 |
 |
 |
 |
 |
|
 |
 |
 |
 |
|
|
 |
[ Overview ] [ Understanding The Physiology ] [ Supporting Research ] [ More Published Studies ] [ Supporting Medical Studies ] SUPPORTING RESEARCH Free Radicals & Autism - James Study Chronic biochemical imbalance is often a primary factor in the development of many complex diseases as well as a possible metabolic basis for autism. A number of researchers have focused on metabolic biomarkers in the brain for the answer. Dr Jill James from the University of Arkansas believes that because individuals with autism share a chronic flaw in the body's natural defense against oxygen free radicals and as a result the free radicals bombard the brain and cause havoc which manifests in autism (James, et al., 2004). Individuals with autism have been found to have a lower than normal or neutralized oxygen free radical system which in turn lowers the binding ability of a chemical (glutathione) produced by all cells in the body, to alter the electron balance and expel free radicals. If this process does not occur, then the maturing neurons and synapses are vulnerable to bio-molecular invasion which James believes may be a trigger for autism. Glutathione functions as an antioxidant, the body's tool for detoxifying and excreting metals. James suggests that environmental mercury contaminants, including a mercury preservative known as thimerosal used extensively in vaccines from 1988 through 2002 in the United States, alter the glutathione balance whereby interfering with the body's ability to neutralize toxic heavy metals, leading to increased risk in the developing brain and nervous system. As a result the unopposed free radicals may affect the gastrointestinal tract and the immune system, common pathology reported to occur in individuals with autism. James and colleagues measured blood samples from 20 United States, Caucasian autistic children (6-8 years old, 14 males and 6 females), and 33 United States, Caucasian control children to determine the levels of protective antioxidant (glutathione). The study determined a correlation between abnormally low antioxidant levels and children with autism, further indicating that there may be a possible connection between brain tissue damaged by mercury concentration whereby interrupting the elimination of toxins, causing a metabolic or "biomarker" imbalance, resulting in characteristics of autism. Concentration of Mercury in Urine- Bradstreet Study At Arizona State University, Jeff Bradstreet et al. (2003) conducted a case control study of thimerosal mercury, first added to childhood immunization vaccines in the 1930's, autism was first described in 1943 among children who were born in the 1930's, suggesting that autism may indeed be an iatrogenic (doctor caused) effect of (thimerosal) burden in children. Two hundred and twenty one children were analyzed with the diagnosis of established ASD comparing mercury excretion after a three-day treatment with an oral chelating agent, meso-2,3-dimercaptosuccinic acid (DMSA) to a matched control group of 18 children without an autism diagnosis among themselves or a sibling or a first-degree family member. The male:female ratio was 4.88:1 and the ages ranged form 3-15 years of age in the cases and 3-16 years of age in the controls. The Bradstreet study (Bradstreet et al., 2003) measured the mercury buildup in the tissues of children to determine if children with autism accumulate a higher concentration level of mercury in their bodies and if so, could the presence of mercury accumulation be due to pre-existing genetic conditions and possibly produce a toxic effect in pre-natal neurodevelopment causing autism. Bradstreet indicated a strong association between increased urinary mercury concentrations after a three day treatment of DMSA and the diagnosis of ASD. Because mercury concentrations in the human brain are six times greater than in the blood, it is possible that thimerosal binds to a free radical and is not excreted from the body. The lack of the ability of the children with autism to excrete mercury may affect the immune system and the central nervous system possibly causing neurochemical and neurophysiolical damage which could manifest in degrees of neurological disorders, including Attention Deficit Disorder (ADD), learning difficulties and speech delay. The analysis confirmed that children who developed ASD had significantly greater accumulated mercury than the controls. The Bradstreet study is in line with previous published epidemiologic reports indicating a direct association between increased mercury from thimerosal-containing childhood vaccines and neurodevelopment disorders (Geier & Geier, 2003). Environmental Insults to the Thyroid System-Porterfield Study Susan Porterfield (Porterfield, 1994), Medical College of Georgia, indicates that the PCB's and dioxins are structurally similar to the thyroid hormone and depending on the amount of toxin exposure, either mimic or decrease the biological action of the thyroid hormone in the body. If either effect occurs during brain development in utero and/or as infants, neurologic development may manifest in behavioral disorders. If there is an absence of the thyroid hormone, myelinization (growth of sheath-like insulating material in the spinal cord developed during the 2nd trimester and continuing until the second year of life, protecting the nervous system and serving as an electrical insulator in development of fine motor control) is delayed along with normal biochemical maturation of neurons, effecting the cerebral and cerebellum cortex if superimposed on a pre-existing maternal or fetal thyroid disorder. If toxins change the thyroid function, they may cause permanent neurological damage including impaired learning and memory, hyperactivity (reported in mice, rats and monkeys), delayed auditory processing (reported in rats and mice), decreased birth weight and litter size in rodents and possible decrease in birth weight in humans (Porterfield, 1994, p. 5). The effects of prenatal and perinatal PCB and dioxin exposure to the neurological system in humans, resembles those associated with fetal or perinatal hypothyroidism. Porterfield concludes that the possibility exists that toxins, may at low levels, be altering neurological development via their action on thyroid hormones available during critical brain development periods of gestation. Molecular Defects in the Autistic Brain White Brain Matter & Autism- Herbert Study Dr. Martha Herbert, pediatrics neurologists at Massachusetts General Hospital at Harvard Medical School, reports that although various brain, biochemical, immunological and genetic abnormalities have been found in individuals with ASD, at present there is no reliable biomarker, making it a syndrome rather than a disease (Herbert, 2004). Dr. Herbert rejects the ideology that conflicting measurement tools and methods for screening is a validity problem in measuring individuals with autism and ASD, but suggests that the variability in studies may be due to the fact that autism may not be a specific biological entity but rather a "final common pathway" (Purcell, Jeon & Pevsner, 2001; Herbert 2004). Furthermore, Herbert argues that environmental toxins are most likely the cause of 20% of US children being diagnosed with some form of PDD, with millions more added each year. Rather than trying to eliminate the variability, Herbert poses the question of just how it can be that such a presumably heterogeneous set of underlying biological abnormalities can eventuate in the same syndrome of behavioral abnormalities. How can we characterize the cognitive neuroscience of the phenomenon of a final common pathway? Herbert hypothesizes that autism is a disorder of systems alteration or disruption and that systems can be impacted in multiple ways and yet yield a similar syndrome of behaviors (Herbert, 2004, p.4). Through Magnetic Resonance Imaging (MRI) and a new procedure known as morphometric analysis (post-mortem brain tissue is divided into small parcels and examined), Dr Herbert measured individual parts of the brain to determine why autistic brains are bigger than normal, specifically the white matter, the color of the fatty material that insulates the nerve cell fibers in the brain (Schumann, Buonocore & Amaral, 2001). White matter develops later in gestation and does not mature until the second year of life. Herbert found that the increase in the white matter, or inflammation, is greatest in the area that transmits information between the brain regions that are closest to each other and on the same side of the brain. As opposed to the white matter transmitters that are long distance and transmit information to and from opposite sides of the brain. Herbert reported the long distance white matter to be relatively unchanged in individuals with autism. More importantly, Herbert discovered that the volume change in white matter is greatest in the front of the brain, which is the area of the brain most connected to all other areas of the brain, and where the most abstract higher-level thinking is believed to take place. Dr. Herbert measured the size of 48 areas of the brain on both sides with MRI. In individuals with autism she found a reversal of brain asymmetry, more areas are bigger on the right side than the left indicating that there is a bias on the right side of the brain, opposite of a typically developing child. Of most interest is the fact that the enlarged brain area of individuals with autism are the areas associated with higher-order thinking and are responsible for tying together information from all other locations in the brain. Herbert also reported a correlation with increased white matter and the right side of the brain, the non-verbal hemisphere, asymmetry and the brains of children with Developmental Language Disorders. Indicating that the anatomical problem may underlie the inability to process complex information such as language and furthermore, that the language disability in autism may be a part of a much more widespread abnormality i.e. there is no difference in a specific Learning Disability (LD) and autism, they are the same disorder but the degree of the disability is how it will manifest as an autism disorder, LD or other neurological disability. "Overall, Herbert suggests that in autism, parts of the brain may not be talking to each other normally. Because white matter grows normally until 9 months of age in the individual with autism, says Herbert, then it goes haywire and by two years of age, excessive white matter is found in the frontal lobes, the cerebellum and higher level processing areas. The reason the enlargement of the brain is not seen in mature individuals with autism is because the brain grows rapidly from 1 to 2 months of age, with another spurt between 6 months and 2 years. A 5 year old with autism has the same size brain as a normal 13 year old child. By mid-adolescence, when normal developing children catch up, the individual with autism's brain is comparatively smaller." (Blakeslee, New York Times, 2005, p. 1). Also of interest is the fact that individuals with autism process the alphabet in that area of the brain where shapes are normally process, suggesting that they are using a basic sensory region of the brain to process higher-level concepts. The analogy that Dr Mathew Belmonte, an autism researcher at the University of Cambridge in England refers to as a computer analogy, "Think of the white matter as fibers that connect neurons in separate areas of the brain and grey matter contains the neurons themselves, white matter are the cables and the grey matter is the circuit board. Even if the circuit board is intact, if the computer cables are disrupted then the computer can't function (Blakeslee, 2005)." |
                 
|
|
|
|
 |
|
|||
|
CLICK HERE FOR DIRECTIONS TO THE OFFICE 100 Manetto Hill Road, Suite 106 | Plainview, NY 11803 | 516-470-9525 |
|
|||
