Re: Lancet Article

[Guest guest]

A Silent Pandemic: Industrial Chemicals Are Impairing the Brain Development

of Children Worldwide

For immediate release: Tuesday, November 07, 2006

Boston, MA ­ Fetal and early childhood exposures to industrial chemicals in

the environment can damage the developing brain and can lead to

neurodevelopmental disorders (NDDs)‹autism, attention deficit disorder

(ADHD), and mental retardation. Still, there has been insufficient research

done to identify the individual chemicals that can cause injury to the

developing brains of children.

In a new review study, published online in The Lancet on November 8, 2006,

and in an upcoming print issue of The Lancet, researchers from the Harvard

School of Public Health and the Mount Sinai School of Medicine

systematically examined publicly available data on chemical toxicity in

order to identify the industrial chemicals that are the most likely to

damage the developing brain.

The researchers found that 202 industrial chemicals have the capacity to

damage the human brain, and they conclude that chemical pollution may have

harmed the brains of millions of children worldwide. The authors conclude

further that the toxic effects of industrial chemicals on children have

generally been overlooked.

To protect children against industrial chemicals that can injure the

developing brain, the researchers urge a precautionary approach for chemical

testing and control. Such an approach is beginning to be applied in the

European Union. It puts in place strong regulations, which could later be

relaxed, if the hazard were less than anticipated, instead of current

regulations that require a high level of proof. At present in the U.S.,

requirements for toxicity testing of chemicals are minimal.

³The human brain is a precious and vulnerable organ. And because optimal

brain function depends on the integrity of the organ, even limited damage

may have serious consequences,² says Philippe Grandjean , adjunct professor

at Harvard School of Public Health and the study¹s lead author.

One out of every six children has a developmental disability, usually

involving the nervous system. Treating NDDs is difficult and costly to both

families and society. In recent decades, a gathering amount of evidence has

linked industrial chemicals to NDDs. Lead, for example, was the first

chemical identified as having toxic effects to early brain development,

though its neurotoxicity to adults had been known for centuries.

A developing brain is much more susceptible to the toxic effects of

chemicals than an adult brain. During development, the brain undergoes a

highly complex series of processes at different stages. An interference‹for

example, from toxic substances‹that disrupts those processes, can have

permanent consequences. That vulnerability lasts from fetal development

through infancy and childhood to adolescence. Research has shown that

environmental toxicants, such as lead or mercury, at low levels of exposure

can have subclinical effects‹not clinically visible, but still important

adverse effects, such as decreases in intelligence or changes in behavior.

Grandjean and co-author Philip J. Landrigan, Professor at Mount Sinai School

of Medicine, compiled a list of 202 environmental chemicals known to be

toxic to the human brain using the Hazardous Substances Data Bank of the

National Library of Medicine and other data sources. (The authors note that

the list should not be regarded as comprehensive; for example, the number of

chemicals that can cause neurotoxicity in laboratory animal tests exceeds

1,000.)

The authors then examined the published literature on the only five

substances on the list‹lead, methylmercury, arsenic, PCBs and toluene‹that

had sufficient documentation of toxicity to the developing human brain in

order to analyze how that toxicity had been first recognized and how it led

to control of exposure. They found a similar pattern in how the risks of

each substance were documented: first, a recognition of adult toxicity and

episodes of poisoning among children, followed by a growing body of

epidemiological evidence that exposure to lower levels of the substances

caused neurobehavioral deficits in children.

³Even if substantial documentation on their toxicity is available, most

chemicals are not regulated to protect the developing brain,² says

Grandjean. ³Only a few substances, such as lead and mercury, are controlled

with the purpose of protecting children. The 200 other chemicals that are

known to be toxic to the human brain are not regulated to prevent adverse

effects on the fetus or a small child.²

Grandjean and Landrigan conclude that industrial chemicals are responsible

for what they call a silent pandemic that has caused impaired brain

development in millions of children worldwide. It is silent because the

subclinical effects of individual toxic chemicals are not apparent in

available health statistics. To point out the subclinical risk to large

populations, the authors note that virtually all children born in

industrialized countries between 1960 and 1980 were exposed to lead from

petrol, which may have reduced IQ scores above 130 (considered superior

intelligence) by more than half and increased the number of scores less than

70. Today, it¹s estimated that the economic costs of lead poisoning in U.S.

children are $43 billion annually; for methylmercury toxicity, $8.7 billion

each year.

³Other harmful consequences from lead exposure include shortened attention

spans, slowed motor coordination and heightened aggressiveness, which can

lead to problems in school and diminished economic productivity as an adult.

And the consequences of childhood neurotoxicant exposure later in life may

include increased risk of Parkinson¹s disease and other neurogenerative

diseases,² says Landrigan.

The researchers believe that the total impact of the pandemic is much

greater than currently recognized. In supplementary documentation (see below

for a link), about half of the 202 chemicals known to be toxic to the brain

are among the chemicals most commonly used.

Testing chemicals for toxicity is a highly efficient public health measure.

However, less than half of the thousands of chemicals currently used in

commerce have been tested to assess acute toxicity and, although new

chemicals undergo more thorough testing, access to the data may be

restricted because companies fear exposing proprietary information. Also,

current toxicity testing rarely includes neurobehavioral functions.

³The brains of our children are our most precious economic resource, and we

haven¹t recognized how vulnerable they are,² says Grandjean. ³We must make

protection of the young brain a paramount goal of public health protection.

You have only one chance to develop a brain.²

To view supplementary documentation on industrial chemicals and risks of

toxic effects on brain development, click here:

http://www.hsph.harvard.edu/neurotoxicant/appendix.doc

Support for this research was provided by the Danish Medical Research

Council, the (U.S.) National Institute of Environmental Health Sciences and

the U.S. Environmental Protection Agency.

( " Developmental Neurotoxicity of Industrial Chemicals, " The Lancet, November

8, 2006- Vol. 368)

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For more information, contact:

Todd Datz

tdatz@...

617-432-3952

[Guest guest]

Thank you, darling Patty, so glad to see you back. The B12 has helped me so much, as far as my digestion goes. This is a great article.

Love you.........Lea

~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~```

Lancet article

http://www.medscape.com/medline/abstract/12826451

Is Candida albicans a trigger in the onset of coeliac disease?

Lancet. 2003; 361(9375):2152-4 (ISSN: 1474-547X)

Nieuwenhuizen WF; Pieters RH; Knippels LM; Jansen MC; Koppelman SJNetherlands Organisation for Applied Scientific Research (TNO) Nutrition and Food Research, PO Box 360, 3700 AJ, Zeist, Netherlands. nieuwenhuizenvoeding (DOT) tno.nl

Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans-hyphal wall protein 1 (HWP1)-contains aminoacid sequences that are identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium.

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[Guest guest]

Hi Lea, I am so glad to hear that you have seen positive results from the B12! My grandmother, who died at 93, had to take B12 shots during the later years of her life....I think B12 can be overlooked even in younger women, so I am glad you are taking it. I am using the spray that 's mom, recommended, and I really like using it--so easy! PattyLea <devans@...> wrote: Thank

you, darling Patty, so glad to see you back. The B12 has helped me so much, as far as my digestion goes. This is a great article. Love you.........Lea ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~``` Lancet article http://www.medscape.com/medline/abstract/12826451 Is Candida albicans a trigger in the onset of coeliac disease? Lancet. 2003; 361(9375):2152-4 (ISSN: 1474-547X) Nieuwenhuizen WF; Pieters RH; Knippels LM; Jansen MC; Koppelman SJNetherlands Organisation for Applied Scientific Research (TNO) Nutrition and Food Research, PO Box 360, 3700 AJ, Zeist, Netherlands. nieuwenhuizenvoeding (DOT) tno.nl Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. We postulate that Candida albicans is a trigger in the onset of coeliac disease. The virulence factor of C albicans-hyphal wall protein 1 (HWP1)-contains aminoacid sequences that are identical or highly homologous to known coeliac disease-related alpha-gliadin and gamma-gliadin T-cell epitopes. HWP1 is a transglutaminase substrate, and is used by C albicans to adhere to the intestinal epithelium. Furthermore, tissue transglutaminase and endomysium components could

become covalently linked to the yeast. Subsequently, C albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium. Ahhh...imagining that irresistible "new car" smell?Check out new cars at Autos.

Ahhh...imagining that irresistible "new car" smell? Check out

new cars at Autos.