A study published in the Journal of Child Neurology examined the question of what is leading to the apparent increase in autism. They expressed that if there is any link between autism and mercury, it is crucial that the first reports of the question are not falsely stating that no link occurs. Researchers determined that a significant relation does exist between the blood levels of mercury and the diagnosis of an autism spectrum disorder.
Journal of Child Neurology
First Published November 1, 2007
M. Catherine DeSoto, PhD, Robert T. Hitlan, PhD
Department of Psychology, University of Northern Iowa, Cedar Falls, Iowa,
The question of what is leading to the apparent increase in autism is of great importance. Like the link between aspirin and heart attack, even a small effect can have major health implications. If there is any link between autism and mercury, it is absolutely crucial that the first reports of the question are not falsely stating that no link occurs. We have reanalyzed the data set originally reported by Ip et al. in 2004 and have found that the original p value was in error and that a significant relation does exist between the blood levels of mercury and diagnosis of an autism spectrum disorder. Moreover, the hair sample analysis results offer some support for the idea that persons with autism may be less efficient and more variable at eliminating mercury from the blood.
A study published in the Journal of Child Neurology noted that autistic spectrum disorders can be associated with mitochondrial dysfunction. Researchers determined that children who have mitochondrial-related dysfunctional cellular energy metabolism might be more prone to undergo autistic regression between 18 and 30 months of age if they also have infections or immunizations at the same time.
Journal of Child Neurology
First Published February 1, 2006
Study – Developmental Regression and Mitochondrial Dysfunction in a Child With Autism
1 – Jon S. Poling, MD, PhD, 2 – Richard E. Frye, MD, PhD, 3 – John Shoffner, MD, 4 – Andrew W. Zimmerman, MD
1 – Department of Neurology and Neurosurgery Johns Hopkins Hospital Baltimore, MD
2 – Department of Neurology Boston Children’s Hospital Boston, MA
3 – Horizon Molecular Medicine Georgia State University Atlanta, GA
4 – Department of Neurology and Neurosurgery Johns Hopkins Hospital Kennedy Krieger Institute Baltimore, MD
Autistic spectrum disorders can be associated with mitochondrial dysfunction. We present a singleton case of developmental regression and oxidative phosphorylation disorder in a 19-month-old girl. Subtle abnormalities in the serum creatine kinase level, aspartate aminotransferase, and serum bicarbonate led us to perform a muscle biopsy, which showed type I myofiber atrophy, increased lipid content, and reduced cytochrome c oxidase activity. There were marked reductions in enzymatic activities for complex I and III. Complex IV (cytochrome c oxidase) activity was near the 5% confidence level. To determine the frequency of routine laboratory abnormalities in similar patients, we performed a retrospective study including 159 patients with autism (Diagnostic and Statistical Manual of Mental Disorders-IV and Childhood Autism Rating Scale) not previously diagnosed with metabolic disorders and 94 age-matched controls with other neurologic disorders. Aspartate aminotransferase was elevated in 38% of patients with autism compared with 15% of controls (P < .0001). The serum creatine kinase level also was abnormally elevated in 22 (47%) of 47 patients with autism. These data suggest that further metabolic evaluation is indicated in autistic patients and that defects of oxidative phosphorylation might be prevalent.
A study conducted by Massachusetts General Hospital at the Centre for Morphometric Analysis by the department of Paediatric Neurology illustrates how autistic brains have a growth spurt shortly after birth and then slow in growth a few short years later. Researchers have determined that neuroinflammation appears to be present in autistic brain tissue from childhood through adulthood. The study excerpt reads:
“Oxidative stress, brain inflammation and microgliosis have been much documented in association with toxic exposures including various heavy metals. The awareness that the brain as well as medical conditions of children with autism may be conditioned by chronic biomedical abnormalities such as inflammation opens the possibility that meaningful biomedical interventions may be possible well past the window of maximal neuroplasticity in early childhood because the basis for assuming that all deficits can be attributed to fixed early developmental alterations in net”
US National Library of Medicine
National Institutes of Health – 2005
Pediatric Neurology, Center for Morphometric Analysis, Massachusetts General Hospital, Charleston, MA 02129, USA. firstname.lastname@example.org
The most replicated finding in autism neuroanatomy-a tendency to unusually large brains-has seemed paradoxical in relation to the specificity of the abnormalities in three behavioral domains that define autism. We now know a range of things about this phenomenon, including that brains in autism have a growth spurt shortly after birth and then slow in growth a few short years afterward, that only younger but not older brains are larger in autism than in controls, that white matter contributes disproportionately to this volume increase and in a nonuniform pattern suggesting postnatal pathology, that functional connectivity among regions of autistic brains is diminished, and that neuroinflammation (including microgliosis and astrogliosis) appears to be present in autistic brain tissue from childhood through adulthood. Alongside these pervasive brain tissue and functional abnormalities, there have arisen theories of pervasive or widespread neural information processing or signal coordination abnormalities (such as weak central coherence, impaired complex processing, and underconnectivity), which are argued to underlie the specific observable behavioral features of autism. This convergence of findings and models suggests that a systems- and chronic disease-based reformulation of function and pathophysiology in autism needs to be considered, and it opens the possibility for new treatment targets.
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1 Corinthians 15 Authorized (King James) Version (AKJV)
1 Moreover, brethren, I declare unto you the gospel which I preached unto you, which also ye have received, and wherein ye stand;
2 by which also ye are saved, if ye keep in memory what I preached unto you, unless ye have believed in vain.
3 For I delivered unto you first of all that which I also received, how that Christ died for our sins according to the scriptures;
4 and that he was buried, and that he rose again the third day according to the scriptures:
Hebrews 6 Authorized (King James) Version (AKJV)
1 Therefore leaving the principles of the doctrine of Christ, let us go on unto perfection; not laying again the foundation of repentance from dead works, and of faith toward God,
2 of the doctrine of baptisms, and of laying on of hands, and of resurrection of the dead, and of eternal judgment.
3 And this will we do, if God permit.
4 For it is impossible for those who were once enlightened, and have tasted of the heavenly gift, and were made partakers of the Holy Ghost,
5 and have tasted the good word of God, and the powers of the world to come,
6 if they shall fall away, to renew them again unto repentance; seeing they crucify to themselves the Son of God afresh, and put him to an open shame.
7 For the earth which drinketh in the rain that cometh oft upon it, and bringeth forth herbs meet for them by whom it is dressed, receiveth blessing from God:
8 but that which beareth thorns and briers is rejected, and is nigh unto cursing; whose end is to be burned.