Editor’s Note: This article is a reprint. It was originally published on March 10, 2019.
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 obtained his Ph.D. in chemistry and biochemistry. He conducted research funded by the National Institutes of Health (NIH) for 25 years at the University of Wyoming and the University of Kentucky. Early in his career, he developed a biochemical detection system known as nucleotide photoaffinity labeling and has published studies on its application. Haley explains:
“I took ATP and made it radioactive, which isn’t a big feat. But then I attached a molecule to it that would explode upon exposure to a photon of light. When it exploded, it created a very reactive intermediate with a half-life of around 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 types of probes to observe the differences between ATP, guanosine diphosphate (GDP), cyclic adenosine monophosphate (AMP), and nicotinamide adenine dinucleotide (NADH) — all these binding proteins, to analyze how the energetics of the cell were changing.”
Haley’s Alzheimer’s Research
He later joined the Alzheimer’s Center, a research institution for Alzheimer’s disease, where he collaborated with a former graduate student of his. Their research, funded by the NIH for five years, utilized Haley’s technology to compare the differences in ATP, GDP, and cyclic AMP binding proteins in normal brains versus those with Alzheimer’s disease.
“There were significant differences,” he notes. For example, the enzyme creatine kinase, a fundamental enzyme, is 98% inhibited in Alzheimer’s patients. They also found that tubulin — a major brain protein responsible for holding an axon in its extended form and controlling the growth direction of axons and dendrites — is inhibited by over 80%.
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 then shares the story of how he faced backlash from the NIH when he decided to explore the impact of heavy metals on Alzheimer’s susceptibility. At that time, a prevalent theory suggested that aluminum toxicity caused Alzheimer’s.
Utilizing his technology, he demonstrated that mercury was the sole heavy metal capable of inducing normal brains to develop the same biochemical abnormalities — including abnormal tubulin — seen in Alzheimer’s disease.
Haley asserts that his research has since been replicated and validated. According to him, mercury leads to the disappearance of synaptic clefts and triggers the formation of neurofibrillary tangles, a key diagnostic feature of Alzheimer’s, by inducing abnormal hyperphosphorylation of tau.
He also published a paper3 in the esteemed medical journal Proceedings of the National Academy of Sciences in 1992, outlining how the presence of glutamine synthetase in the cerebrospinal fluid could serve as a potential diagnostic biochemical marker of Alzheimer’s disease, along with more than 100 other studies,4 including a review on the relationship between mercury and autism,5 as well as research demonstrating how the chelating agent he developed, emeramide (NBMI), protects against the cytotoxic effects of mercury.6
Biochemical Abnormalities Are Triggered by Mercury
Beta-amyloid, often associated with Alzheimer’s, is not the primary cause of the disease. It is merely a marker; a consequence of the disease. Nevertheless, treating neurons with mercury can result in the buildup of beta-amyloid in the brain.
“Mercury inhibits the expression of neprilysin, the main protease in the brain responsible for breaking down beta-amyloid. Mercury doesn’t directly impact beta-amyloid, but it prevents the expression of the protease, the cleanup enzyme,” he explains.
“When you expose tissues that will survive for some time to very low levels of mercury, you’ll observe an accumulation of beta-amyloid protein. In essence, 6 out of 6 major biochemical abnormalities and pathological hallmarks of Alzheimer’s disease can be induced by adding mercury.
I can tell you that this was something the top officials at the NIH did not want to acknowledge … They argued that beta-amyloid was the cause of Alzheimer’s disease. This made them heroes — they identified the cause, so naturally, they would discover the cure …
But they were unwilling to consider a simple solution. No profits are to be made by advising people, ‘Avoid exposure to mercury if you want to prevent Alzheimer’s disease.’
Mercury is not the sole cause. I have never claimed that, and I never will. I stated, ‘Mercury is the primary exacerbating factor7 because we place dental amalgams in our mouths, and the primary source of mercury in our bodies comes from these dental amalgams, according to the World Health Organization (WHO).'”
The Journey of a Skeptic
Interestingly, Haley was initially skeptical about the idea that dental amalgam released mercury before he delved into the subject. Like many others, he assumed that the U.S. Food and Drug Administration and the American Dental Association would not permit something genuinely toxic to be placed in people’s mouths.
His scientific inquiries ultimately convinced him that amalgams are a significant source of mercury exposure that can exacerbate and trigger chronic illnesses — a concept he elaborates on in his 2014 paper,8 “Evidence Supporting a Link Between Dental Amalgams and Chronic Illness, Fatigue, Depression, Anxiety, and Suicide.”
Haley also reflects on the twists and turns that led him to investigate the connections between mercury toxicity and autism, as well as how vaccines can contribute to toxic mercury exposure. Although thimerosal has been removed from many childhood vaccines, it is still used in some. One study from 1977 at Toronto Hospital found that 10 out of 13 infants died after being treated with merthiolate (which contains thimerosal) in their umbilical region. It was discovered that these infants died from mercury toxicity. Despite this, the U.S. Centers for Disease Control and Prevention approved thimerosal as a preservative for vaccines given to newborns and infants.
Genetics play a role in how the body eliminates mercury, with the ApoE2 gene being protective due to its ability to bind effectively to mercury, while the ApoE4 gene does not. Therapeutic interventions like emeramide can help address mercury toxicity by binding tightly to mercury and free iron.
Popular chelating agents like DMSA and DMPS have drawbacks in detoxifying mercury as they can cause renal failure and do not effectively remove mercury from cells. Dr. Haley developed emeramide as a better chelating agent after failed attempts to raise awareness about the dangers of thimerosal.
Emeramide is nontoxic, binds tightly to mercury, and can pass the blood-brain barrier to enter cells, making it an effective treatment for mercury toxicity. It is a highly potent antioxidant, equipped with two glutathione “arms” that play a crucial role in detoxifying mercury and other harmful toxins in the body. Haley suggests that the antioxidant capabilities stem from the glutathione elements, which actively combat hydroxyl free radicals. Research has revealed that each emeramide molecule can neutralize three hydroxyl free radicals, effectively preventing toxicity. However, it does not possess the ability to repair any existing damage, necessitating alternative treatment methods.
The initial product created by Haley, known as Oxidative Stress Relief (OSR) and sold from 2008 to 2010, faced FDA shutdown in 2010 following a complaint. The FDA altered regulations to target Haley, leading to the closure of his business without formal legal repercussions. This drove Haley to develop emeramide, a chemical chelator required to undergo drug approval due to its non-natural composition.
Emeramide, labeled as Irminix, serves as the active pharmaceutical ingredient (API) and has gained orphan drug status for mercury chelation in the U.S. and the European Union. Phase I trials conducted in Sweden exhibited no adverse effects at high doses, indicating its safety and efficacy in humans. Subsequent Phase II studies on Ecuadorian gold miners demonstrated a substantial reduction in mercury levels, showcasing the drug’s potential in treating mercury toxicity and associated symptoms.
Emeramide’s ability to eliminate mercury without the need for binders makes it a promising solution for various conditions linked to mercury exposure, including neurodegenerative diseases and COPD caused by smoking. Haley himself has been using emeramide preventatively since 2006 and attributes his cognitive health at 83 years old to its benefits, boasting a blood glutathione level akin to that of a teenager. Se ha realizado un estudio de Fase II en pacientes con EPOC para asegurarse de que no es tóxico para este grupo de pacientes.
Más Información
Emeramide todavía está en desarrollo de medicamentos pero se puede obtener a través de acceso ampliado, uso de pacientes nombrados, uso compasivo o uso especial, dependiendo del país en el que te encuentres. Una solicitud de acceso temprano y una receta, requerida por la EMA, están disponibles en el sitio web de la compañía, EmeraMed.com, junto con más detalles por país.
Si tienes preguntas sobre la compañía en sí, que tiene su sede en Irlanda, puedes solicitar un paquete de información por correo electrónico a [email protected]. Aunque el producto se regala de forma gratuita a aquellos que califican para el acceso temprano, un paquete de tratamiento de dos semanas cuesta alrededor de $600 por gastos de la junta médica irlandesa, seguro y envío.
OSR solía venderse por $30 por un mes de tratamiento y se vendía como un antioxidante dietético. “Cuando lo conviertes en un medicamento, es mucho más caro”, dice Haley. Aún no está claro cuánto costará Irminix (también conocido ahora como emeramide y OSR#1).
“Quiero decir que definitivamente no va a ser nada como ($600)”, dice Haley. “El verdadero obstáculo aquí es que si vas a obtener la aprobación de un medicamento, debes demostrar que no es tóxico. Debes hacer el estudio de Fase I. Y luego debes hacer el estudio de Fase II y el estudio de Fase III. Esas son pruebas de eficacia para demostrar que tu medicamento funciona.
¿Cómo muestras que tu medicamento está uniendo mercurio en un grupo de estadounidenses en los que ninguno de ellos —según la FDA o la ciencia o los NIH— es tóxico por mercurio? Porque debes estar [en un cierto nivel] en tu nivel de orina para ser [considerado] tóxico por mercurio.
Eso es científicamente incorrecto porque las personas que no excretan mercurio tienen niveles muy bajos en orina y sangre. Lo acumulan en sus células, y eso es lo que disminuye [al usar Irminix]…
Hemos encontrado un grupo [de prueba] en Colombia, Sudamérica —Un niño encontró un frasco de mercurio líquido. Lo llevó a su escuela, lo compartió con sus amigos. El proceso de todo eso hizo que alrededor de 125 personas estuvieran muy intoxicadas por mercurio, y no son mineros de oro, por lo que no están siendo [continuamente] expuestos. Iniciamos un estudio en Colombia en esas personas, porque … tienen niveles muy altos. Eso podrá demostrar [que emeramide funciona].”
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