Candida Yeast

According to Henry Butt, M.D. of the University of Melbourne, a person’s general health depends largely on how well his or her body is able to absorb the byproducts of naturally present “gut flora.” Changes to our internal physical environment, especially persistent ones, can cause a variety of gastro-intestinal symptoms, such as diarrhea or abdominal distention. Patients with autism seem to be prone to such GI issues, which may be caused by an overabundance of yeast. According to some schools of thought, elevated yeast levels can cause a variety of autism-like symptoms, including increased sensory defensiveness, inappropriate laughter, and inattention. To date, however, there has been no proof that an elevated yeast level actually causes autism, and the etiology of autism remains unknown.

Ultimately, what Dr. Butt’s research shows is that while we are not yet able to pinpoint the causes of autism, we are reaching a point where we are able to ascertain whether or not secondary treatments, such as diet modification, are able to lessen some of the symptoms associated with autism. By additional outside factors that contribute to autism-like behaviors, we will perhaps be one step closer to finding the ultimate cause of this very prevalent disease.

An abstract of the lecture he presented at the 2011 ARMS Global Autism Conference can be found in HERE.

For more information on the validity of dietary changes and their effect on autism, please see the Mayo Clinic articles on autism and candida cleanse diets.

ICare4Autism Founder and President, Joshua Weinstein with Dr. W. Ted Brown

The Fragile X Syndrome is the most common inherited cause of intellectual disability. Fragile X has a population incidence of approximately 1 in 4,000 affected (full-mutation) males, 1 in 6,000 affected females, 1 in 700 premutation carrier males and 1 in 260 carrier females. This disorder typically causes moderate to severe intellectual deficiency in affected males, and milder deficiency in affected females.  It is associated with autism or PDD-NOS in about 50% of affected males, and most affected individuals evidence some autistic-like behaviors. 

Fragile X syndrome is considered to be the most common known single gene cause of autism. It is estimated that Fragile X accounts for 2-4% of intellectual deficiency overall, and is second to Down syndrome, which is not inherited, as a genetic cause of intellectual deficiency. The fragile X mutation results in the lack of expression of the Fragile X Protein (FMRP), an mRNA finding protein, which results in overexpression of the glutamate (stimulatory) and under-expression of the GABA (inhibitory) pathways in the brain.

Current experimental treatment trails are being carried out in Fragile X and in autism with glutamate receptor blockers and GABA stimulatory drugs.  The underlying defects in neurochemical pathways in both conditions appear to have much in common, involving the ERK, mTOR and PI3K signaling pathways.

Dr. W. Ted Brown will be speaking at the upcoming ICare4Autism International Conference on Autism, in Israel, about the relationship between Fragile X syndrome and autism.

W. Ted Brown, MD, PhD, is the Director of the New York State Institute for Basic Research (IBR) in Developmental Disabilities, Chair of the IBR Department of Human Genetics and Director of the IBR Jervis Clinic.  He is a fellow of the American College of Medical Genetics and Professor at the State University of New York- Downstate Medical Center in Brooklyn.

In 1991, he was appointed the Director of IBR’s Jervis Clinic and in 2005 became IBR’s Director. He is the author of more than 350 publications.  At IBR, he began research focused on the Fragile X syndrome, which was then newly recognized and is now considered to be the most common inherited cause of intellectual deficiency or mental retardation. At IBR, he established a DNA diagnostic and molecular laboratory. He developed a screening and prenatal testing program for Fragile X.

His work on Fragile X has ranged from clinical studies relating to phenotype, to family inheritance studies, to mouse model development, and to basic molecular research. His current research is focused on autism genetics and the Fragile X syndrome.

Eyal Ben-David and Sagiv Shifman, Hebrew University of Jerusalem

It is widely understood that different genes interact with environmental factors to influence autism, but new research finds a common ground as the various genes involved in autism appear to influence special processes in the brain.

Autism is influenced by many different genes, and different genes are involved in different individuals, making it hard to find the common genetic ground between patients.

Now, research conducted at the Hebrew University of Jerusalem has shown that the different genes involved in autism tend to be involved in specific processes in the brain. This can explain similarities in the behavioral symptoms of different people with autism, but also the large spectrum of behaviors observed in different individuals with autism.

The Hebrew University research, conducted by Dr. Sagiv Shifman and his doctoral student Eyal Ben-David of the Department of Genetics at the Alexander Silberman Institute of Life Sciences, has potential implications for early diagnosis as well as for treatment of autism in the future.

Dr. Shifman’s areas of interest are the genetics of schizophrenia and autism and genetics of variation in gene expression.  He will be speaking about this research “Shared neuronal pathways affected by common and rare variants in autism spectrum disorders” at ICare4Autism’s upcoming International Autism Conference in Jerusalem.

The mission of the Hebrew University project was to test the contribution of rare genetic mutations, as well as the genetic variations which are common in the population, and to see whether these different types of genetic risk factors are related. Instead of testing individual genes, the researchers chose to study gene collections, in an attempt to understand general pathways involved in autism.

Based on genetic data from thousands of families with autistic children, the researchers studied the contribution of different groups of genes to autism.

To their surprise, they found – when looking at mutations found in autism as well as thousands of common gene variants that are more frequently seen in individuals with autism – that these mutations and variations are located in specific functional groups.

When looking at families with one individual with autism (sporadic cases), and in families where there is more than one affected individual (multiplex cases), the same variants were seen acting in both cases. These groups of genes are highly active in the first year of life, and are involved in processes of learning, memory, and sensory perception.

The Hebrew University scientists believe that their work could pave the way for large-scale genetic scans in the future that could allow for early diagnosis of autism. Further, the results of their study provide a ray of hope that by concentrating on specific gene groups, it will one day be possible to design drugs which could alleviate symptom

Ben-David E, Shifman S (2012) Networks of Neuronal Genes Affected by Common and Rare Variants in Autism Spectrum Disorders. PLoS Genet 8(3):e1002556. doi:10.1371/journal.pgen.1002556

http://medicalxpress.com/news/2012-05-genetic-disrupted-autistic-brain.html

The study, led by Gladstone Investigator Jorge J. Palop, PhD, revealed that low levels of a protein, called Nav1.1, disrupt the electrical activity between brain cells. Such activity is crucial for healthy brain function and memory. Indeed, the researchers found that restoring Nav1.1 levels in mice that were genetically modified to mimic key aspects of Alzheimer’s disease (AD-mice) improved learning and memory functions and increased their lifespan.

“It is estimated that more than 30 million people worldwide suffer from Alzheimer’s disease and that number is expected to rise dramatically in the near future,” said Lennart Mucke, MD, who directs neurological research at Gladstone, an independent and nonprofit biomedical-research organization. “This research improves our understanding of the biological processes that underlie cognitive dysfunction in this disease and could open the door for new therapeutic interventions.”

In the brain, neurons form highly interconnected networks, using chemical and electrical signals to communicate with each other. The researchers investigated whether this communication between neurons is disrupted in AD-mice, and if so, how this may affect the symptoms of Alzheimer’s disease.

“Like a conductor in an orchestra, PV cells regulate brain rhythms by precisely controlling excitatory brain activity,” said Laure Verret, PhD, postdoctoral fellow and lead author. “We found that PV cells in patients with Alzheimer’s and in AD-mice have low levels of the protein Nav1.1 – likely contributing to PV cell dysfunction. As a consequence, AD-mice had abnormal brain rhythms. By restoring Nav1.1 levels, we were able to re-establish normal brain function.”

Indeed, the scientists found that increasing Nav1.1 levels in PV cells improves brain wave activity, learning, memory and survival rates in AD-mice.

“Enhancing Nav1.1 activity, and consequently improving PV cell function, may help in the treatment of Alzheimer’s disease and other neurological disorders associated with gamma-wave alterations and cognitive impairments such as epilepsy, autism and schizophrenia,” said Dr. Palop, who is also an assistant professor of neurology at the University of California, San Francisco, with which Gladstone is affiliated. “These findings may allow us to develop therapies to help patients with these devastating diseases.”

Gladstone Institutes. (2012, April 29). “Mechanism May Aid Treatment For Alzheimer’s And Neurological Disorders Associated With Gamma-Wave Alterations And Cognitive Impairments.“ Medical News Today. Retrieved from http://www.medicalnewstoday.com/releases/244665.php.

Verret, Laure; Mann, Edward O.; Hang, Giao B.; Barth, Albert M.I.; Cobos, Inma; Ho, Kaitlyn; Devidze, Nino; Masliah, Eliezer; Kreitzer, Anatol C.; Mody, Istvan; Mucke, Lennart; Palop, Jorge J. Inhibitory Interneuron Deficit Links Altered Network Activity and Cognitive Dysfunction in Alzheimer Model.  Cell doi:10.1016/j.cell.2012.02.046 (volume 149 issue 3 pp.708 – 721)

Philip Landrigan, MD, MSc, a world-renowned leader in children’s environmental health and Director of the Children’s Environmental Health Center (CEHC) at Mount Sinai School of Medicine, co-authored the editorial, entitled “A Research Strategy to Discover the Environmental Causes of Autism and Neurodevelopmental Disabilities,” along with Luca Lambertini, PhD, MPH, MSc, Assistant Professor of Preventive Medicine at Mount Sinai and Linda Birnbaum, Director of the National Institute OF Environmental Health Sciences.

The National Academy of Sciences reports that 3 percent of all neurobehavioral disorders in children, such as autism spectrum disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD), are caused by toxic exposures in the environment and that another 25 percent are caused by interactions between environmental factors and genetics. But the precise environmental causes are not yet known. While genetic research has demonstrated that ASD and certain other neurodevelopmental disorders have a strong hereditary component, many believe that environmental causes may also play a role – and Mount Sinai is leading an effort to understand the role of these toxins in a condition that now affects between 400,000 and 600,000 of the 4 million children born in the United States each year.

“A large number of the chemicals in widest use have not undergone even minimal assessment of potential toxicity and this is of great concern,” says Dr. Landrigan. “Knowledge of environmental causes of neurodevelopmental disorders is critically important because they are potentially preventable.”

CEHC developed the list of ten chemicals found in consumer products that are suspected to contribute to autism and learning disabilities to guide a research strategy to discover potentially preventable environmental causes. The top ten chemicals are:

1. Lead
2. Methylmercury
3. PCBs
4. Organophosphate pesticides
5. Organochlorine pesticides
6. Endocrine disruptors
7. Automotive exhaust
8. Polycyclic aromatic hydrocarbons
9. Brominated flame retardants
10. Perfluorinated compounds

In addition to the editorial, there were four papers published which also call for increased research to identify the possible environmental causes of autism in America’s children.

Source: Mount Sinai Hospital

Furthermore, this kind of research could lead to better treatments for a subset of children with elevated levels of certain compounds in their urine, said James Woods, a researcher at the University of Washington who worked with Battelle researchers on the project.

While the study was relatively small, including 76 boys, Nick Heyer, a senior research scientist at Battelle’s Seattle lab, who worked on the study and said he’s hopeful it can be replicated on a larger scale and lead to a widely available screening test for babies.

“If it can detect increased risk of autism at age 1, that would be fantastic,” he said. “It’s the only biomarker (test) I’m aware of that could be done non-invasively and fairly inexpensively.

“I’m really pretty optimistic and excited about getting it retested.”

Heyer said he is trying to incorporate the urine test into a study that will include 1,200 mothers who have autistic children and are pregnant again. The researchers would follow the new babies’ development through age 3. He’s also working with a laboratory in South Korea to reproduce the study in a larger group.

The test looks for elevated levels of compounds called porphyrins and costs between $50 and $100. Woods said the cost would come down if the test were used frequently to screen babies.

Woods said everybody has the compounds in their urine, but some of the children in the study had clearly elevated levels.

The study included only boys, who are much more likely to have autism than girls, but the test likely would work for both genders based on other research, Woods said.

Heyer said there’s been speculation that elevated porphyrin levels are connected to mercury exposure in children with autism, but the research team found no link to increased exposure to mercury, leaving open the question of why the compounds are higher in some children with autism.

“I’m not a supporter of the concept that this is due to mercury exposure,” he said. “There’s no evidence in my mind that that should be the reason for this.”

Woods JS, Armel SE, Fulton DI, Allen J, Wessels K, et al. 2010 Urinary Porphyrin Excretion in Neurotypical and Autistic Children. Environ Health Perspect 118(10): doi:10.1289/ehp.0901713

Overall, they found autism had been diagnosed in 10 percent to 11 percent of full siblings and 5 percent to 7 percent of half-siblings.

The new finding may not be a surprise – given that half-siblings share about 25 percent of their genes – but provides new clues to how autism is inherited.

The study included more than 5,000 U.S. families enrolled in a nationwide autism registry in which there was a child with autism and at least one other sibling. Included were 619 families with at least one maternal half-sibling, meaning the children shared the same mother but not the same father. The researchers compared autism recurrence among the half-siblings to the rate among the full siblings.

The researchers also looked at half-siblings in a group of St. Louis families to try to replicate the findings from the larger study.

“We found that autism risk for half-siblings is about half of what it is for full siblings,” principal investigator Dr. John Constantino, director of child and adolescent psychiatry at the Washington University School of Medicine in St. Louis and psychiatrist-in-chief at St. Louis Children’s Hospital, said in a university news release.

“Most of the half-siblings we studied had the same mothers. Given that half of the risk of transmission was lost and half was preserved among those maternal half-siblings, mothers and fathers appear to be transmitting risk equally in families in which autism recurs,” Constantino said.

The findings also suggest that in many families, the transmission of autism from parents to children is the result of the effects of many genes, with each contributing a small proportion of the risk, he said.

The study was published online April 16 in the journal Molecular Psychiatry.

Sources:

J N Constantino, A Todorov, C Hilton, P Law, Y Zhang, E Molloy, R Fitzgerald, D Geschwind. Autism recurrence in half siblings: strong support for genetic mechanisms of transmission in ASD. Molecular Psychiatry, 2012; DOI:10.1038/mp.2012.9

Washington University in St. Louis (2012, April 17). Study of half siblings provides genetic clues to autism. ScienceDaily. Retrieved April 23, 2012, from http://www.sciencedaily.com­/releases/2012/04/120417143849.htm

Attendees at past ICare4Autism International Autism Conference

On August 1-2, 2012, more than 1,500 leaders in autism research, educationand policy from every continent will gather in Jerusalem, Israel, for ICare4Autism‘s 2012 International Conference, “Autism: A Global Perspective“.

Dr.Joshua Weinstein, CEO & Founder indicated that the, “Conference will highlight groundbreaking research into the causes and treatments of Autism Spectrum Disorders, and serve as a catalyst for powerful new collaborations to tackle the global autism crisis”.

Students from around the world are invited to present their autism research at a poster session. One poster will be selected by the review committee to receive a scholarship to attend the Conference.  The scholarship will cover travel, hotel accommodations and conference registration fee. The scholarship winner will also be invited to participate on one of the Conference panels. The Poster Session consists of physical displays (aka posters) of information shown during a 60-90 minute session, with presenters standing by their poster reporting empirical research and pilot projects for future research.  Attendees have the opportunity to speak with the presenters about their work.

Dame Stephanie Shirley, The British Government’s Founding Ambassador for Philanthropy, and Chairman of the Shirley Foundation, will deliver the Keynote Address and The First Lady of Panama Mrs. Marta Linares de Martinelli will be giving opening remarks.

They will be joined by distinguished researchers and practitioners from more than 20 countries who will unveil their latest biomedical discoveries andeducational innovations.

Groundbreaking biomedical research will be presented; notably Henry Markram, Ph.D, the Director of Blue Brain Project, Coordinator of the Human Brain Project and Professor at Swiss Federal Institute for Technology (EPFL) will present, “Prospects of using detailed brain simulations to explore possible causes and treatments of Autism”

Innovativeeducational practices will be featured in presentations by Dr. S. Mariam Aljunied (Senior Autism Specialist, Singapore Ministry of Education); Dr.Carlos MarcinSalazar (Director of the National Autism Clinic of Mexico); and Dr. Pamela Wolfberg (Director, Autism Spectrum Program,UniversityofCalifornia San Francisco). Attendees will tour the campus where ICare4Autism will open the world’s first Global Autism Research andEducationCenterin 2015.

ICare4Autism (InternationalCenterfor Autism Research & Education) is a charitable organization, founded in 2004 to catalyze breakthrough innovations in autism research, diagnosis and treatment.

Among them will be Beth Israel Deaconess Medical Center (BIDMC) neuroscientist Lindsay Oberman, PhD, using noninvasive brain stimulation and neuroimaging tools to study the brain in children and adults with autism spectrum disorders.

“The work that Lindsay will be pursuing has the potential to impact the lives of many individuals with these devastating disorders, as well as the lives of their families,” explains Alvaro Pascual-Leone, MD, PhD, Director of the Berenson-Allen Center for Noninvasive Brain Stimulation at BIDMC and Oberman’s Harvard Catalyst mentor. “This MeRIT program support enables junior scientists to advance their research so that they can reach the next level as clinical and translational scientists.”

Oberman uses transcranial magnetic stimulation (TMS) to probe brain plasticity in ASD patients. TMS is a noninvasive technique in which a magnetic field is generated through a flat “paddle” placed against a patient’s scalp. The painless procedure results in the induction of electric currents and enables Oberman to target small areas of the brain to either enhance or reduce activity and measure the effects on subjects’ neural circuitry.

“Plasticity refers to changes in the brain that stem from new experiences, such as studying a new language or any other learning experience,” explains Oberman, who is also an Instructor of Neurology at Harvard Medical School. “In patients with ASD, we think that these mechanisms of plasticity are abnormally high or ‘hyperplastic.’

“Our research is demonstrating that in individuals with no evidence of autism, these changes in the brain last about 30 minutes,” she explains. But, she adds, among adults with ASD, the brain changes last much longer, 90 minutes on average.

“This suggests that for ASD patients any new experiences are causing lasting brain changes, thereby leading to the communication and social deficits that often characterize these conditions,” says Oberman.

In addition, hyperplasticity may also explain some savant abilities demonstrated by some ASD patients; in such instances, patients are extremely gifted in one area, such as musical ability, in contrast to their overall developmental limitations. But, adds Oberman, on balance, it appears that hyperplasticity results in more problems than benefits for these individuals.

“If our studies in children are consistent with the data we’ve gathered from our adult research subjects, we may eventually be able to use hyperplasticity as a means of diagnosing autism in young children, before the onset of behavioral symptoms,” explains Oberman.

http://www.bidmc.org/News/InResearch/2010/January/LindsayOberman.aspx

In particular, of the 29 cytokine levels investigated, the researchers found disturbed levels in five related to the T-helper cell immune system and three involved in hematopoiesis or the production of blood cells possibly affecting antibody production required for normal functioning of the immune system.

Both the immune system and genetic factors have been implicated in the biological basis for autism, said Merlin G. Butler, professor of psychiatry at the KU Medical Center. “Our study further supports a disturbed immune system in children with classic autism that may be related to genetic factors as cytokine proteins are coded by genes distributed among the human chromosomes.”

Additionally, studies in families with autism have shown the significant contribution of genetics, including deletions and duplications of chromosomes and mutations or variants found in specific genes involved with brain development and function, he said.

“The importance of identifying early immunological disturbances that may contribute to autism has implications for identifying risk factors, diagnosis and possibly intervention as cytokines may play a role in the function of the developing brain,” he said.

The study was one of the largest of its kind to date, analyzing the plasma of 99 children with AD between 5 and 10 years of age and that of 40 age- and gender- matched unrelated healthy siblings without AD under the same clinical assessments, specimen processing and laboratory conditions. The male-to-female ratio closely matches that seen in the ASD population, and there were gender-based differences found in five cytokines.

Butler said that the purpose of this research is linking the genes encoding immune-related proteins and cytokines to ASD along with identifying the sequence of the events during critical periods of brain and neurological development. This could allow for earlier recognition, diagnosis and potential treatment.

Ann Manzardo, assistant professor of psychiatry, was the first author on the study. The study was published in the April 2012 International Journal of Developmental Neuroscience.