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JANUARY
20 – 22, 2012 American Legion, Philadelphia, NY 58 Main Street
Friday: Pasta Dinner: 5:00
– 7:00 $8.00
Dinner & Dance: $12.00 Dance Only: $5.00 8:00 – 11:00 Saturday: Psychic Fair 10:00
– 4:00 Sunday: Craft Fair, Bake Sale
11:00 – 4:00 Hamburgs, hot dogs, chili Raffles, Wilson’s book sale
Research proposes common link between autism, diabetes Study implicates hyperinsulinemia
in increased incidence of autism HOUSTON -- (Oct. 19, 2011) -- A review of the genetic and biochemical abnormalities associated
with autism reveals a possible link between the widely diagnosed neurological disorder and Type 2 diabetes, another medical
disorder on the rise in recent decades. "It appears that both Type 2 diabetes and autism have a common underlying
mechanism -- impaired glucose tolerance and hyperinsulinemia," said Rice University biochemist Michael Stern, author
of the opinion paper, which appears online in this month's issue of Frontiers in Cellular Endocrinology. Hyperinsulinemia,
often a precursor to insulin resistance, is a condition characterized by excess levels of insulin in the bloodstream. Insulin
resistance is often associated with both obesity and Type 2 diabetes. "It will be very easy for clinicians
to test my hypothesis," said Stern, professor of biochemistry and cell biology at Rice. "They could do this by
putting autistic children on low-carbohydrate diets that minimize insulin secretion and see if their symptoms improve."
Stern said the new finding also suggests that glucose tolerance in pregnant women may need to be addressed more seriously
than it is now. Stern said he first realized there could be a common link between Type 2 diabetes and autism a few
years ago, but he assumed someone else had already thought of the idea. Stern's lab, which is located at Rice's BioScience
Research Collaborative, specializes in investigating the genetic interactions associated with genetic diseases like neurofibromatosis,
a disorder in which patients are several times more likely to be afflicted with autism and autism spectrum disorders (ASD)
like Asperger's syndrome. Autism and ASD are neurological disorders that have a strong but poorly understood genetic
basis. The U.S. Centers for Disease Control and Prevention estimates that about nine out of 1,000 U.S. children are diagnosed
with ASD. Stern said at least four genes associated with increased frequency in autism are known to produce proteins
that play key roles in a biochemical pathway known as PI3K/Tor. Stern said he had been studying a form of abnormal function
in the synapses of fruit flies that was remarkably similar to abnormalities observed in rats and mice with defects in a
different pathway known as mGluR-mediated long-term depression. "I had also spent a lot of time thinking about
insulin signaling because another project in my lab is an endocrinology project in which we're studying how key proteins
involved in insulin signaling affect the timing of metamorphosis in fruit flies," Stern said. From his studies
in both areas, Stern knew two things: PI3K/Tor was the major pathway for insulin signals within cells, and insulin could
affect synapses in a remarkably similar way to the mGluR defects associated with autism. "When I read that
the incidence of autism was increasing, and combined that with the fact that the incidence of Type 2 diabetes is also increasing,
it seemed reasonable that each increase could have the same ultimate cause -- the increase in hyperinsulinemia in the general
population," Stern said. "I didn't do anything with this notion for a few years because it seemed so obvious that
I figured everyone already knew this hypothesis, or had tested it and found it was not true." Stern said he
changed his mind a few months ago when a health care consulting firm asked him to provide input about autism. "In
preparing for this interview, I discovered that gestational diabetes was the most important identified maternal risk factor
for autism, but that 'no known mechanism could account for this,'" Stern recalled. "When I read this, I was speechless.
That's when I realized that this was not obvious to others in the field, so I decided to write this up with the hope that
clinicians might become aware of this and treat their patients accordingly." In writing the article, Stern said
he learned that the role of insulin in cognitive function is becoming more widely accepted. "I was checking to
see if insulin was known to affect synaptic function, and I learned that the nasal application of insulin is already being
tested to see if it is beneficial for both Alzheimer's and schizophrenia." Stern said he also found preliminary
studies that indicated that low-carb diets were therapeutic for some individuals with autism and ASD. "Based
on what's already in the literature, insulin needs to be taken seriously as a causative element in autism," Stern said.
"I hope that clinicians will take the next step and put this to a rigorous test and determine how to best use this
information to benefit patients." ### VIDEO is available at: http://www.youtube.com/watch?v=GGizH7NaRxY A high-resolution image is available for download at: http://www.media.rice.edu/images/media/NEWSRELS/Stern.jpg
CAPTION: Michael Stern
CREDIT: Jeff Fitlow/Rice University The opinion article is available at: bit.ly/r4SALm Located on a 300-acre forested campus in Houston, Rice University is consistently ranked among the nation's top
20 universities by U.S. News & World Report. Rice has highly respected schools of Architecture, Business, Continuing
Studies, Engineering, Humanities, Music, Natural Sciences and Social Sciences and is known for its "unconventional
wisdom." With 3,485 undergraduates and 2,275 graduate students, Rice's undergraduate student-to-faculty ratio is less
than 6-to-1. Its residential college system builds close-knit communities and lifelong friendships, just one reason why
Rice has been ranked No. 1 for best quality of life multiple times by the Princeton Review and No. 4 for "best value"
among private universities by Kiplinger's Personal Finance. To read "What they're saying about Rice," go to http://futureowls.rice.edu/images/futureowls/Rice_Brag_Sheet.pdf.
CHEST: Airway Anomaly Linked to Autism
By Todd Neale, Senior Staff Writer, MedPage Today
Published: October 25, 2011
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse
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HONOLULU -- A specific airway
abnormality may be an objective marker for autism spectrum disorders in children, a small study showed. A doubling
of the take-off to the lower airways occurred in 49 children who underwent a bronchoscopy, all of whom had been diagnosed
previously with an autism spectrum disorder, according to Barbara Stewart, MD, a pediatric pulmonologist at Nemours Children's
Clinic in Pensacola, Fla. A search of the literature revealed that such an abnormality has never been described
before in any individual, regardless of autism status, she reported at the CHEST meeting here.
Action
Points
- Note that this study was published as an abstract and presented
at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
- Explain that a pediatric pulmonologist found a double take-off to the lower airways in 49 children
undergoing bronchoscopy for the workup of chronic cough, a finding she had not observed previously.
- Point
out that later, when looking for shared characteristics in these children, she noted that all of them had been diagnosed
with autism spectrum disorder.
Thus, the presence of "doublets" could provide objective support
for an autism diagnosis, which is provided subjectively through observing the behaviors of the child. Stewart stressed,
however, that bronchoscopy should not be performed for the purpose of making or confirming an autism spectrum disorder diagnosis
because it is an invasive procedure that carries some risks. If children with autism "have another reason to have
a bronchoscopy, it would be okay to look for doublets," she said, "but I wouldn't do it on anybody just to see
if they have a diagnosis of autism." Stewart added that she is not aware of a less invasive way to observe the doublets.
She said that it took about seven years for her to make the connection between this airway abnormality and autism spectrum
disorders. In children with the doublets, the trachea appears normal, but there are two take-offs into each of the
lobes of the lung instead of the normal one. All 49 of the patients on whom Stewart performed a bronchoscopy (mean
age 3 years) presented with a cough that was unresponsive to therapy. The bronchoscopy was part of the diagnostic work-up.
When Stewart retrospectively reviewed the charts to try to find a factor connecting all of the children, she came up with
only one -- the diagnosis of an autism spectrum disorder. The doublets may result in higher airway resistance, which
could explain why autistic children are not generally very athletic, Stewart said. "They may tire quicker and
they may get short of breath, and that may be secondary to their doubling in their airway," she said. She said
the next steps would be to confirm the findings and also examine the genetic cause of the airway abnormality. Stewart reported that she had no conflicts of interest. |
Primary source: CHEST 2011
Source reference:
Stewart B "Can bronchoscopic
airway anatomy be an indicator of autism?" CHEST 2011; Abstract 388A.
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Genetic variant and autoantibodies linked to having a child with autism
Font size:   Finding may lead to screening test to identify susceptibility to having an autistic child
(SACRAMENTO, Calif.) — A study by researchers
at UC Davis has found that pregnant women with a particular gene variation are more likely to produce autoantibodies to
the brains of their developing fetuses and that the children of these mothers are at greater risk of later being diagnosed
with autism. The finding is the first to demonstrate a genetic mechanism at play in the development
of the neurodevelopmental disorder among some children -- offering the possibility of a genetic test for some women
at risk for having a child with autism, said Judy Van de Water, an immunologist and the study's co-principal investigator. Judy Van
de Water (right) works with student researcher (left).  "Association of a MET genetic variant with autism-associated maternal autoantibodies to fetal brain proteins
and cytokine expression," is published online today in the journal Translational Psychiatry, a Nature publication.
"Our study gives strong support for the idea that, in at least some cases,
autism results from maternal immunity gone overboard," said Judy Van de Water, a professor of internal medicine and
a researcher affiliated with the UC Davis MIND Institute. "This is the first time that a genetic factor known to be important in autism and its effects have been demonstrated."
Autism is a neurodevelopmental disorder that affects a child's ability to learn and communicate socially. It affects
an estimated 1 in 110 children in the United States, according to the U.S. Centers for Disease Control and Prevention.
For the study, Van de Water and her colleagues examined the action of the MET gene, which has a known association with
autism, among 200 mothers of children with autism and 150 mothers of typically developing children enrolled in the Northern
California-based Childhood Autism Risks from Genetics and the Environment (CHARGE) Study. All of the study
participants were between 24 and 60 months of age at the time of study enrollment, lived with one biological parent, and
spoke either English or Spanish. The researchers found that the C-allele of the MET gene is more common in mothers
with several immunologic abnormalities that might contribute to the development of autism. Analysis of the MET C-allele
is a method of determining susceptibility for immune dysregulation in the mothers. One abnormality they attributed
to the MET C allele is the presence of antibodies against fetal brain proteins in the blood of the mothers. These brain-attacking
antibodies occur in some mothers with an autistic child, but are not found in mothers of typically developing children.
It is believed that these antibodies somehow injure the developing brain of the fetus, and in some instances may cause
autism. Researchers do not yet know when or how the antibodies are formed, or precisely what happens to the brain
tissue exposed to them, but based on a collaborative paper with Loren Martin at Azuza Pacific University, they appear
to have pathologic significance, or a functional effect on brain development, changing the way the brain develops. Van
de Water and her group are still working on the precise effect of these maternal antibodies on the developing brain.
The investigators also found that MET protein levels are reduced in cells from mothers with one C allele and one normal
allele, and were even lower in those with two C alleles. Lower MET protein on the cell surface may increase susceptibility
to a more intense and prolonged immune response when the cells are activated, like exposure to a bacteria or virus. This,
in turn, could make these individuals more prone to forming antibodies against 'self' proteins, such as those found in
the fetal brain. In addition, the investigators evaluated the functional polymorphism in the study participants'
immunological cytokines, molecules that tell other cells what to do. The cytokine IL-10, an important anti-inflammatory
marker, was reduced in women with the MET C allele. IL-10 is a well-studied immunosuppressive molecule that is important
for preventing autoimmunity. A reduction in IL-10 would increase the chances that an inflammatory response would continue
unchecked. "The convergence of these two distinct associations with autism risk -- that of maternal antibodies
to fetal brain proteins and the MET C allele -- provides the first link between an autism susceptibility gene and its
effects," Van de Water said. Daniel B. Campbell, assistant professor of psychiatry and the behavioral sciences
at the Zilkha Neurogenetic Institute of the University of Southern California, is co-principal investigator of the
study. "The presence of maternal antibodies to fetal blood proteins is one of the best markers known for autism,
accounting for about 12 percent of cases. In contrast, genetic factors previously identified in children with autism account
for only 2 or 3 percent of cases," Campbell said. "Now we not only have a marker, but we are starting
to understand the actual mechanisms of what causes autism," Campbell said. "These findings can greatly enhance
our understanding of the origins of some cases of autism and may directly lead to screening tests and treatments to prevent
it." Why women with the C allele form antibodies against fetal brain proteins is another important area of
interest, according to Van de Water, because it suggests a hyper-responsive immune system. Proteins associated with the
MET gene function as key blockers of immune activity. "Our study has found that a kind of safety switch that
regulates the immune system and prevents it from targeting the brain of the developing fetus is defective in some mothers
of children who later develop autism," Van de Water said. Van de Water said the relationship between autism
and aberrations in the immune system, once a radical notion in the scientific community, is now becoming a well-accepted
and very fruitful focus of research. "While it is not known how the antibody response against fetal brain proteins
arise, it may be possible to one day treat susceptible women to reduce the likelihood of having an autistic child,"
Van de Water said. Other study authors include Paul Ashwood, Luke Heuer, and Daniel Braunschweig, all of UC
Davis. At the UC Davis MIND Institute, world-renowned scientists engage in research to find improved treatments as
well as the causes and cures for autism, attention-deficit/hyperactivity disorder, fragile X syndrome, Tourette syndrome
and other neurodevelopmental disorders. Advances in neuroscience, molecular biology, genetics, pharmacology and behavioral
sciences are making inroads into a better understanding of brain function. The UC Davis MIND Institute draws from these
and other disciplines to conduct collaborative, multidisciplinary research. For more information, visit mindinstitute.ucdavis.edu.
Study: Many Sunscreens May
Be Accelerating CancerWASHINGTON
(May 24) -- Almost half of the 500 most popular sunscreen products may actually increase the speed at which malignant cells
develop and spread skin cancer because they contain vitamin A or its derivatives, according to an evaluation of those products
released today. AOL News also has learned through documents and interviews that the Food and Drug Administration
has known of the potential danger for as long as a decade without alerting the public, which the FDA denies. The
study was released with Memorial Day weekend approaching. Store shelves throughout the country are already crammed with tubes,
jars, bottles and spray cans of sunscreen. The white goop, creams and ointments might prevent sunburn. But don't
count on them to keep the ultraviolet light from destroying your skin cells and causing tumors and lesions, according to researchers
at Environmental Working Group. In their annual report to consumers on sunscreen, they say that only 39 of the
500 products they examined were considered safe and effective to use. The report cites these problems with bogus
sun protection factor (SPF) numbers: - The use of the hormone-disrupting chemical oxybenzone, which penetrates the skin
and enters the bloodstream.
- Overstated claims about performance.
- The lack of needed regulations and oversight
by the Food and Drug Administration.
But the most alarming disclosure in this year's report is the finding
that vitamin A and its derivatives, retinol and retinyl palmitate, may speed up the cancer that sunscreen is used to prevent.  Environmental Working Group The industry
includes vitamin A in its sunscreen formulations because it is an anti-oxidant that slows skin aging. But the
EWG researchers found the initial findings of an FDA study of vitamin A's photocarcinogenic properties, meaning the possibility
that it results in cancerous tumors when used on skin exposed to sunlight. "In that yearlong study, tumors
and lesions developed up to 21 percent faster in lab animals coated in a vitamin A-laced cream than animals treated with a
vitamin-free cream," the report said. The conclusion came from EWG's analysis of initial findings released
last fall by the FDA and the National Toxicology Program, the federal government's principle evaluator of substances that
raise public health concerns. EWG's conclusions were subsequently scrutinized by outside toxicologists. Based on the strength of the findings by FDA's own scientists, many in the public health community say they can't believe
nor understand why the agency hasn't already notified the public of the possible danger. "There was enough
evidence 10 years ago for FDA to caution consumers against the use of vitamin A in sunscreens," Jane Houlihan, EWG's
senior vice president for research, told AOL News. "FDA launched this one-year study, completed their research
and now 10 years later, they say nothing about it, just silence." On Friday, the FDA said the allegations
are not true. "We have thoroughly checked and are not aware of any studies," an FDA spokesperson told
AOL News. She said she checked with bosses throughout the agency and found no one who knew of the vitamin A sunscreen research
being done by or on behalf of the agency. But documents from the FDA and the National Toxicology Program showed
that the agency had done the research. "Retinyl palmitate was selected by (FDA's) Center for Food Safety
and Applied Nutrition for photo-toxicity and photocarcinogenicity testing based on the increasingly widespread use of this
compound in cosmetic retail products for use on sun-exposed skin," said an October 2000 report by the National Toxicology
Program. FDA's own website said the animal studies were done at its National Center for Toxicological Research
in Jefferson, Ark. And it was scientists from the FDA center and National Toxicology Program who posted the study data last
fall. In a perfect worldThe ideal sunscreen would completely block the UV rays that
cause sunburn, immune suppression and damaging free radicals. It would remain effective on the skin for several hours and
not form harmful ingredients when degraded by UV light, the report said.  National Cancer Institute Graph of melanoma of the skin rates from 1975 to
2006. APC stands for annual percent change and AAPC stands for average annual percent change. But in the
U.S., there is currently no sunscreen that meets all of these criteria. European countries have more chemical combinations
to offer, but in the U.S. the major choice is between the "chemical" sunscreens, which have inferior stability,
penetrate the skin and may disrupt the body's hormone systems, and "mineral" sunscreens zinc and titanium dioxide.
Increasingly, as AOL News reported in March, the industry is using titanium dioxide that is made nanosized, which a growing number of researchers believe have
serious health implications. The sunscreen industry cringes when EWG releases its yearly report -- this is its
fourth. The industry charges that the advocacy group wants to do away with all sunscreen products, a claim that is not accurate.
The report's researchers clearly say that an effective sunscreen prevents more damage than it causes, but it wants
consumers to have accurate information on the limitations of what they buy and on the potentially harmful chemicals in some
of those products. EWG does warn consumers not to depend on any sunscreen for primary protection from the sun's
harmful ultraviolet rays. Hats, clothing and shade are still the most reliable sun protection available, they say. Don't count on the numbers Some of us are old enough to remember when the idea of having a
tan was good, a sign of health, when billboards and magazine ads featured the Coppertone girl showing off her tan when a puppy
pulls down her bathing suit bottom. Going for that tan, we coated our kids and ourselves with sun blockers with
sun protection factors of 1 or 2. Some overly cautious parents might have smeared on a 4 during the hottest part of a day. But we've learned of the dangers that come from exposure to the sun's rays, especially ultraviolet A and B. So today,
drugstore shelves are crammed with sunscreens boasting SPFs of 30, 45, 80 or even higher. However, the new report
says those numbers are often meaningless and dangerous because products with high SPF ratings sell a false sense of security,
encouraging people using them to stay out in the sun longer. "People don't get the high SPF they pay for,"
the report says. "People apply about a quarter of the recommended amount. So in everyday practice, a product labeled
SPF 100 really performs like SPF 3.2, an SPF 30 rating equates to a 2.3 and an SPF 15 translates to 2." In
2007, the report says, the FDA published proposed regulations that would prohibit manufacturers from labeling sunscreens with
an SPF higher than "SPF 50." The agency wrote that higher values would be "inherently misleading," given
that "there is no assurance that the specific values themselves are in fact truthful." This is being
widely ignored by the sunscreen makers who are heavily advertising their 80, 90 and 100 SPF products. "Flouting
FDA's proposed regulation," companies substantially increased their high-SPF offerings in 2010 with one in six brands
now listing SPF values higher than 50. "Neutrogena and Banana Boat stand out among the offenders, with six and four products
labeled as 'SPF 100,' respectively," the new report says. The full list of the best and worst sunscreens can
be found on the EWG's searchable database. (Update: The database has been loading slowly today. You may want to try it again later.)
http://www.aolnews.com/2010/05/24/study-many-sunscreens-may-be-accelerating-cancer/
News To Help Keep You Informed Recall...there
is a recall of Romaine lettuce produced by Freshway Foods effective May 6, 2010 since E.coli 0145 has been linked to a recent
foodborne outbreak in New York, Michigan and Ohio in which 12 people have been hospitalized, 3 with possible life-threatening
complications called hemolytic uremic syndrome (HUS).
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