Roger Masters, Ph.D.
Presentation + Questions & Answers
For ADD-Holistic Discussion Group
http://www.HolisticMed.Com/add/
To: add-holistic@mLists.net
From: mgold@tiac.net
Subject: ADD Introduction of Visiting Expert!
Date: Sun, 14 Nov 1999 14:37:39 -0700 (MST)
Hi!
I am very pleased to introduce our Visiting Expert, Roger D. Masters,
Ph.D. Dr. Masters is Nelson D. Rockefeller Professor Emeritus in the
Dartmouth College Department of Government. He heads the Dartmouth
Foundation for Neuroscience and Society. For several decades he has
researched the causes of violence and other dysfunctional human behavior
such as ADD, ADHD, drug abuse and the like. His viewpoint, which has been
published widely, is that toxins in the environment have subtle effects on
brain and neural functions which are ultimately manifested in behaviors
which many social scientists and politicians prefer to attribute to social
dynamics.
Dr. Masters presented a groundbreaking study related to lead and
silicofluorides at the recent 17th International Neurotoxicology
Conference ( "Children's Health and the Environment," Little Rock,
Arkansas, October 17-20, 1999). I feel fortunate that Dr. Masters has
agreed to take some time to help us better understand the behavioral
effects of lead and other toxins. Please join me in welcoming Dr. Masters
to our online discussion group! [Clap, clap, clap, clap!]
Dr. Masters' opening email will be sent out tomorrow (Monday).
Below are a few relevent excerpts from his Curriculum Vitae:
Education:
Harvard College, 1951-55 (., Summa cum Laude, 1955)
University of Chicago, 1957-58 (M.A., 1958)
Institut d'Etudes Politiques, Paris, 1958-59 (Auditor)
University of Chicago, 1959-61 (Ph. D., 1961)
Behavioral Research (1995-1998)
Cultural Attache, U.S. Embassy, Paris, France (1969-71)
Visiting Lecturer, Yale Law School (1988)
Adjunct Professor, Vermont Law School (Fall, 1993, 1994)
Awards:
Fulbright Fellowship to France (1958-59)
Joint Yale-S.S.R.C. Fellowship (1964-65)
John Simon Guggenheim Fellowship (1967-68)
John Sloan Dickey Third Century Professor of Government,
Dartmouth College (1979-1985)
Director d'Etudes, Ecole des Hautes Etudes en
Sciences Sociales, Paris, France (1986)
Work in progress: Analysis of neurotoxicity associated with
pollution, poor diet, and lifestyle as risk factors in vi`
crime, health, and social behavior.
Publications:
Editor and co-translator, Rousseau's First and Second Discourses (New
York: St. Martin's, 1964)
The Nation is Burdened: American Foreign Policy in a Changing World
(New York: Knopf, 1967)
The Political Philosophy of Rousseau (Princeton: Princeton
University Press, 1968)
Editor, Rousseau's Social Contract, with Geneva Manuscript and
Political Economy (New York: St. Martin's Press, 1978)
Co-Editor with Margaret Gruter, Ostracism: a Biological and Social
Phenomenon (New York: Elsevier Science Publishers, 1986)
The Nature of Politics (New Haven: Yale University Press, 1989)
Co-Editor with Christopher Kelly, Rousseau, Judge of Jean-Jacques;
Collected Writings of Rousseau, Vol. 1 (Hanover, NH: University
Press of New England, 1990).
Co-Editor with Glendon Schubert, Primate Politics (Carbondale, IL:
Southern Illinois University Press, 1991); paperback, with new
Preface (University Press of America, 1994).
Co-Editor with Margaret Gruter, The Sense of Justice: Biological
Foundations of Law (Newbury Park, CA: Sage, 1992)
Co-Editor with Christopher Kelly, Rousseau's First Discourse and
Polemics; Collected Writings of Rousseau, Vol. 2 (Hanover, NH:
University Press of New England, 1992).
Co-Editor with Christopher Kelly, Rousseau's Second Discourse.
Polemics, and Political Economy; Collected Writings of Rousseau,
Vol. 3 (Hanover, NH: University Press of New England, 1993)
Beyond Relativism: Science and Human Values (Hanover, NH:
University Press of New England, 1993)
Co-Editor, with Michael T. McGuire, The Neurotransmitter
Revolution (Carbondale, IL: Southern Illinois University Press,
1994)
General Editor, Gruter Institute Reader: Biology, Law, and Human
Behavior (Computerized Database for Customized Books of Readings;
New York: McGraw Hill [Primis])
Co-Editor with Christopher Kelly, Rousseau's Socal Contract, Essay
on the Virtue of Heroes, Geneva Manuscript; Collected Writings of
Rousseau, Vol. 4 (Hanover, NH: University Press of New England,
1994)
Co-Editor with Christopher Kelly, Rousseau's Confessions, Collected
Writings of Rousseau, Vol. 5 (Hanover, NH: University Press of New
England, 1996)
Machiavelli, Leonardo, and the Science of Power (University of
Notre Dame Press. 1996)
Fortune is a River: Leonardo da Vinci and Niccole Machiavelli's
Magnificent Dream to Change the Course of Florentine History (New
York: Free Press, 1998). Paperback edition, New York: Plume,
1999).
Over 150 scholarly articles and journalistic essays in English,
French, and German, including contributions to Quarterly Review of
Biology, Ethology and Sociobiology, American Political Science
Review, World Politics, Politics and Life Sciences, Environmental
Toxicology, International Journal of Environmental Studies, etc.
Neuroscience, Toxic Chemicals and ADD/ADHD
Roger D. Masters
Dartmouth College
Most current discussions of ADD/ADHD have paid insufficient attention to
recent work in cognitive neuroscience. The education establishment, the
medical community, and the public at large often seem to believe that each
of these conditions is a single category for which drug therapy (e.g.,
with ritalin) is the normal response. I believe this is superficial
and, indeed, dangerous for two reasons. First, among the many sources of
the behaviors associated with ADD and ADHD are the exposure to and uptake
of lead and other heavy metals that are toxic to brain cells. Realization
of this evidence has clear implications for treatment. Second, the
biological or psychological effects of a prolonged course of drug therapy
with ritalin or other comparable treatments are, to my knowledge, unknown.
Although numerous specialists have privately agreed with this concern, it
is rarely emphasized in the press that the nearly ubiquitous reliance on
drug treatment without long-term testing may be risky for some if not most
children.
These points are related, since there is an alternative approach to the
portion of the ADD/ADHD population whose symptoms are the result of heavy
metal neurotoxicity.
First, the issue of etiology. There is little question that the frequency
of ADD/ADHD has greatly increased in recent years (though some still
pretend it is simply more visible than in the past). I saw one report
from Milwaukee that suggested as much as a doubling in ADD/ADHD cases over
the last decade. Such large increases usually do not come from increased
visibility of a genetic condition that influences a fixed percentage of
children.
One factor that can explain this is heavy metal absorption in the brain
(Minder, et al., 1994; Needleman, 1999). Although not all studies confirm
the association (e.g., Kahn, Kelly, and Walker, 1995), Tuthill (1996) also
found that a large proportion of ADHD children in one Massachusetts
community had absorbed high levels of lead. Others have suggested similar
effects of manganese toxicity. In animal studies, moreover, impulsive
responses are significantly increased by lead exposure (Brockel and
Cory-Slechta, 1997).
Mechanisms that can explain this associated are also known. Lead is
known to downregulate several neurotransmitters, including dopamine and
glutamate; manganese downregulates serotonin (Bryce-Smith, 1983;
Needleman, 1991, 1996). In addition, these heavy metals have effects
related to the crucial role of calcium, which functions as a
neurotransmitter and co-factor in many brain systems.
Uptake of heavy metals from the environment is increased by dietary
deficits in calcium, which is a divalent cation -- that is, an element
with a positive ionic chage of 2. Heavy metals like lead, cadmium, and
manganese are also divalent cations, so they can occupy sites on or in
neurons normally occupied by calcium. Hence heavy metal neurotoxicity
both downregulates essential neurotransmitters, including those required
for impulse control, and reduces the normal effect of calcium (Aschner &
Kimelberg, 1996; Masters, Hone and Doshi, 1998).
It takes only a brief look at a textbook in cognitive neuroscience to see
how important these effects can be. For example, the inhibitory function
of the basal ganglia relies in part on dopamine, which is downregulated by
lead (e.g., Gazzaniga, et al., 1998: pp. 413-420). And calcium plays a
key role in the hippocampus, essential to the basic learning process known
as "Long Term Potentiation" or LTP (Gazzaniga, et al., 1998: pp. 283-288).
Not surprisingly, ADHD has been linked to deficits in dopamine function
(Cook, et al., 1995).
Hence there are plausible explanations for the observation that heavy
metals could account for a substantial portion of ADD/ADHD cases,
especially since early lead exposure is so widespread and damaging to
children (Aschengau, et al, 1993; Bellinger, et al., 1994; Mielke, 1998;
Levitt, 1999). In one early study by Chisholm, although said to be
flawed by many neuroscientists, chelation improved the symptoms of a small
number of ADHD children with high lead levels. More work is badly needed
in this area, since lead chelation might replace drug treatment for a
subset of ADD/ADHD cases.
Another major approach, focusing on prevention, is suggested by research
that I have been conducting with Myron Coplan. We have found that lead
levels in children are significantly increased by exposure to water
treated with either fluosilicic acid or sodium silicofluoride. These
"silicofluorides" (which are used for over 94% of the water fluoridation
in the U.S.) have never been fully tested, though early studies in the
1930's showed substantial differences in metabolism between sodium
silicofluoride and sodium fluoride (the chemical used in tests of
fluoridation safety by supporters and critics alike, even though it is
employed in only about 6% of American water fluoridation).
In general, silicofluorides enhance the uptake of lead from old houses or
public water supplies, particularly among the poor and minorities whose
diets are insufficient in calcium and other essential minerals.
Reanalyzing a Massachusetts survey of lead levels in 280,000 children
(Bailey et al., 1994), we found significantly higher lead levels in SiF
treated communities, controlling for other risk factors for lead toxicity
(Masters and Coplan, 1999). This finding has now been confirmed using the
national sample in NHANES III as well as in a sample of over 120,000
children from New York towns of 15,000 to 75,000 population (Masters,
Coplan, and Hone, 1999).
By reanalyzing a NIJ sample of urinalysis of over 30,000 criminals in 24
cities, we have also found higher rates of alcoholism, substance abuse and
crime to be associated with SiF usage (Masters and Coplan, in press).
Indeed, in the communities covered by our other studies, we also see more
crime and alcoholism associated with SiF usage. Since Manuzza (1989,
1998) and others have indicated that there is a correlation between
hyperactivity and criminal behavior, these associations are probably
linked elements of a pattern of weakened impulse control.
We are actively seeking information on ADD/ADHD rates, and would
appreciate any reliable geographic data that would allow us to compare
numbers of children receiving drug treatment and/or special education
services in communities using different approaches to water treatment.
(For a sample of 16 towns in New York, we found that the percent of
enrolled high school students reported by the school nurse to take
medication for ADD/ADHD is 38% higher where SiF is in use, as compared to
non-fluoridating communities of similar size).
We would welcome collaboration with any researchers who have relevant
data. It may well be, for example, that OTHER environmental factors are
associated with higher rates of ADD/ADHD. Given the importance of the
issue, it is rather astonishing that so little geographic data has been
collected. And since neurotoxicity is probably one of the etiological
pathways (along with early developmental insults of other sorts and
probably genetics), such ecological data would be especially valuable.
NOTE: For copies of our publications, please send an e-mail request with
your address to: Suzanne.Saxton@Dartmouth.edu
BIBLIOGRAPHY
Aschengau, A., Ziegler, S., and Cohen. 1993. "A. Quality of Community
Drinking Water and the Occurrence of Late Adverse Pregnancy Outcomes,"
Archives of Environmental Health 48: 105-113.
Aschner, M. and Kimelberg, M. 1996. The Role of Glia in Neurotoxicity.
Boca Raton,FL, CRC Press.
Bailey, A.J., Sargent, J.D., Goodman, D.C., Freeman, J., and Brown, M.J.
1994. Poisoned Landscapes: The Epidemiology of Environmental Lead
Exposure in Massachusetts Children 1990-1991. Social Science Medicine 39:
757-776.
Bellinger D et al, "Pre-and Postnatal Lead Exposure and Behavior Problems
in School-Aged Children", Environmental Research, v 66 (1), p 12-30, (July
1994)
Brockel, Becky A., Cory-Slechta, Deborah A. "Lead, Attention, and
Impulsive Behavior: Changes in a Fixed-Ratio Waiting-for-Reward
Paradigm", Pharmacology Biochemistry and Behavior , June 1998,Vol.60, No.
2: 545-552.
Bryce-Smith, D. 1986. " Environmental Chemical Influences on Behaviour
and Mentation," Chemical Sciety Review, 15, 93-123.
Cook, E. H Jr.,et al. 1995. "Association of Attention Deficit disorder
and the dopamine Transporter gene. "American Journal of Human Genetics,56,
Gazzaniga, Michael, Ivry, Richard B. and Mangun, George R. 1998.
Cognitive Neuroscience. New York: W. W. Norton.
Kahn, CA., Kelly, PC., Walker, WO. 1995. "Lead screening in children with
attention deficit hyperactivity disorder and developmental delay",
Clinical Pediatrics,, Sept 1995, Vol 34, No. 9: 498-501.
Minder, Barbara, Das-Smaal, Edith A., Brand, Eddy F. J. M., Orlebeke,
Jacob F. 1994. "Exposure to Lead and Specific Attentional Problems in
Schoolchildren",
Journal of Learning Disabilities , June/July 1994, Vol. 27, no. 6:
393-398.
Levitt, Miriam. 1999. "Toxic Metals, Preconception, and Early Childhood
Development," Social Science Information, 38: 179-201.
Manuzza, S., et al. 1989. "Hyperactive Boys Almost Grown Up," Archives of
General Psychiatry, 46: 1073-1079.
Manuzza, S., et al., 1998. "Adult Psychiatric Status of Hyperactive Boys
Grown Up," American Journal Of Psychiatry 155: 493-498.
Masters, Roger D. and Coplan, Myron. J. 1999a. "Water Treatment with
Silicofluorides and Lead Toxicity," International Journal of Environmental
Studies, 56: 435-449.
Masters, Roger D. and Coplan, Myron J. 1999b. "A Dynamic, Multifactorial
Model of Alcohol, Drug Abuse, and Crime: Linking Neuroscience and Behavior
to Toxicology," Social Science Information. In press.
Masters, Roger D., Coplan, Myron J. and Hone, Brian T. 1999a.
"Silicofluoride Usage, Tooth Decay, and Children s Blood Lead," Poster
Presentation, Environmantal Influences on Children: Brain, Development,
and Behavior, Conference at New York Academy of Medicine, New York, NY,
May 24-25, 1999.
Masters, Roger D., Coplan, Myron J. and Hone, Brian T. 1999b. "Heavy
Metal Toxicity, Development, and Behavior," Poster Presentation, 17th
International Neurotoxicology Conference, Doubletree Hotel, Little Rock,
ARK., October 17-20, 1999.
Masters, Roger D., Hone, Brian T., and Doshi, Anil. 1998. "Environmental
Pollution, Neurotoxicity, and Criminal Violence," in J. Rose., ed.,
Environmental Toxicology (London: Gordon and Breach), pp. 13-48.
Mendelsohn, Alan L.; Dreyer, Benard P.; Fierman, Arthur H.; Rosen, Carolyn
M.; Legano, Lori A.; Kruger, Hillary A.; Limß, Sylvia W. and Courtlandt,
Cheryl D. 1998. "Low-Level Lead Exposure and Behavior in Early Childhood"
Pediatrics, Vol. 101 No. 3 March 1998, p. e10.
Mielke, H. 1998. "Lead in the Inner Cities," American Scientist,
87:62-73.
Needleman, Herbert L., ed. 1991. Human Lead Exposure. Boca Raton, FL:
CRC Press.
Needleman, Herbert L., et al., 1996. "Bone Lead Levels and Delinquent
Behavior, JAMA 275: 363-69.
Needleman, Herbert L. 1999. "Environmental Neurotoxins and Attention
Deficit Disorder," Presentation at Conference on Environmental Neurotoxins
and Developmental Disability, N. Y. Academy of Medicine, New York (May
24-25, 1999).
Tuthill, R. W. 1996. "Head Lead Levels Related to Children s Classrooom
Attention-Deficit Behavior," Archives of Environmental Health, 51: 214-20.
To: add-holistic@mLists.net
From: "Dr. Gary Erkfritz"
Subject: Re: ADD Introduction of Visiting Expert!
Date: Sun, 14 Nov 1999 14:16:52 -0800
Dr. Masters, the first thing I'd like to know if how and why you
made from government to toxicology? That must be an interesting
story.
Gary
To: add-holistic@mLists.net
From: Roger.D.Masters@Dartmouth.EDU
Subject: Re: ADD Introduction of Visiting Expert!
Date: Mon, 15 Nov 1999 22:29:32 -0700 (MST)
>To: add-holistic@mLists.net
>From: "Dr. Gary Erkfritz"
>Subject: Re: ADD Introduction of Visiting Expert!
>Dr. Masters, the first thing I'd like to know if how and why you made
>from government to toxicology? That must be an interesting story.
I was trained as a political philosopher (studying with Leo Strauss at
Chicago), and working primarily on Rousseau. In 1968 I decided to look at
modern biology and evolutionary theory (because Rousseau claimed that
humans descended from -- or were originally -- primates like gorillas or
chimpanzees). One thing led to another and I spent years on the biology
of behavior (focusing on experimental studies of the nonverbal displays of
presidential candidates and their effects on voters). IN 1989, published
THE NATURE OF POLITICS (with both this empirical work and theoretical
discussion). See also BEYOND RELATIVISM and MACHIAVELLI, LEONARDO & THE
SCIENCE OF POWER). I then did a good deal of work with lawyers on biology
and law, which led to a request from the Commissioner of Corrections of
Vermont (where I live) that I study brain chemistry and crime. Since I'd
done a book with Michael McGuire on serotonin and social behavior
(including low 5HT and aggressive behavior), I agreed. That led to a
meeting where I met an independent researcher who was studying manganese
toxicity and crime. I originally thought the idea nonsense, set out to
disprove it with EPA Toxic Release data, and confirmed it! I also began
to study lead, and that resulting in the question from Myron Coplan if I
had ever studied fluoride as a toxin. One thing led to another, including
several grants, and now I'm over my head!
roger masters
To:
From: "Dale Goudey"
Subject: Re: ADD Introduction of Visiting Expert!
Date: Tue, 16 Nov 1999 10:23:00 -0800
Dr. Rodger Masters,
>One thing led to another, including several grants, and now I'm over my
>head!
If you ever start to see daylight, please consider looking into the toxic
plight of kids with autism. There are SPEC scans of children with autism
which imply that autism is the same thing as ADD/ADHD, only worse. See
this site. www.nids.net Many of the kids have a damaged sulfur
detoxification pathway. One toxin that can cause this is mercury, which
crosses the placenta. Some of the children are being chelated to remove
this toxin.
Polly
To: add-holistic@mLists.net
From: Roger.D.Masters@Dartmouth.EDU (Roger D. Masters)
Subject: Re: ADD Introduction of Visiting Expert!
Date: 16 Nov 1999 14:47:24 EST
I would be very happy to work WITH you (or anyone else) on the
environmental factors associated with Autism. I've been trying for some
time to locate geographic data on rates of incidence. If you know of any
sources, they would be invaluable.
I've been conscious of possible neurochemical links to autism ever since a
dermatologist explained that rubbing the skin releases nitric oxide (which
functions as a muscle relaxant). I had the hunch at the time (based on
hearing an interview with Temple Grandin) that this mechanism might
explain the use of pressure on the skin which she (and others) have found
to be effective.
If there are neurochemical dysfunctions involved, then of course
neurotoxicity is a possible candidate for etiology. In many cases, of
course, more than one neurotoxin (alone or in synergistic interaction) is
often responsible for the symptoms. This makes the analysis VERY
difficult, but if one starts out expecting complexity, it is easier to
find.
If anyone knows a source of funding for this research, I am President of a
small foundation (as yet, we have no money, only dreams) that can serve as
the basis for grants. I'm also happy to recruit Dartmouth undergraduates
to help with the research (they can be extremely good). My principal
problem is the limitation of my own time. However, since I have a
colleague with an autistic child, I have a personal incentive to help.
roger masters
To: add-holistic@mLists.net
From: "John V DOMmisse, MD"
Subject: Re: ADD Introduction of Visiting Expert!
Date: Mon, 15 Nov 1999 23:10:46 -0700
Roger.D.Masters@Dartmouth.EDU wrote:
> .... > meeting where I met an independent researcher who was studying
> manganese toxicity and crime. I originally thought the idea nonsense,
> set out to disprove it with EPA Toxic Release data, and confirmed it! I
> also began to study lead, and that resulting in the question from Myron
> Coplan if I had ever studied fluoride as a toxin. One thing led to
> another, including several grants, and now I'm over my head!
Dr Masters,
Have you come across Steven
Schoenthaler's work on nutrient deficiencies and juvenile delinquency,
violent behavior, etc.? I believe he is still at the U of Ca at
Stanislaus, a PhD in psychology who has ventured into nutrient
biochemistry and behavior.
John Dommisse MD
Nutritional & Metabolic (Tele)Medicine
http://www.galaxymall.com/health/Nutrnl_Mtblc
Tucson,AZ,USA 85718-5892 Fax 520-577-1743 Ph.-1940
To: add-holistic@mLists.net
From: Roger.D.Masters@Dartmouth.EDU (Roger D. Masters)
Subject: Re: ADD Introduction of Visiting Expert!
Date: 16 Nov 1999 14:49:27 EST
Yes. Schoenthaler's work was among the first that I noted (see the
chapter with Hone and Doshi in J. Rose, ed., ENVIRONMENTAL TOXICOLOGY,
Gordon & Breach, 1998). More generally, this type of research - esp. with
the use of head hair analysis for a broad spectrum of toxins -- is
extremely useful as a means of monitoring toxic uptake.
roger masters
To: add-holistic@mLists.net
From: "John V DOMmisse, MD"
Subject: Re: ADD: Neuroscience, Toxic Chemicals and ADD/ADHD
Date: Mon, 15 Nov 1999 22:51:15 -0700
Prof. Masters,
I applaud your
reference-based exposition of this subject. I attempted the same approach
in a paper that is published only on my website (I haven't had the time to
submit it anywhere); if you have the time, I'd appreciate your taking a
quick look at it and letting me know what you think of it. I don't recall
but hope that at least one of my references is to your work!
John Dommisse
John V DOMmisse MBChB(CapeTown), FRCP(Canada)
Nutritional & Metabolic (Tele)Medicine
http://www.galaxymall.com/health/Nutrnl_Mtblc
http://Thyroid.about.com/library/weekly/aa092299.htm
1840 E River Rd, Ste 210
Tucson,AZ,USA 85718-5892 Fax 520-577-1743 Ph.-1940
To: add-holistic@mLists.net
From: Roger.D.Masters@Dartmouth.EDU (Roger D. Masters)
Subject: Re: ADD: Neuroscience, Toxic Chemicals and ADD/ADHD
Date: 16 Nov 1999 14:52:44 EST
I would be very happy to look at your paper.
roger masters
To: add-holistic@mLists.net
From: mgold@tiac.net
Subject: Questions for Visiting Expert
Dr. Masters,
I have several questions. Your thoughts would be helpful to me and I
believe would interest list members as well.
- If I remember correctly, some of the the earlier
studies related to lead and behavioral effects were criticized
because socioeconomic factors were not factored into the
calculations. In other words, some people said that ADD/ADHD
was more common in families with lower socioeconomic status.
Higher lead exposure was also more common in families with
lower socioeconomic status. Therefore the lead-ADD connection
might just be a coincidence.
It is my understanding that Tuthill, R.W. put this criticism
to rest by controlling for socioeconomic factors, thereby showing
a connection between lead exposure and ADD.
Is this your understanding of the issue? Are there any other
recent studies that controlled for socioeconomic status?
- I have heard that some common sources for lead exposure include
lead in soil dust, lead paint dust (including exterior paint),
pollution from factories, lead dust on hands during food
preparation, ????.
Are there any steps that families can take to reduce their likely
exposure to lead? We have many parents on our discussion group
and any practical steps or ideas to consider would be extremely
useful.
- Are there any steps that families can take to reduce their changes
of overexposure to manganese?
- There are some people who might consider EDTA chelation for
lead. I am aware a study led by Dr. Boyd Haley of the Univ.
of Kentucky showing potential adverse effects on the brain
from EDTA chelation with concurrent exposure
to mercury (Hg) from food, mercury amalgam fillings, endogenous Hg,
etc. I have heard from a third party that Dr. Haley suggests avoiding
EDTA chelation until mercury urine measurements are below a certain
level. (I haven't spoken with Dr. Haley myself.)
On the other hand, I believe that EDTA chelation is often
given with various nutrients (e.g., magnesium) that may
help to protect the brain during chelation.
Large-scale use of EDTA chelation in children would concern
me not only for possible clinically-obvious effects, but
potential subtle effects. On the other hand, maybe
the positive of chelation would outweigh any risk.
Anyway, I have included the abstract at the end of this email and
would be interested in your thoughts on the subject.
- I have read that a significant portion of lead in blood is
from recirculated lead that was in the bones (from previous
exposure). Do you know if EDTA chelation helps remove lead
from the bones?
- Are you aware of any nutrients that would tend to reduce the
toxic effects of lead or manganese? Or, are their specific
nutrient *deficiencies* that would tend to increase the toxicity
of lead or manganese.
Abstract Mentioned Above
Duhr EF, Pendergrass JC, Slevin JT & Haley BE
HgEDTA complex inhibits GTP interactions with the E-site of
brain beta-tubulin.
Toxicol Appl Pharmacol 122(2):273-280
(1993)
ABSTRACT: "We have found that EDTA and EGTA complexes of Hg2+, which
conventional wisdom has assumed are biologically inert, are
potentially injurious to the neuronal cytoskeleton. Tubulin, a major
protein component of the neuronal cytoskeleton, is the target of
multiple toxicants,including many heavy metal ions. Among the mercurials,
inorganic mercuric ion (Hg2+) is one of the most potent inhibitors
of microtubule polymerization both in vivo and in vitro.
In contrast to other heavy metals, the capacity of Hg2+ to
inhibit microtubule polymerization or disrupt formed microtubules
cannot be prevented by the addition of EDTA and
EGTA, both of which bind Hg2+ with very high affinity. To the contrary, the
addition of these two chelating agents potentiates Hg2+ inhibition
of tubulin polymerization. Results herein show that HgEDTA and HgEGTA
inhibit tubulin polymerization by disrupting the interaction of GTP with the
E-site of brain beta-tubulin, an obligatory step in the polymerization of
tubulin.
Both HgEDTA and HgEGTA, but not free Hg2+, prevented binding of
[32P]8N3GTP, a photoaffinity nucleotide analog of GTP, to the E-site and
displaced bound [32P]8N3GTP at low micromolar concentrations. This
complete inhibition of photoinsertion into the E-site occurred in a
concentration- and time-dependent fashion and was specific for Hg2+
complexes of EDTA and EGTA, among the chelating agents tested. Given the
ubiquity of Hg2+ in the environment and the widespread use of EDTA
in foodstuffs and medicine, these mercury complexes may pose a potentially
serious threat to human health and play a role in diseases of the
neuronal cytoskeleton."
**************
Mark D. Gold
mgold@tiac.net
To: add-holistic@mLists.net
From: Roger.D.Masters@Dartmouth.EDU (Roger D. Masters)
Subject: ADD Re: Questions for Visiting Expert
Date: 16 Nov 1999 15:01:57 EST
FOR SIMPLICITY, MY ANSWERS ARE IN CAPS AFTER EACH QUESTION.
> It is my understanding that Tuthill, R.W. put this criticism
> to rest by controlling for socioeconomic factors, thereby showing
> a connection between lead exposure and ADD.
> Is this your understanding of the issue? Are there any other
> recent studies that controlled for socioeconomic status?
OUR WORK HAS CONSISTENTLY CONTROLLED FOR SOCIOECONOMIC STATUS, AND FOR
OTHER ECOLOGICAL FACTORS (E.G., THE PRESENCE OF OLD HOUSING, INDUSTRIAL
POLLUTION, EDUCATION, ETC. AS WELL AS RACE, AGE, AND SEX). THIS IS
TREMENDOUSLY IMPORTANT BECAUSE WE FIND WHAT STATISTICIANS CALL
"INTERACTION" EFFECTS: X (FOR EXAMPLE, SILICOFLUORIDE TREATED WATER) IS
ASSOCIATED WITH HIGHER BLOOD LEAD IF AND ONLY IF THE CHILD IS IN A TOWN
WITH A HIGH PERCENTAGE OF OLDER HOUSING, AND/OR A HIGH FIRST DRAW LEAD
LEVEL. THESE INTERACTIONS REFLECT CHEMICAL MECHANISMS IN THE TOXIN (THIS
CASE SILICOFLUORIDES) THAT ENHANCE THE UPTAKE OF ANOTHER TOXIN (IN THIS
CASE A DIVALENT CATION LIKE LEAD, WHICH THEN CHANGES NEUROTRANSMITTER
FUNCTION).
> Are there any steps that families can take to reduce their likely
> exposure to lead? We have many parents on our discussion group
> and any practical steps or ideas to consider would be extremely
> useful.
I KNOW THAT THE ISSUE OF LEAD PAINT REMOVAL IS HOTLY CONTESTED, WITH MANY
EXPERTS FAVORING "CAPPING" THE PAINT. THE FIRST AND SIMPLEST DEVICE, AND
IT SHOULD BE FOLLOWED *URGENTLY* EVERYWHERE, IS TO PROVIDE CALCIUM
SUPPLEMENTS, ESP. ALONG WITH VITAMIN D. UPTAKE OF HEAVY METALS WITH AN
IONIC CHARGE OF 2 (THAT IS WHAT IS MEANT BY "DIVALENT CATION" ABOVE) ARE
OFTEN SUBSTITUTED FOR EACH OTHER ON THE SURFACE OF NEURONS OR INSIDE THEM;
IF CALCIUM LEVELS ARE ADEQUATE, LEAD UPTAKE (OR MANGANESE UPTAKE) IS LOWER
OR ABSENT. LITHIUM HAS AN EFFECT LIKE CALCIUM, BY THE WAY.
A SECOND ISSUE IS WATER. USE BOTTLED WATER FOR BABY FORMULA. FILTERS ON
FAUCETS. BE ESPECIALLY CAREFUL THE HIGHER UP IN A BUILDING AN APARTMENT
IS LOCATED: TOP FLOORS ARE ALWAYS WORSE.
LEAD IN SOIL IS A PROBLEM (THE WORK OF HOWARD MIELKE) BECAUSE LEAD TASTES
SWEET, AND KIDS LICK THEIR FINGERS.
>3. Are there any steps that families can take to reduce their changes
> of overexposure to manganese?
AS FAR AS I CAN SEE, THE PROCESS IS SIMILAR FOR LEAD AND MANGANESE.
>4. There are some people who might consider EDTA chelation for
> lead. I am aware a study led by Dr. Boyd Haley of the Univ.
> of Kentucky showing potential adverse effects on the brain
> from EDTA chelation with concurrent exposure
> to mercury (Hg) from food, mercury amalgam fillings, endogenous Hg,
I AM SIMPLY NOT WELL-ENOUGH INFORMED TO MAKE A SCIENTIFIC JUDGMENT
>5. I have read that a significant portion of lead in blood is
> from recirculated lead that was in the bones (from previous
> exposure). Do you know if EDTA chelation helps remove lead
> from the bones?
ASK HERBERT NEEDLEMAN AT U OF PITTSBURGH
>6. Are you aware of any nutrients that would tend to reduce the
> toxic effects of lead or manganese? Or, are their specific
> nutrient *deficiencies* that would tend to increase the toxicity
> of lead or manganese.
SEE ABOVE
To: add-holistic@mLists.net
From: mgold@tiac.net
Subject: ADD Dr. Master's Current Focus
Date: Fri, 19 Nov 1999 20:57:57 -0700 (MST)
Dr. Masters,
You alluded to current interestin your CV related to "neurotixicity
associated with pollution, poor diet, and lifestyle risk factors...."
Can you tell us a little bit about this effort? Will it involve new
surveys of diet, pollution, lifestyle, and behavior, or do you plan to do
a meta-anaylsis of existing scientific literature?
By the way, for everyone else on the group. The work Dr. Masters is doing
is very important (in my opinion) in furthering our understanding of the
contributing factors to behavioral changes. If any of the organizational
representatives or others on the group know of either 1) funding sources
for Dr. Masters' foundation or 2) reliable geographic incidence data for
ADD/ADHD or Autism, it would be helpful to forward that information to
Dr. Masters.
- Mark D. Gold
mgold@tiac.net
To: add-holistic@mLists.net
From: Roger.D.Masters@Dartmouth.EDU
Subject: Re: ADD Dr. Master's Current Focus
Date: 22 Nov 1999 09:41:35 EST
Thanks for your kind words. Our next papes will focus on the risk factors
that are linked to lead uptake in the samples of NHANES III and New York:
in both cases, we find that silicofluoride water treatment significantly
enhances the effect of all risk factors.
A future goal, as soon as we get these papers completed, is to locate and
analyze geographic (or time-series) data on such factors as drug usage to
treat ADD/ADHD. It has seemed to me that if we can locate such data, it
might provide a clear way of analyzing whether environmental toxins play a
role in disease incidence.
Let me know if I can be of further assistance,
roger masters