Archive for category ‘Neurodevelopment‘

Mercury exposure, nutritional deficiencies and metabolic disruptions may affect learning in children

Children with learning disabilityAmong dietary factors, learning and behavior are influenced not only by nutrients, but also by exposure to toxic food contaminants such as mercury that can disrupt metabolic processes and alter neuronal plasticity. 

Neurons lacking in plasticity are a factor in neurodevelopmental disorders such as autism and mental retardation. Essential nutrients help maintain normal neuronal plasticity. Nutritional deficiencies, including deficiencies in the long chain polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid, the amino acid methionine, and the trace minerals zinc and selenium, have been shown to influence neuronal function and produce defects in neuronal plasticity, as well as impact behavior in children with attention deficit hyperactivity disorder. 

Nutritional deficiencies and mercury exposure have been shown to alter neuronal function and increase oxidative stress among children with autism. These dietary factors may be directly related to the development of behavior disorders and learning disabilities. 

Mercury, either individually or in concert with other factors, may be harmful if ingested in above average amounts or by sensitive individuals. High fructose corn syrup has been shown to contain trace amounts of mercury as a result of some manufacturing processes, and its consumption can also lead to zinc loss. Consumption of certain artificial food color additives has also been shown to lead to zinc deficiency. Dietary zinc is essential for maintaining the metabolic processes required for mercury elimination.

Since high fructose corn syrup and artificial food color additives are common ingredients in many foodstuffs, their consumption should be considered in those individuals with nutritional deficits such as zinc deficiency or who are allergic or sensitive to the effects of mercury or unable to effectively metabolize and eliminate it from the body. 

Reference:

Dufault R, Schnoll R, Lukiw WJ, Leblanc B, Cornett C, Patrick L, Wallinga D, Gilbert SG, Crider R., Mercury exposure, nutritional deficiencies and metabolic disruptions may affect learning in children, Behav. Brain Funct. 2009 Oct 27;5(1):44.

UCLA study reveals how tiny levels of carbon monoxide damage fetal brains

CO Exposure could make them more vulnerable to disease

A UCLA study has discovered that chronic exposure during pregnancy to miniscule levels of carbon monoxide damages the cells of the fetal brain, resulting in permanent impairment. The journal BMC (BioMed Central ) Neuroscience published the findings June 22 in its online edition.

“We expected the placenta to protect fetuses from the mother’s exposure to tiny amounts of carbon monoxide,” said John Edmond, professor emeritus of biological chemistry at the David Geffen School of Medicine at UCLA. “But we found that not to be the case.”

The researchers exposed pregnant rats to 25 parts per million carbon monoxide in the air, an exposure level established as safe by Cal/OSHA, California’s division of occupational health and safety.

Dr. Ivan Lopez, UCLA associate professor of head and neck surgery, tested the rats litters 20 days after birth. Rats born to animals who had inhaled the gas suffered chronic oxidative stress, a harmful condition caused by an excess of harmful free radicals or insufficient antioxidants.

“Oxidative stress damaged the baby rats brain cells, leading to a drop in proteins essential for proper function,” said Lopez. “Oxidative stress is a risk factor linked to many disorders, including autism, cancer, Alzheimer’s, Parkinson’s, Lou Gehrig’s disease, multiple sclerosis and cardiovascular disease. We know that it exacerbates disease.”

“We believe that the minute levels of carbon monoxide in the mother rats environment made their offspring more vulnerable to illness,” added Edmond. “Our findings highlight the need for policy makers to tighten their regulation of carbon monoxide.”

Tobacco smoke, gas heaters, stoves and ovens all emit carbon monoxide, which can rise to high concentrations in well-insulated homes. Infants and children are particularly vulnerable to carbon monoxide exposure because they spend a great deal of time in the home.

No policies exist to regulate the gas in the home. Most commercial home monitors sound an alarm only hours after concentrations reaches 70 parts per million – nearly three times the 25 parts per million limit set by Cal/OSHA.

A grant from the University of California’s Tobacco-related Disease Research Program supported the research.

Reference: Elaine Schmidt, UCLA study reveals how tiny levels of carbon monoxide damage fetal brains, UCLA, 6/25/2009

Exposure to phthalates may be a risk factor for low birth weight in infants

Phthalates are ubiquitous in newbornsMany parents worry about their child’s exposure to phthalates, the chemical compounds used as plasticizers in a wide variety of personal care products, children’s toys, and medical devices. Phthalate exposure can begin in the womb and has been associated with negative changes in endocrine function. A new study soon to be published in the Journal of Pediatrics examines the possibility that in utero phthalate exposure contributes to low birth weight in infants. Low birth weight is the leading cause of death in children under 5 years of age and increases the risk of cardiovascular and metabolic disease in adulthood.  

To investigate the associations between in utero phthalate exposure and low birth weight, Dr. Renshan Ge of the Population Council and colleagues from Fudan University and Second Military Medical University in Shanghai studied 201 pairs of newborns and their mothers between 2005 and 2006. Of the 201 infants studied, 88 were born with low birth weight. The researchers analyzed samples of the infants’ meconium, the first bowel movement that occurs after birth, and cord blood to determine phthalate levels.  

They found quantifiable levels of phthalate and phthalate metabolites in more than 70% of the samples. Infants with low birth weight had consistently higher levels of phthalates. According to Dr. Ge, “The results showed that phthalate exposure was ubiquitous in these newborns, and that prenatal phthalate exposure might be an environmental risk factor for low birth weight in infants.” Although these associations are not conclusive, this study supports the accelerating efforts to minimize phthalate exposure. 

Reference: The study, reported in “Phthalate Levels and Low Birth Weight: A Nested Case-Control Study of Chinese Newborns” by Zhang Y, PhD, Lin L, MD, Cao Y, PhD, Chen B, MD, Zheng L, MSC, Ge R, MD, appears in the Journal of Pediatrics, DOI 10.1016/j.jpeds.2009.04.007, published by Elsevier. EurekAlert, June 25, 2009.

Newborn weights affected by environmental contaminants

newborn-baby with low body weight

Recent epidemiological studies have revealed an increase in the frequency of genital malformations in male newborns (e.g., un-descended testes) and a decrease in male fertility.  

The role played by the growing presence in our environment of contaminants that reduce male hormone action could explain this phenomenon. 

It is known that the birth weight of males is higher than that of females due to the action of male hormones on the male fetus.If the exposure of pregnant women to environmental contaminants that diminish the action of male hormones has increased over the years, one would expect to see a decrease in the sex difference in birth weight.

This is exactly what a new study published in the July 2009 issue of Epidemiology shows. Investigators analyzed the Public Health Agency of Canada’s database on the birth weights of more than five million children born in Canada between 1981 and 2003.  

Using statistical methods that control for changes over time of mother’s age and parity, the investigators effectively show a sustained decrease in birth weight differences between boys and girls, which supports the hypothesis of growing endocrine disruption related to environmental contaminants. Contaminants found in plastic materials represent plausible candidates, since they are known to diminish the action of male hormones. 

“Our study underlines the importance of probing the impact of environmental contaminants on the health of mothers and fetuses and on the reproductive potential of future generations,” says lead researcher Dr. Guy Van Vliet, a pediatric endocrinologist and investigator at the Sainte-Justine University Hospital Research Center and a professor at the Department of Pediatrics of the Université de Montréal.

Reference: Sainte-Justine University Hospital Research Center, Newborn weights affected by environmental contaminants, University of Montreal, McGill University and Public Health Agency of Canada, June 15, 2009  

Bisphenol A exposure in pregnant mice permanently changes DNA of offspring

DNA

Exposure during pregnancy to the chemical bisphenol A, or BPA, found in many common plastic household items, is known to cause a fertility defect in the mother’s offspring in animal studies, and now researchers have found how the defect occurs. The results of the new study will be presented Saturday at The Endocrine Society’s 91st Annual Meeting in Washington, D.C.

The study, funded partly by the National Institutes of Health, joins a growing body of animal research showing the toxic health effects of BPA, including reproductive and developmental problems. Last August the U.S. Food and Drug Administration found BPA to be safe as currently used but later said more research on its safety is needed. BPA is used to make hard polycarbonate plastic, such as for baby bottles, refillable water bottles and food containers, as well as to make the linings of metal food cans.

BPA has estrogen-like properties and in pregnant animals has been linked to female infertility.

“The big mystery is how does exposure to this estrogen-like substance during a brief period in pregnancy lead to a change in uterine function,” said study co-author Hugh Taylor, MD, professor and chief of the reproductive endocrinology section at Yale University School of Medicine.

To find the answer to that question, Taylor and his co-workers at Yale injected pregnant mice with a low dose of BPA on pregnancy days 9 to 16. After the mice gave birth, the scientists analyzed the uterus of female offspring and extracted DNA.

They found that BPA exposure during pregnancy had a lasting effect on one of the genes that is responsible for uterine development and subsequent fertility in both mice and humans (HOXA10). Furthermore, these changes in the offspring’s uterine DNA resulted in a permanent increase in estrogen sensitivity. The authors believe that this process causes the overexpression of the HOXA10 gene in adult mice that they found in previous studies.

The permanent DNA changes in the BPA-exposed offspring were not apparent in the offspring of mice that did not receive BPA injection (the controls). This finding demonstrates that the fetus is sensitive to BPA in mice and likely also in humans, Taylor said.

“We don’t know what a safe level of BPA is, so pregnant women should avoid BPA exposure,” Taylor said. “There is nothing to lose by avoiding items made with BPA—and maybe a lot to gain.”

Reference: The Endocrine Society, Bisphenol A exposure in pregnant mice permanently changes DNA of offspring, 10-Jun-2009