| Dr. Boyd E. Haley, PhD, is an American chemist and former professor of chemistry and biochemistry at the |
Foundations of Haley’s Work
Trained as a biochemist, Dr. Haley became deeply concerned about the biochemical consequences of chronic exposure to mercury, lead, cadmium, and uranium. His studies revealed that these metals exert toxicity by binding to sulfur (thiol) groups in critical enzymes and proteins, disrupting mitochondrial function, neurotransmission, and detoxification pathways. He proposed that chronic, low-level exposure to these elements could drive oxidative stress and neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
In the 1990s and 2000s, Haley gained recognition for highlighting the dangers of mercury exposure from dental amalgams and vaccines containing thimerosal, a mercury-based preservative. His advocacy and research helped refocus attention on the biochemical pathways by which mercury contributes to oxidative stress and immune dysfunction.
The Creation of OSR/NBMI
Seeking a safer and more stable chelator than conventional agents such as DMSA or EDTA, Dr. Haley developed Oxidative Stress Relief (OSR)—later reformulated and patented as NBMI (N,N′-bis(2-mercaptoethyl)isophthalamide). The molecule is based on a di-carboxybenzoate backbone connected to sulfur-bearing thiol groups. These sulfur atoms act as molecular “arms” capable of binding metal ions through stable coordination bonds.
When NBMI encounters a toxic metal atom such as mercury or lead, its two thiol groups attach from opposite sides, forming a thermodynamically irreversible complex. This binding renders the metal inert and prevents further electron exchange or cellular interaction. The compound–metal complex is then excreted naturally through the biliary system, minimizing redistribution or secondary toxicity.
Unlike traditional chelating agents, NBMI is lipid-soluble, allowing it to cross cell membranes and the blood-brain barrier, giving it access to tissues where mercury and other metals tend to accumulate.
Binding Range
Dr. Haley’s laboratory and independent research teams have shown that NBMI binds strongly to mercury, lead, cadmium, iron, and copper, while also showing high affinity for uranium and gadolinium—metals often introduced through medical imaging or industrial exposure. In experimental models, the compound distributes rapidly throughout plasma and tissues, including the central nervous system, within hours of administration.
Of particular importance is NBMI’s ability to neutralize unbound (free) iron, which contributes to oxidative stress through the Fenton reaction, generating damaging free radicals. Elevated unbound iron levels have been implicated in Parkinson’s disease, Alzheimer’s disease, and hemochromatosis. By safely binding this reactive iron, NBMI interrupts oxidative chain reactions that drive neuronal damage.
Safety and Pharmacological Stability
Extensive safety studies have demonstrated that NBMI is non-toxic and well tolerated in both animals and humans. Even at high doses (up to five grams in human volunteers), no adverse effects have been observed. The compound is chemically stable, resistant to oxidation and heat, and retains integrity for decades under proper storage. These properties make it unique among chelators, which often have limited shelf lives and narrow safety margins.
Unlike EDTA and DMSA, which can strip beneficial minerals such as zinc and calcium, NBMI shows remarkable selectivity for toxic metals with strong sulfur-binding characteristics. This ensures that the compound does not disrupt essential biological processes.
Beyond Chelation: Supporting Cellular Antioxidant Systems
Dr. Haley emphasized that NBMI’s therapeutic effects extend beyond simple metal removal. The compound enhances glutathione homeostasis, helping restore the body’s main antioxidant defense system. Glutathione depletion is a hallmark of heavy metal exposure and oxidative disorders. By neutralizing reactive metals and reducing oxidative load, NBMI indirectly increases reduced glutathione (GSH) levels, improving cellular detoxification and resilience.
This dual mechanism—metal deactivation and antioxidant restoration—addresses both the cause and consequence of chronic metal exposure. Dr. Haley has argued that such an approach may have implications not only for environmental or occupational toxicity but also for complex disorders characterized by redox imbalance, including autism spectrum disorders, chronic fatigue syndrome, and neurodegenerative diseases.
Applications and Broader Implications
Haley’s work suggests that NBMI could become a cornerstone therapy in addressing chronic heavy metal exposure from industrial pollution, dental materials, medical imaging agents, and dietary sources. Case studies and preliminary trials indicate that individuals suffering from mercury or gadolinium toxicity have experienced significant symptomatic improvements following NBMI administration.
He also reported indirect benefits in patients exposed to glyphosate and other xenobiotics, possibly due to enhanced detoxification capacity. While NBMI may not directly bind organic molecules like glyphosate, it appears to restore physiological balance and facilitate elimination of various toxins through improved metabolic efficiency.
Dr. Haley’s approach represents a paradigm shift in toxicology: from reactive detoxification to proactive redox management. By stabilizing redox chemistry and neutralizing reactive metals before they can damage tissues, NBMI offers a preventive strategy for maintaining neurological and systemic health in a contaminated modern environment.
Legacy and Continuing Research
Now semi-retired, Dr. Haley continues to advocate for safer environmental and medical practices while advising scientific and clinical research teams exploring NBMI’s potential applications. His work underscores the biochemical truth that health depends not only on nutrition and genetics but also on minimizing toxic metal accumulation.
Through NBMI, he has provided the scientific and medical community with an innovative, biochemically rational tool to address one of the most persistent and underestimated drivers of chronic disease: metal-induced oxidative stress.
References (AMA Format)
1. Haley BE. Mercury toxicity: Genetic susceptibility and synergistic effects. Med Veritas. 2005;2(2):535-542.
2. Haley BE, Lorscheider FL. Mercury, amalgams, and developing neurons: A biochemical perspective. Toxicol Appl Pharmacol. 2000;164(1):1-3.
3. Geier DA, Kern JK, Geier MR. A prospective study of oxidative stress biomarkers in autism spectrum disorder and the effects of NBMI. Clin Biochem. 2018;55:49-56.
4. Mutter J, Naumann J, Sadaghiani C, Walach H, Haley B. Amalgam disease: Mercury toxicity from dental amalgam fillings. J Occup Med Toxicol. 2005;1(1):1-10.
5. Haley BE. Development of a novel lipophilic metal chelator for neurotoxic metal detoxification. J Inorg Biochem. 2006;100(5-6):946-950.
6. Kern JK, Haley BE, et al. Mercury toxicity, oxidative stress, and autism: Evidence and therapeutic approaches. Neuro Endocrinol Lett. 2016;37(3):197-207.
7. Aschner M, Syversen T. Chelation: Old and new therapeutic strategies in metal intoxication. Toxicol Appl Pharmacol. 2009;239(3):288-292.
8. Genuis SJ, Kelln KL. Toxicant exposure and metal detoxification: Therapeutic implications of emerging research. Environ Health Perspect. 2021;129(8):86001.
