Study Of Genes, Toxic Metals In Children With Autism Spectrum Disorders Launched By UT Houston, Jamaica Researchers
Main Category: AutismAlso Included In: Genetics; Pediatrics / Children's Health; Psychology / Psychiatry
Article Date: 01 Oct 2009 - 0:00 PDT
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Researchers at The University of Texas Health Science Center at Houston and the University of the West Indies have joined forces to launch a study of Jamaican children that they hope will unlock the secrets of how genetics and environment may interact to cause autism spectrum disorders.
The research, funded with a two-year, $300,000 exploratory grant from the National Institute of Child Health and Human Development (NICHD) and Fogarty International Center, will train Jamaican health professionals in the most current autism diagnostics; identify an initial sample of Jamaican children ages 3 to 8 who have an autism spectrum disorder; and test the children for specific genes that may interact with exposure to toxins that could affect their neurodevelopment.
"This study will help us identify if autism is related to gene-environment interaction," said Mohammad Hossein Rahbar, Ph.D., principal investigator and professor of epidemiology and biostatistics at The University of Texas School of Public Health. "Jamaica has a stable population, which can help us get a better estimate of the prevalence of autism spectrum disorders linked to environmental causes. In addition, over 90 percent of the population is of African descent, which means less variation in genetics."
Autism spectrum disorders (ASD) are complex, neurodevelopmental and behavioral disorders characterized by impairments in social interaction and communication and repetitive, sometimes obsessive, behaviors. According to the NICHD, a conservative estimate is that one in every 1,000 children has an autism disorder. The national group Autism Speaks puts the number at 1 in 150.
The study will enroll 150 children with autistic disorders from the existing Jamaican ASD database established by Maureen Samms-Vaughan, M.D., Ph.D., principal investigator of the University of the West Indies subcontract. Another group of 150 age- and sex-matched children will be enrolled in this study to serve as a control group and will be compared with children diagnosed with ASD.
"By utilizing the most current available diagnostic methods in Jamaica, our study in the future will promote the earlier identification of children there who are on the autism spectrum," said Katherine Loveland, Ph.D., co-investigator and professor of psychiatry and behavioral sciences at The University of Texas Medical School at Houston. "Also, because most children in Jamaica who need developmental assessment receive it at the clinic directed by Dr. Samms-Vaughan, we will ultimately have the unique opportunity to reach and to research autism in the majority of children in Jamaica who have an autism spectrum disorder."
Samms-Vaughan, professor of child health, child development and behavior at UWI, Mona Campus, is the only developmental and behavioral pediatrician in Jamaica and one of four in the Caribbean. She founded the Child and Family Clinic for Developmental and Behavioral Disorders of Childhood.
"This grant allows us to utilize the most recent diagnostic methods available for participants in the study," Samms-Vaughan said. "There is a lot of information on autism in developed countries, but more limited information from developing countries. Researching similarities and differences across nations will better inform us of the causes. If we can unearth the causes, we will be well on our way to preventing the disabling condition that autism is."
Eric Boerwinkle, Ph.D., professor and director of the Division of Epidemiology at the UT School of Public Health, will lead the project's study of variations in the glutathione-S-transferase genes in relation to autism, as well as their possible interaction with genes involved in contaminant metabolism and metals involved in developmental toxicity. Those metals include mercury, lead, arsenic and cadmium. The study team will collaborate with geneticist Wayne McLaughlin, Ph.D., from UWI's Caribbean Genetics Lab and Gerald Lalor, Ph.D., from UWI's International Centre for Environment and Nuclear Science. The genetic research is funded in part with an additional grant to Boerwinkle from the National Institute of General Medical Sciences. The grant examines genomic sequence information for predicting health and disease beyond traditional risk factors.
The pilot study will set the ground work for large, population-based studies of ASD in Jamaica and help build the infrastructure there for the two universities to train researchers and conduct joint research, said Rahbar, who is director of the Biostatistics, Epidemiology and Research Design Core of the Center for Clinical and Translational Sciences at the UT Health Science Center at Houston.
Co-investigators from the UT School of Public Health are Deborah del Junco, Ph.D., associate professor of epidemiology; and Jan Bressler, Ph.D., assistant professor in the Human Genetics Center. Co-investigator Clara Lajonchere, Ph.D., is vice-president of clinical programs for Cure Autism Now/Autism Speaks and research assistant professor at the University of Southern California.
Source:
Deborah Lake
University of Texas Health Science Center at Houston
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Fertility Drugs and Autism
posted by Terence Mix on 4 Oct 2010 at 7:06 amFertility drugs appear likely to be at least one cause of autism spectrum disorder (ASD). On May 20, 2010, researchers from the Harvard School of Public Health presented their findings from a study exploring the possible relationship between the use of fertility drugs and autism spectrum disorder. The scientists reported to attendees at the International Meeting for Autism Research in Philadelphia that women who used fertility drugs to get pregnant had almost double the risk of having a child with ASD verses nonusers. The drugs studied included Clomid (clomiphene citrate) and Pergonal (gonadotropin).
Some have expressed skepticism about the study. However, although its value cannot be fully assessed until it appears in a peer-reviewed journal, there are several factors that argue in favor of its merits. In an effort to rule out other causes, Dr. Lyall and her colleagues made an “adjustment for pregnancy complications, maternal age, and other possible risk factors,” before making a determination that use of fertility drugs represented a 91% increased risk. This was at a highly significant statistical level – namely, the odds that their data did not occur by chance were 993 out of 1,000 (P=0.007). They also determined that a history of infertility – exclusive of fertility drugs – was not significantly associated with ASD, and that the “odds ratio for autism spectrum disorder increased with the number of reports of use of ovulation inducing drugs” (P=0.008).
This recent study is part of a growing body of research that strengthens the argument that Clomid and other fertility drugs are a cause of ASD via their ability to deny cholesterol to a developing embryo shortly after conception. About 58% of ASD children have low total cholesterol (
Fertility Drugs and Autism
posted by Terence Mix on 12 Oct 2010 at 11:30 amTo complete my posting of October 4, 2010: About 58% of ASD children have low total cholesterol and about 19% have a total cholesterol count below 100. It has also been observed that a high percentage of children (71-86%) born with Smith-Lemli-Opitz syndrome (SLOS), in addition to a wide array of birth defects are also born with ASD. Infants with SLOS are born with a defective enzyme that impairs the body’s ability to produce cholesterol. Cholesterol is essential for growth of the myelin membranes that cover the brain and abnormalities in the myelin sheath are believed to be a contributing cause of ASD. Many experts thus believe that low cholesterol during early embryonic development is one of the causes of ASD.
Clomid has a long half-life and is present during the embryonic period (first 8 weeks) even when taken before conception. Studies have shown it to be biologically active for up to 54 days after ingestion and that it can accumulate over successive cycles of treatment. A critically important fact is that Clomid is a cholesterol inhibitor and impairs its production by acting upon enzymes in the body similar to Lipitor and other statin drugs.
The GOOD NEWS is that many ASD children with low cholesterol, treated with cholesterol supplementation, have shown dramatic improvement. Better yet, once we have a full understanding about one of the causes of ASD, some day in the future we might be in a position to eliminate that cause. As I postulated over two years ago, maintaining an optimum level of cholesterol throughout pregnancy could likely eliminate many cases of birth defects and autism spectrum disorder.
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