Vaccine News – Study – Blood Levels of Mercury Are Related to Diagnosis of Autism: A Reanalysis of an Important Data Set & VAXXED TV – Vaccines gave my son autism

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

Study – Blood Levels of Mercury Are Related to Diagnosis of Autism: A Reanalysis of an Important Data Set

M. Catherine DeSoto, PhD, Robert T. Hitlan, PhD
Department of Psychology, University of Northern Iowa, Cedar Falls, Iowa,

Abstract
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

Abstract
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

Study – Large brains in autism: the challenge of pervasive abnormality

Herbert MR.
Author information
Pediatric Neurology, Center for Morphometric Analysis, Massachusetts General Hospital, Charleston, MA 02129, USA. mherbert1@partners.org

Abstract
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.

VAXXED TV – Unvaccinated family with no cancer

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I’m a former pro vaccine nurse

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How to accept Jesus Christ as your personal Saviour

Testimony by Phil Robertson from Duck Dynasty

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.

 

Autism related studies

Autism related studies
Fever plus mitochondrial disease could be risk factors for autistic regression.

Abstract
Autistic spectrum disorders encompass etiologically heterogeneous persons, with many genetic causes. A subgroup of these individuals has mitochondrial disease. Because a variety of metabolic disorders, including mitochondrial disease show regression with fever, a retrospective chart review was performed and identified 28 patients who met diagnostic criteria for autistic spectrum disorders and mitochondrial disease. Autistic regression occurred in 60.7% (17 of 28), a statistically significant increase over the general autistic spectrum disorder population (P < .0001). Of the 17 individuals with autistic regression, 70.6% (12 of 17) regressed with fever and 29.4% (5 of 17) regressed without identifiable linkage to fever or vaccinations. None showed regression with vaccination unless a febrile response was present. Although the study is small, a subgroup of patients with mitochondrial disease may be at risk of autistic regression with fever. Although recommended vaccinations schedules are appropriate in mitochondrial disease, fever management appears important for decreasing regression risk.

Is fever a predictive factor in the autism spectrum disorders?

If it is confirmed that autistic children with high fevers are of higher functionality, it is possible for preventive intervention programs to be developed where children are exposed to the least possible chemical drugs intervention (antipyretics, antibiotics, etc.) or even selective vaccination. Further experimental, epidemiological and clinical studies are necessary to investigate the above.

Prevalence of autism spectrum disorders–Autism and Developmental Disabilities Monitoring Network, 14 sites, United States, 2008.

RESULTS:
For 2008, the overall estimated prevalence of ASDs among the 14 ADDM sites was 11.3 per 1,000 (one in 88) children aged 8 years who were living in these communities during 2008. Overall ASD prevalence estimates varied widely across all sites (range: 4.8-21.2 per 1,000 children aged 8 years). ASD prevalence estimates also varied widely by sex and by racial/ethnic group. Approximately one in 54 boys and one in 252 girls living in the ADDM Network communities were identified as having ASDs. Comparison of 2008 findings with those for earlier surveillance years indicated an increase in estimated ASD prevalence of 23% when the 2008 data were compared with the data for 2006 (from 9.0 per 1,000 children aged 8 years in 2006 to 11.0 in 2008 for the 11 sites that provided data for both surveillance years) and an estimated increase of 78% when the 2008 data were compared with the data for 2002 (from 6.4 per 1,000 children aged 8 years in 2002 to 11.4 in 2008 for the 13 sites that provided data for both surveillance years). Because the ADDM Network sites do not make up a nationally representative sample, these combined prevalence estimates should not be generalized to the United States as a whole.

Bactericidal Antibiotics Induce Mitochondrial Dysfunction and Oxidative Damage in Mammalian Cells

Abstract
Prolonged antibiotic treatment can lead to detrimental side effects in patients, including ototoxicity, nephrotoxicity, and tendinopathy, yet the mechanisms underlying the effects of antibiotics in mammalian systems remain unclear. It has been suggested that bactericidal antibiotics induce the formation of toxic reactive oxygen species (ROS) in bacteria. We show that clinically relevant doses of bactericidal antibiotics—quinolones, aminoglycosides, and β-lactams—cause mitochondrial dysfunction and ROS overproduction in mammalian cells. We demonstrate that these bactericidal antibiotic–induced effects lead to oxidative damage to DNA, proteins, and membrane lipids. Mice treated with bactericidal antibiotics exhibited elevated oxidative stress markers in the blood, oxidative tissue damage, and up-regulated expression of key genes involved in antioxidant defense mechanisms, which points to the potential physiological relevance of these antibiotic effects. The deleterious effects of bactericidal antibiotics were alleviated in cell culture and in mice by the administration of the antioxidant N-acetyl-L-cysteine or prevented by preferential use of bacteriostatic antibiotics. This work highlights the role of antibiotics in the production of oxidative tissue damage in mammalian cells and presents strategies to mitigate or prevent the resulting damage, with the goal of improving the safety of antibiotic treatment in people.