Richard Deth
From Wikipedia, the free encyclopedia
Richard Deth, Ph.D., is a neuropharmacologist, professor of pharmacology at Northeastern University in Boston, Massachusetts and is on the scientific advisory board of the National Autism Association. Deth has become a significant voice in the escalating controversies in autism and vaccine controversy, due to his ongoing research backing his theory that certain children are more at risk than others because they lack the normal ability to excrete neurotoxic metals.
Deth has published many studies on the role of D4 dopamine receptors in schizophrenia, autism, and ADHD, including papers on the role of thimerosal and genetics in these disorders, "Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and Thimerosal," and "How Genetic and Environmental Factors can Synergize with Inflammation to Impair Methylation and Cause Developmental Disorders." He has also written the book, Molecular Origins of Human Attention: The Dopamine-Folate Connection.
Contents |
[edit] Research focus
The primary realms of research conducted by Deth involve the role of D4 dopamine receptors in schizophrenia and attention. He has focused on understanding the molecular basis of transmembrane signaling by G protein-coupled receptors, the study of their structure using three-dimensional molecular graphics, and modeling how the binding of various drugs causes a shift in their molecular form. Deficits in D4 receptor-mediated phospholipid methylation, according to Deth, may contribute to the etiology of several neuropsychiatric disorders, including schizophrenia and depression. Deth has characterized the conformation-dependent participation of D4 dopamine receptors in the process of phospholipid methylation and found that different states of methylation yield varying degrees of spontaneous activity with regard to G protein coupling.
[edit] Neurodevelopmental toxins and thimerosal
Deth's research has uncovered evidence thimerosal creates deficits in the D4 receptor-mediated phospholipids methylation essential for detoxification and sustaining attention to tasks. The research provides the first scientific link between attention deficits and autism. Deth has identified the metabolic process, called methylation, whereby thimerosal can cause the brain damage associated with autism. When Deth exposed human neuronal cells to low doses of thimerosal, the chemical activity called methylation dropped significantly.
Deth believes the dramatic rise in autism and ADHD cases in recent years can be blamed on mercury poisoning due to vaccine-related thimerosal exposure.[1] "During the first years of life networks of neurons that represent the matrix for learning are being developed in the brain," says Deth. "Methylation and the development of neuronal cells to create these networks are critical during this time. If the process is interrupted, the ability to learn and pay attention would naturally be impaired.["http://www.sciencenews.org/articles/20041113/bob8.asp]
An enzyme critical to methylation, methionine synthase, uses an active form of vitamin B12 to complete its chemical function, according to Deth. Thimerosal interferes with the conversion of dietary forms of B12 into the active form and so impedes DNA methylation and disrupts some normal gene actions.I
Deth has found that insulin-like growth factor-1 (IGF-1) and the neurotransmitter dopamine both stimulated folate-dependent methylation pathways in neuronal cells, while compounds like thimerosal, ethanol and metals (like lead and mercury) effectively inhibited these same biochemical pathways at concentrations that are typically found following vaccination or other sources of exposure.
"Taken together," Deth has said, "increased exposure to thimerosal has combined with genetic risk factors in a sensitive subpopulation to cause the recent rise in autism.... This molecular understanding should lead to new and improved treatments for autism and should provide a scientifically sound basis for the removal of thimerosal from all vaccines."
[edit] Acceptance
Studies by Columbia University professor Dr. Mady Hornig and Deth were presented to the Institute of Medicine Committee for review at the agencies' February 8, 2004, meeting, convened to address the growing furor over that has arisen globally over mass vaccination campaigns. However, because the IOM was directed by the Centers for Disease Control (CDC) to examine only epidemiological studies; neither study was considered in the subsequent IOM report, which strongly rejected a thimerosal-autism association and recommended diversion of research efforts to other areas.[2]
In a hearing chaired by Dan Burton, (R-IN), Deth spoke before Congress members concerning the role of thimerosal in neurodevelopmental disorders. Following repeated statements about the importance of vaccines and immunization programs, the Burton scolded a panel representing the CDC, IOM and other Federal health safety agencies for placing the vaccine program's image ahead of the health of children who cannot excrete mercury normally. Despite pleas from the chair to remain for the testimony of Deth and other scientists, government officials walked out, rather than remaining to witness presentations of evidence potentially linking vaccines to autism and other developmental disorders.[3]
On October 5, 2004, Deth further described his findings to a Congressional Labor and Health and Human Services subcommittee in Washington, D.C., explaining to the panel that his team had determined the specific molecular mechanism by which thimerosal inhibits methylation.
[edit] See also
[edit] External links
- NEU.edu - Richard Deth (homepage), Northeastern University
- EurekAlert.org - 'A link between thimerosal and the brain: Can vaccines affect central nervous system function?' (February 5, 2004)
- MedMutual.com - 'Study Suggests Vaccine, Autism Link', WebMD (Feb. 5, 2004)
