against Alzheimer’s if you are metabolically flexible and regularly engage in intermittent or partial fasting.<\/p>\n

Therapeutic Interventions to Address Mercury Toxicity<\/strong><\/h2>\n
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Alzheimer’s disease is associated with oxidative stress. While mercury is not a redox metal, meaning it cannot create hydroxyl free radicals, mercury does displace iron and kaempferol, and when mercury displaces iron, it stops ATP production in that electron transport system.<\/div>\n<\/div>\n<\/div>\n

By displacing iron from the iron sulfur centers mercury also blocks the cytochromes, as cytochromes require iron to work. “There are publications now showing that mercury exposure totally screws up the metabolism of iron in the body,” Haley says.<\/p>\n

The chelating compound he developed, called emeramide or NBMI,9<\/a>\u00a0tightly binds to both mercury and free iron, which is also highly toxic. As such, emeramide can also be used in the treatment of hemochromatosis, a genetic disease that causes chronic iron overload.<\/p>\n

Drawbacks of Most Popular Chelating Agents for Mercury<\/strong><\/h2>\n