MERCURY TOXICITY-NEUROLOGICAL ILLNESS

April 20, 2006

Interview with Dr. Boyd E. Haley: Biomarkers supporting mercury toxicity as the

major exacerbator of neurological illness, recent evidence via the urinary

porphyrin tests

Boyd E. Haley, PhD

Professor, Department of Chemistry

University of Kentucky

Lexington, Kentucky

Boyd E. Haley, PhD and Teri Small

Medical Veritas 3(2006) 1-14

Abstract

In the recent past, several biological finds have supported the hypothesis that

early exposure of infants to Thimerosal was the major exacerbation factor in the

increase in autism-related disorders since the advent of the mandated vaccine

program. These initially included the observations of a genetic susceptibility

impairing the excretion of mercury and the increased retention of mercury by

autistic children. This was followed by data indicating that autistics have low

levels of the natural compound glutathione that is necessary for the bilary

excretion of mercury, possibly explaining the genetic susceptibility. Other

observations clearly point out that various biochemical processes are inhibited

at exceptionally low nanomolar levels of Thimerosal, including the killing of

neurons in culture, the inhibition of the enzyme that makes methyl-B12, the

inhibition of phagocytosis (the first step in the innate and acquired immune

system), the inhibition of nerve growth factor

function at levels not cytotoxic, and the negative effect on brain dendritic

cells. It is also now quite clear from primate studies that Thimerosal, or more

correctly, the ethylmercury from Thimerosal delivers mercury to the brain, and

causes brain inorganic mercury levels higher than equal levels of methylmercury.

Most recently, one study showed that 53% of autistic children had aberrant

prophyrin profiles similar to mercury toxic individuals. Treatment of these

children with a mercury chelator brought these porphyrins back towards normal

levels indicating mercury toxicity was the cause, not genetic impairment.

Porphyrin profiles are one of the most sensitive methods of measuring toxic

mercury exposures. Recently, in a major advance it was shown that about 15% of

individuals in one population displayed a marked sensitivity to mercury exposure

in their porphyrin physiology, again supporting the concept of a genetically

susceptible population that is more sensitive to mercury than the general

population. This observation on porphyrin aberrancies brings into

consideration other possible effects of mercury toxicity that are secondary to

porphyrin depletion. Porphyrins are the precursors to heme synthesis. Heme is

the oxygen binding prosthetic group in hemoglobin and depletion of heme

would affect oxygen delivery to the mitochondria and decrease energy

production. Also, heme is a component of the electron transport system of

mitochondria and a prosthetic group in the P450 enzymes which are fundamental in

the detox of the body from many organic toxicants including pesticides and PCBs.

Just recently, a report was released implying that lack of heme was the major

reason why ß-amyloid plaques build up in the brains of Alzheimer’s diseased

subjects. It seems that heme attaches to ß-amyloid helping it remain soluble and

excretable. Without adequate heme one of the major pathological diagnostic

hallmarks of Alzheimer’s disease appears. It is well known that mercury rapidly

disrupts the normal polymerization of tubulin into microtubulin in brain tissue

and aberrant tubulin polymerization is a consistent factor observed in

Alzheimer’s diseased brain. Therefore, it is the multiple inhibitions of mercury

that can cause various neurological and systemic problems

and many of these are secondary to the primary site of mercury binding. To

view the entire transcript of the interview, click here. Article-in-press;

Medical Veritas: The Journal of Medical Truth; Volume 3, Issue 1; April 2006.

Medical Veritas is the journal of Medical Veritas International

http://www.usautism.org/speakers.htm#boyh

Boyd Haley, PhD

Boyd Haley, PhD, former Chairman of the Department of Chemistry at the

University of Kentucky from 1996-2005, has now chosen to devote additional time

to research, in addition to his being an active professor. An NIH Postdoctoral

Scholar in the Department of Physiology, Yale University Medical School from

1971 to 1974, in the past 17 years, Dr. Haley has emphasized studies on the

biochemistry of Alzheimer’s disease. His research in the biochemical aberrancies

in Alzheimer’s disease also led to his identifying mercury toxicity as a major

factor in this disease. He was one of the first to propose that the

organic-mercury preservative (Thimerosal) in infant vaccines was the most likely

toxic agent involved in Gulf War Syndrome and autism related disorders. Dr.

Haley has testified before numerous government agencies on the effects of

mercury toxicity from dental amalgams and vaccines. His articles include Reduced

Levels of Mercury in First Baby Haircuts of Autistic Children,

which was published in the International Journal of Toxicology.

Teri Small

http://www.autismone.org/radio/

________________________________________

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May 8, 2006

Grammy, I'm just getting cuaght up... thanks for sending this article.

Agape,

Grammy Bauer wrote:

Interview with Dr. Boyd E. Haley: Biomarkers supporting mercury toxicity as

the major exacerbator of neurological illness, recent evidence via the urinary