"The doctor of the future will give no medicine, but will interest his patients in the care of the human frame, in diet and in the cause and prevention of disease."
- Thomas Edison
Bland, Jeffrey S., Genetic Nutritioneering, McGraw-Hill, 1999.
Williams, Roger, Biochemical Individuality, McGraw-Hill, 1998.
This page contains several articles related to the health of children.
Posted by Joel Sol:
NAS 354 page review 2000 says ~50% failed pregnancies
Has anyone heard of this? The Committee on Developmental Toxicology has eminent members. JS
Scientific Frontiers in Developmental Toxicology and Risk Assessment Committee on Developmental Toxicology, Board on Environmental Studies and Toxicology, National Research Council
354 pages, 6 x 9, 2000, hardback, $ 47.20
Thanks much to: "Ashley Hotz" <firstname.lastname@example.org>
Approx 1/2 of all pregnancies in U.S. result in miscarriage or unhealthy babies.. a stunning, hidden report
This stunning press release came out of the National Research Council of the National Academy of Science Institute of Medicine in June 2000 -- but the public did not hear about it and Congress and the states have not followed-up. I first heard about it from Betty Mekdeci, Executive Director of Birth Defect Research for Children, Inc. I searched several times over the past two years but was unable to find a web-based link to the NAS site until today. The full 354 page report is accessible from the NAS site but requires payment. Here is a riveting quote from the second paragraph of the press release:
"Approximately half of all pregnancies in the United States result in prenatal or postnatal death or an otherwise less than healthy baby." NAS says that manufactured chemicals should be assessed for developmental effects before marketing. See report at:
And here is the text:
Date: June 1, 2000
Contacts: Bill Kearney, Media Relations Associate
Megan O'Neill, Media Relations Assistant
(202) 334-2138; e-mail <email@example.com>
FOR IMMEDIATE RELEASE
Major Advances in Biology Should Be Used to Assess
Birth Defects From Toxic Chemicals
WASHINGTON -- New discoveries in developmental biology and genetics should be used when scientists analyze chemicals for their potential to cause birth defects, says a new report from the National Research Council of the National Academies. Given recent advances in understanding how the process of normal development occurs, methods can now be devised to determine how chemicals disrupt it in humans.
Approximately half of all pregnancies in the United States result in prenatal or postnatal death or an otherwise less than healthy baby. And major developmental defects, such as neural tube and heart deformities, occur in approximately 120,000 of the 4 million infants born here each year. Exposure to toxic chemicals, both manufactured and natural, cause about 3 percent of all developmental defects, and at least 25 percent might be the result of a combination of genetic and environmental factors.
"Many manufactured chemicals, as well as chemicals that occur in nature, have not been adequately evaluated for developmental toxicity," said Elaine Faustman, chair of the committee that wrote the report and professor of environmental health and director of the Institute for Risk Analysis and Risk Communication, University of Washington, Seattle.
"Our report provides a blueprint for using new findings about the dynamic processes involved in normal development to further our understanding of how human development may be affected by potentially toxic chemicals. Collaboration among scientists from many disciplines will be key in this endeavor, as will the integration of information from various databases."
New approaches to developmental toxicology are needed that emphasize simultaneous research on several fronts by experts from multiple scientific disciplines, the report says. It urges scientists to take advantage of new knowledge about the human genome when studying how genes and the environment interact to cause developmental defects. The report also calls for an intensified effort to expand the understanding of how even the smallest, simplest laboratory animals can serve as toxicological models for human biological systems, given recent advances in this area.
In most animals -- including those commonly used in laboratories, such as the fruit fly, roundworm, zebrafish, and mouse -- scientists recently have discovered how specific cells communicate with each other, ultimately activating proteins that turn particular genes on and off, thus regulating development. These "signaling pathways" are used repeatedly in various combinations at different times and locations in the embryo and fetus. Chemical disruption of these pathways could lead to abnormal development. Strikingly similar pathways are found in a wide range of animal species, including humans, and have changed very little over the course of time, which means that studying the effects of chemicals on signaling pathways in animal models could help facilitate understanding of abnormal development in humans, the report says.
Relatively simple assessments using animal models, such as the roundworm and fruit fly, could be used more effectively to provide clues about which developmental pathways are most affected by specific chemicals, the committee said. Based on findings from these tests or general concern about a chemical's prevalence in the environment, more extensive studies could be conducted on animals whose biological systems more closely resemble those of humans.
In addition, major new advances in genetics will help researchers gain insight into how chemicals affect human development, the report says. Mapping the human genome will increase understanding of gene function and expression, and help researchers identify unique alterations in genes, known as polymorphisms. Recent research has shown that individuals with certain polymorphisms, who are also exposed to certain chemicals in utero, have a higher occurrence of specific developmental defects than the general population. New information on genetic variability in humans, especially polymorphisms, is seen as key to understanding how the relationship between genes and the environment leads to developmental defects.
The committee emphasized that all stages of human development -- from conception to puberty -- should be examined in toxicity studies, since all developmental periods are potentially susceptible to toxic agents. In addition, there is a need to look at all adverse developmental outcomes, including growth retardation, behavioral effects, and death. The vast amounts of data that could be generated by testing thousands of chemicals for potential developmental toxicity will require new databases capable of organizing this information in a way that is useful for risk assessment, the committee said. The databases should include information from industry, academia, and government researchers, and be linked with existing databases of developmental biology and genomics, as well as those describing how drugs and chemicals are metabolized by the body. A separate relational database should be set up for chemicals that are found to interact with particular signaling pathways. This would help researchers study whether different chemicals that affect the same pathway are acting in a similar manner.
The lack of opportunities for collaboration among scientists from different fields has impeded the application of new information to improve developmental toxicology and risk assessment, the committee said. To overcome this, educational programs and professional workshops should be organized to facilitate interaction among researchers in developmental toxicology, developmental biology, genomics, medical genetics, epidemiology, and biostatistics.
The study was sponsored by the American Industrial Health Council, Centers for Disease Control and Prevention, U.S. Department of Defense, U.S. Environmental Protection Agency, U.S. Department of Veterans Affairs, National Center for Toxicological Research, National Institute of Environmental Health Sciences, National Institute of Child Health and Human Development, and National Institute for Occupational Safety and Health. The National Research Council is the principal operating arm of the National Academy of Sciences and the National Academy of Engineering. It is a private, nonprofit organization that provides advice on science and technology under a congressional charter. A committee roster follows.
Read the full text of Scientific Frontiers in Developmental Toxicology and Risk Assessment for free on the Web, as well as more than 1,800 other publications from the National Academies. Printed copies are available for purchase from the National Academy Press Web site or at the mailing address in the letterhead; tel. (202) 334-3313 or 1-800-624-6242. Reporters may obtain a pre-publication copy from the Office of News and Public Information at the letterhead address (contacts listed above).
NATIONAL RESEARCH COUNCIL
Commission on Life Sciences
Board on Environmental Studies and Toxicology
Toxicology and Risk Assessment Program
Committee on Developmental Toxicology
Elaine M. Faustman, Ph.D. (chair)
Professor, Department of Environmental Health, and
Director, Institute for Risk Analysis and Risk Communication
University of Washington, Seattle
John C. Gerhart, Ph.D. (vice chair)*
Professor, Department of Molecular and Cell Biology
University of California, Berkeley
Nigel A. Brown, Ph.D.
Professor of Developmental Biology
Department of Anatomy and Developmental Biology
St. George's Hospital Medical School, London
George P. Daston, Ph.D.
Miami Valley Laboratories
Procter & Gamble Co., Cincinnati
Mark C. Fishman, M.D.
Chief of Cardiology; Director, Cardiovascular Research Center, and
Chief, Developmental Biology Laboratory
Massachusetts General Hospital, and
Professor of Medicine
Harvard Medical School, Boston
Joseph F. Holson, Ph.D.
President and Director
WIL Research Laboratories Inc., Ashland, Ohio
Herman B.W.M. KoŽter, Ph.D.
Environmental Health and Safety Division
Organization for Economic Cooperation and Development, Paris
Anthony P. Mahowald, Ph.D. *
Louis Block Professor and Chair
Department of Molecular Genetics and Cell Biology
University of Chicago, Chicago
Jeanne M. Manson, Ph.D.
Fellow, Center for Clinical Epidemiology and Biostatistics
University of Pennsylvania, Philadelphia
Richard K. Miller, Ph.D.
Professor and Associate Chair of Obstetrics and Gynecology, and
Professor of Environmental Medicine
University of Rochester School of Medicine and Dentistry, Rochester, N.Y.
Philip E. Mirkes, Ph.D.
Research Professor, Department of Pediatrics
University of Washington, Seattle
Daniel W. Nebert, M.D.
Professor, Department of Environmental Health
University of Cincinnati Medical Center, and
Professor, Department of Pediatrics
Division of Human Genetics
Children's Hospital Medical Center, Cincinnati
Drew M. Noden, Ph.D.
Professor of Embryology
Department of Biomedical Sciences
College of Veterinary Medicine
Cornell University, Ithaca, N.Y.
Virginia E. Papaioannou, Ph.D.
Professor of Genetics and Development
College of Physicians and Surgeons
Columbia University, New York City
Gary C. Schoenwolf, Ph.D.
Professor of Neurobiology and Anatomy, and
Member, Huntsman Cancer Institute
School of Medicine
University of Utah, Salt Lake City
Frank Welsch, D.V.M.
Senior Scientist and Head, Teratology Laboratory
Chemical Industry Institute of Toxicology
Research Triangle Park, N.C.
William B. Wood, Ph.D. *
Professor, Department of Molecular, Cellular, and Developmental Biology
University of Colorado, Boulder, and
Member, Cancer Institute
University of Colorado Health Sciences Center, Denver
RESEARCH COUNCIL STAFF
Carol A. Maczka, Ph.D.,
Director, Toxicology and Risk
Abigail E. Stack, Ph.D.
* Member, National Academy of Sciences
"I believe the strain on our enzyme "bank account," caused by diets of cooked food, is one of the paramount causes of premature aging and early death. I also believe it is the underlying cause of almost all degenerative diseases." - Dr. Edward Howell, The Status of Food Enzymes in Digestion and Metabolism, 1946.
"Another expert in this area was Dr. Francis Pottenger. His famous experiments with cats in the 1930s are just as relevant today as ever. He took two groups of cats and for years personally supervised their feeding. One group was given exclusively raw, uncooked food. The other was given only cooked food. Results were overwhelmingly clear: the raw food cats all lived a long, disease-free life. Cooked food cats became sick and died much younger. (Bieler, p 192)
Also notable was that cats who became sick on a long term all cooked diet could not regain their health even when placed on a raw foods diet. Irreversible damage. Cooked food cats produced only two sickly generations, the second of which was invariably sterile. Natural selection." - Dr. Tim O'Shea
Moyers on PBS May 10 toxins & kids
"In New York City, a groundbreaking study led by Dr. Frederica Perera at Columbia University's Mailman School of Public Health, follows more than 500 expectant mothers. These women are wearing air quality monitors in backpacks to trap the environmental toxins they breathe. As their children are born and as they grow, Dr. Perera and her team will look for links between the chemicals that the mothers were exposed to while their babies were developing in the womb and asthma, cancer risk, and learning disabilities.... Dr. Perera's team at Columbia is also studying the way that chemicals can actually bind to human DNA in the womb and cause a mutation called an "adduct." Work by Dr. Perera has shown that the greater the number of adducts, the greater the risk for cancer. "And that's the missing link in all of this," says Dr. Steingraber. "That's the link we're beginning to fill in.""
This rang a bell in my mind--
Life Sci June 26 1998; 63(5): 337-49
Formaldehyde derived from dietary aspartame binds to tissue components in vivo. ["Trok-ho"] Trocho C, Pardo R, Rafecas I, Virgili J, Remesar X, Fernandez-Lopez JA, Alemany M, Departament de Bioquimica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Spain. Maria Alemany, PhD firstname.lastname@example.org "The administration of labeled aspartame to a group of cirrhotic rats resulted in comparable label retention by tissue components, which suggests that liver function (or its defect) has little effect on formaldehyde formation from aspartame and binding to biological components. The chronic treatment of a series of rats with 200 mg/kg of non-labeled aspartame during 10 days results in the accumulation of even more label when given the radioactive bolus, suggesting that the amount of formaldehyde adducts coming from aspartame in tissue proteins
and nucleic acids may be cumulative.
It is concluded that aspartame consumption may constitute a hazard because of its contribution to the formation of formaldehyde adducts."
Are we making our children sick?- May 10
Kids and chemicals, a special report
Bill Moyers tracks the scientific search for answers about how the
environmental toxins affect America's children
Premieres Friday, May 10 at 9:00 (ET) on PBS (check local listings)
It is a medical mystery marked "urgent."
Across America growing numbers of children are suffering from asthma, childhood cancers like leukemia, as well as learning and behavioral disabilities. Scientists are searching for clues to the causes of these illnesses, and a growing body of research suggests that everyday environmental toxins-- what kids eat, drink, and breathe-- may put them at risk. Equipped with new technology and more sophisticated analysis, these scientists are asking compelling questions about the health risks to children growing up exposed to an ever-increasing number of untested chemicals in our environment.
Kids and Chemicals, a special edition of NOW with Bill Moyers to be broadcast on PBS, Friday, May 10 at 9 p.m. (ET), features medical investigators and health officials engaged in the latest research on links between childhood illness and environmental contamination. The program looks at families around the country who are coping with the consequences to their children of potentially toxic exposures.
"The disturbing increases in childhood illness in America cannot be ignored," says Bill Moyers. "How does the exposure affect children's health? The new research is studying how chemicals enter the human body, and posing questions that they could never ask before: Do chemicals affect children, babies and unborn fetuses more than adults? What factors increase toxicity, and how can we protect children from harm?"
Kids and Chemicals' producers Gail Ablow and Greg Henry go to Fallon, Nevada, a small desert town that has had 15 recorded cases of childhood leukemia in just five years. Alarmed, Dr. Mary Guinan, who was one of Nevada's top health officials, called in the Centers for Disease Control and Prevention to investigate the potential links between this childhood cancer and the environment. Could toxic substances in water, food, air, schools, homes or the ground in Fallon be responsible for this "cancer cluster"? If so, which chemicals? Without clear evidence of a specific cause, everything-- from jet fuel emissions to pesticides to naturally occurring arsenic in the water-- is suspect.
As Moyers and his team learn in Fallon, research on cancer clusters once focused mainly on gathering environmental samples because investigators simply didn't have tools sensitive enough to measure which toxins had been absorbed into people.
Dr. Richard Jackson, the director of the National Center for Environmental Health at the Centers for Disease Control and Prevention, explains how his laboratories are using the latest instruments. His research scientists are using sophisticated blood and urine analysis to test for minute traces of toxins in the bodies of the sick children and their families in Fallon.
This work is part of a larger movement in children's environmental health unfolding nationwide. Dr. Phillip Landrigan of the Mount Sinai School of Medicine in New York City works with scientists around the country to understand how kids are affected by exposure to chemicals. "Of the 3000 high production volume chemicals in use in this country today, only 43% have been even minimally tested," he tells Moyers. "Only about 10% have been thoroughly tested to examine their potential effects on children's health and development."
Speaking with Landrigan, Moyers learns that children are potentially more vulnerable to chemicals than adults. "First of all they're more heavily exposed pound for pound," says Landrigan. "They eat more food, they drink more water, they breathe more air. Then, of course, kids play on the ground. They live low, they put their hands in their mouth and so they transfer more toxic chemicals into their body than we do."
Traveling to Research Triangle Park, North Carolina, Moyers meets Dr. Linda Sheldon of the Environmental Protection Agency's National Exposure Research Lab. Sheldon demonstrates how her team of scientists is gathering evidence of exposure to everyday chemicals in nursery schools, homes and daycare centers.
In New York City, a groundbreaking study led by Dr. Frederica Perera at Columbia University's Mailman School of Public Health, follows more than 500 expectant mothers. These women are wearing air quality monitors in backpacks to trap the environmental toxins they breathe. As their children are born and as they grow, Dr. Perera and her team will look for links between the chemicals that the mothers were exposed to while their babies were developing in the womb and asthma, cancer risk, and learning disabilities.
Dr. Sandra Steingraber, a biologist at Cornell University, joins Dr. Landrigan in asserting that exposure during pregnancy doesn't, by itself, mean a child will get ill. What matters is the intensity of the exposure and when it occurs during fetal development. A chemical exposure occurring early in pregnancy might cause a miscarriage, argue the researchers. If it occurs later on, it might cause physical birth defects. Later still, it might damage brain cells. Scientists are trying to precisely identify these "windows of vulnerability." Says Dr. Steingraber: "Maybe certain problems that we understand . . . as attention deficit disorders, hyperactivity, the inability to pay attention, aggressive and violent behaviors, might have their origins during those windows of vulnerability during pregnancy and these questions are just being asked. Data is just beginning to come in."
Dr. Perera's team at Columbia is also studying the way that chemicals can actually bind to human DNA in the womb and cause a mutation called an "adduct." Work by Dr. Perera has shown that the greater the number of adducts, the greater the risk for cancer. "And that's the missing link in all of this," says Dr. Steingraber. "That's the link we're beginning to fill in."
To place the current studies in a public health policy context, Moyers revisits the firestorm over lead research; recalling the revolutionary work of Dr. Herbert Needleman, who correlated low-level lead exposure to lower IQ's in children in 1979. Twelve years later, Needleman's work was attacked by the lead industry as it tried to protect its economic stake in lead products. Ultimately, the validity of Dr. Needleman's work was fully vindicated, and new public policy required unleaded gasoline and restrictions on lead paint. And many scientists believe that, as a result, children's IQ scores have risen, on average, three points. Yet, as Moyers points out, lead remains the number one environmental threat to children's health; many old houses and even many school buildings are still testing positive for lead today.
In Herculaneum, Missouri, lead contamination is a very current issue. The community is up in arms about the astonishingly high levels of lead to which their families have been exposed because the town's primary industry, the Doe Run lead smelter, failed to comply with EPA standards. "Doe Run played a really good game," Robyn Warden, a mother, tells Moyers. "They told people everything was under control and we were safe. And people weren't educated enough to know any different. It took people actually investigating lead to figure out that we were being lied to."
Dr. Steingraber knows the importance of informed parenting. Even in a seemingly pristine environment in rural New York, she knows there are possibilities of risk. "Just because there are no smoke stacks visible around us, just because you live a long way from the source of these chemicals, doesn't mean that nature won't bring them to you in some way," she says. A mother who breast feeds her infant son, Dr. Steingraber also realizes that she passes toxins directly to her baby every time she nurses. "No woman has uncontaminated breast milk on this planet," she states. Dr. Steingraber tries to reduce her children's exposure at home by using non-toxic products. "But we can't shop our way out of our current situation," she warns. "We still need to take action. It's time that our public policy takes action to get our kids out of harm's way."
There are unknown answers to many questions. Moyers reports on a proposed new project called "The National Children's Study," which will track 100,000 children from the womb to age 18 if it receives full funding from Congress. This long-term study may provide the definitive answers necessary for new regulations and laws protecting children from exposure to toxins. "Without conclusive science," Moyers says, "it is a constant fight to protect children's health."
Find out more about how scientists are studying environmental toxins and join the ongoing discussion about the critical issues covered in NOW online at http://www.PBS.org/now
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Diet Trumping Genes
Most geneticists are still focussing on gene sequences to find out which gene variants go with which diseases. But that's a serious mistake, and for more reasons than one. Dr. Mae-Wan Ho reports.
Sources for this report are posted on ISIS members' website. Full details here
Evidence is accumulating that environmental factors, like diet, stress and maternal nutrition, can change gene function epigenetically, i.e., without altering the DNA sequence. These factors have been shown to play a role in cancer, stroke, diabetes, schizophrenia, manic depression and other diseases, as well as in shaping behaviour in offspring.
Prenatal and early nutrition can indeed affect people's susceptibility to chronic diseases later on in life; and the effects can persist through successive generations. This goes counter to the intuition of most geneticists, and the molecular mechanisms involved remain largely unknown.
One theory is that it has to do with patterns of gene expression in the genome, which are 'reprogrammed' in the early embryo, when chemical modifications of the DNA takes place, determining patterns of gene expression that become maintained thereafter.
A common modification involves adding a methyl group (CH3-) to CpG (cytosine-guanine) dinucleotides in the DNA of promoters (gene switches necessary for gene expression), which silences the genes occurring downstream. The metabolic intermediate donating the methyl group to CpG is S-adenosylmethionine; and its availability will be influenced by dietary intake of methyl-donors and other co-factors necessary for its synthesis. That may be one way early nutrition can affect adult propensity to disease.
Patterns of DNA methylation are in part determined by transposable elements - mobile genetic units - scattered throughout the human genome, making up more than 35% of the genome. Most transposons are silenced by methylation, but a subset of them is metastable (not quite stable), and can change in methylation, thereby affecting the expression of nearby genes.
Two researchers in the Department of Radiation Oncology, Duke University Medical Center in Durham, USA, suspected that the epigenetic instability of these transposons make them targets for nutritional influence during early development, and designed a test using a strain of yellow agouti (Avy) mice.
The agouti gene encodes a signalling molecule that causes hair-forming cells to switch from producing black melanin to yellow phaeomelanin. Transcription of the gene is initiated from a hair-cycle specific promoter in exon 2 of the agouti (A) allele (variant of the gene). Transient agouti expression in hair follicles during a specific stage of hair growth results in a yellow band on each hair just below the tip, giving the brown (agouti) coat colour of wild-type mice. The nonagouti (a) allele is due to loss of function of the A allele, so a/a homozygotes are black.
The Avy allele of the yellow agouti mice results from the insertion of a retrotransposon into the tail end of the A allele, which causes alternative initiation of transcription from a promoter in the retrotransposon. This results in a wide variation in individual coat colour, which is associated with degree of obesity, glucose tolerance and susceptibility to tumours among littermates that are all heterozygous Avy/a. This was a sign of epigenetic instability.
Previous research had shown that dietary supplements promoting methylation of a/a pregnant mothers shifted the coat colour distribution of the Avy/a offspring, and that the coat colour correlated with the methylation of Avy, suggesting that the dietary supplement altered the coat colour through changing the methylation of Avy.
In a study published in Molecular and Cellular Biology, August 2003, virgin a/a (black) females, 8 weeks of age, were assigned randomly to be fed a control diet or a diet supplemented with the methyl donors and cofactors: folic acid, vitamin B12, choline chloride and anhydrous betaine for two weeks before the females were mated with Avy/a males, and continued throughout pregnancy and lactation. On weaning at age 21 days, the Avy/a offspring were weighed, a sample of DNA taken from the tips of their tail, and the mice photographed, and rated for coat colour.
The coat colour of the offspring ranged from yellow, to slight mottled, mottled, heavily mottled and pseudoagouti (for colour that was almost the same as agouti, indicating the almost complete silencing of the Avy agouti gene expression). The results cleared showed a significant increase in proportions of heavily mottled and pseudoagouti and a significant decrease in proportions of yellow and slightly mottled offspring from mothers given dietary methyl supplements compared to offspring from mothers fed the control diet.
The coat colours were strongly correlated with degree of methylation of the Avy allele associated with the retrotransposon insertion, increasing from 5% or less in yellow, to 10 to 20% in slightly mottled, 25-40% in mottled, 65 to 75% in heavily mottled and 85 to 95% in pseudoagouti.
When these mice produced the next generation the epigenetic effect will persist, so yellow females will tend to produce fewer pseudoagouti offspring than pseudoagouti females. This maternal effect is thought to be due to incomplete erasing of the epigenetic modification at the Avy gene in the female germ line.
This research underlines the importance of maternal nutrition on the long-term health prospects of their offspring. Previous research has already shown that severe methyl donor deficiency (of folic acid) induced gene-specific DNA hypomethylation in rats as well as DNA breaks. The new results show that merely supplementing a mother's diet with extra folic acid, vitamin B12, choline and betaine can also permanently affect the offspring's DNA. The researchers commented, "This finding supports the conjecture that population-based supplementation with folic acid, intended to reduce the incidence of neural tube defects, may have unintended influences on the establishment of epigenetic gene-regulatory mechanisms during human embryonic development."
What it means is that dietary supplements can have unintended effects on gene expression. But in this particular case, while dietary deficiency had been shown to be harmful, no harmful unintended effects have resulted from dietary supplements.
On the contrary, according to a report published in October in the New York Times, another effect of the supplements, pointedly not mentioned in the scientific paper, is that the yellow mice with the active Avy allele, are also obese, while the pseudoagouti mice with the same gene turned off by methylation, are lean and healthy. And obese yellow mothers given the supplements gave birth to healthy brown mice.
Dr. Randy Jirtle, Professor of radiation oncology in Duke University and the lead researcher of the latest scientific paper, was quoted as saying, "Scientists have long known that what pregnant mother eat - whether they are mice, fruit flies or humans - can profoundly affect the susceptibility of their offspring to disease. But until now they have not understood why."
Dr. Thomas Insel, director of the National Institute of Mental Health, remarked that these epigenetic effects could turn out to be much more important than the sequences of genes that most geneticists are still focused on. "The field is revolutionary," he said, "and humbling."
Dr. Arturas Petonis, an associate professor of psychiatry at the Center for Adiction and Mental Health at the University of Toronto, also believes epigenetics may hold the answer to many mysteries that are baffling to classical genetics: why does one identical twin develop schizophrenia and not the other? Why do certain disease genes affect some people much more than others? Why do diseases like autism turn up more frequently in boys than girls?
It now appears that stresses to germ cells and embryos associated with assisted reproductive technologies are also turning up similar epigenetic effects in 'gene imprinting' that have both immediate and long term impacts on the health of the unborn (see "What' wrong with assisted reproductive technologies?" to appear).
Not just gene expression is modifiable by environmental factors. We at ISIS have documented how toxic environmental agents can shuffle genes and cause chronic illnesses (see Health and the fluid genome mini-series, SiS 19).
Isn't it time we leave genetic determinism well behind and concentrate on cleaning up our environment and providing healthy nutrition to all, especially for mothers.
For more on exposing the myth of genetic determinism, read Living with the Fluid Genome.
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Bland, Jeffrey S., Genetic Nutritioneering, McGraw-Hill, 1999.
Williams, Roger, Biochemical Individuality, McGraw-Hill, 1998.