
News 26 juni 2009
Vitamine C and prevention of autism
caused by heavy metals toxicity
Phil Bate PhD autism study request
I am still trying desperately to get my
simple, cheap, and effective autism prevention therapy broadcast to the world. It is very
difficult to get people interested that can help me. I am asking for you to help if you
will. There's no money involved. Those of you who belong to "social networks"
such as YouTube, Twitter, etc, please send the following message to your account on all
o;f these sites:
There is a new simple, cheap, and effective
Autism Prevention method. Here it is: Less than 1% of all MD's in the USA are even aware
that vitamin C takes all minerals, including heavy metals out of the body. It's not true
chelation, as vitamin C combines metabolically, but it's the same result. Take out all,
and put back in needed. Most MD's even believe that the RDA of 75 mg is correct for good
health, when 4000 mg is the zoo RDA for a 150 pound ape. (Apes are more valuable it
seems.) Mineral analysis of people who use 2000-5000 mg (2-5 grams) per day of vitamin C
for a year or so show heavy metals toxicity so low as to be immeasurable. We have an
epidemic of autism, mostly caused by mercury, aluminum, and/or lead toxicity.
This toxicity is increasing in our culture
and pregnant women are more and more subject to this environmental poisoning. This is
creating infant toxicity before birth such that the infant liver may be near toxic levels,
and the addition of vaccines using these preservatives overloads the infant liver and
actually kills brain cells. A simple and cheap prevention is to have any pregnant woman
start on 4 grams per day of cheap vitamin C (less than $30 for 9 months supply at Costco).
If she takes 2 1000 mg tablets at breakfast and 2 more at dinner, and then takes pre-natal
vitamins and vitamins at lunch, the "shared" blood stream of mother and fetus
will be gradually cleared of mercury and other heavy metals. This allows the birth of a
baby that is not near toxic levels in that tiny liver, and now is able to handle further
toxic loads. Autism is a "bankruptcy" disease to families. Instead of spending
millions on "cure", let's spend a small amount on prevention. But, MD's need to
be re-educated about vitamin C. Big Pharma has done a job with their refutation of Linus
Pauling, and the other scientists work below: Dr. Frederick R. Klenner's Clinical Guide to
the Use of Vitamin C is posted in its entirety at Link
His work on mercury toxic doses and vitamin
C is particularly to the point. The complete text of Irwin Stone's book The Healing Factor
is posted for free reading at link. A
very large number of full-text papers on curing illness with vitamin C are posted at Link . These include Frederick R.
Klenner. Link by Andrew Saul
As the only psychologist in the
Orthomolecular Medical Society for many years and a personal friend of Abram Hoffer and
Carl Pfeiffer, I know the above vitamin C facts as true. I have personally taken 4 grams
per day of vitamin C (as above), for a number of years, my recent mineral analysis shows
the only heavy metals even measurable are aluminum and arsenic, and both are extremely low
on the toxic level. (My wife cooks with aluminum, and we get fresh vegetables from
possible insecticide sprayed fields.) I have personally used vitamin C in my former
practice to solve many cases of schizophrenia caused by excessive copper using 10 grams
per day of vitamin C very successfully. These cases included both the Wilson's family
gene, and some women that the birth control pill had been involved in the copper uptake. I
have also used vitamin C to chelate out mercury in cases of depression successfully. This
simple and cheap therapy has the potential to stop the current epidemic of autism, and at
least bring it back to the 1 case in 10,000, instead of the current 1 in less than 150.
Also, simple to test the validity. Find 100-1000 recently pregnant women, and start this
regimen. If under 6 months left in pregnancy, go to 3 grams per dose, etc. I am retired
and have a net worth around $100,000, so cannot fund such myself. Help me to publicize it.
None of the many "charitable"
groups seem to be interested in preventing autism. Perhaps they remember what happened to
"March of Dimes" after Salk found the polio vaccine? Thanks to all who do the
above. You may have saved families from aautism bankruptcy. Please forward the above also
to all pregnant women you know, and ask them to forward it again. If everyone does this to
just 2 people, we'll cover the world shortly, and save a lot of unborn babies from autism.
Phil Bate PhD (drbate@bellsouth.net)
Inventor of Neuroliminal Training
Tip: Marjan Reuvers
Migraine and Increased Risk of
Cardiovascular Disease
Women who have migraines with aura may be more likely to have a stroke or heart attack
than women who dont have the condition, and the association varies by migraine
frequency, according to research published in the June 24, 2009, online issue of
Neurology®, the medical journal of the American Academy of Neurology. An aura is a visual
or other sensory disturbance that occurs before the migraine starts, such as seeing bright
lights. The study found that women with migraine with aura whose migraines occur at least
once a week are more than four times as likely to have a stroke as women who do not have
migraines. Women with migraine with aura who have migraines less than once a month were
more than twice as likely to have a heart attack and nearly twice as likely to have had
heart procedures such as coronary artery bypass surgery or angioplasty. In contrast, women
who had migraines with aura once a month had no increased risk of stroke or heart
problems. These results should be interpreted with caution, since the number of
migraine and migraine features were self-reported and there were relatively low numbers of
stroke and heart problems in the large study group, said study author and member of
the American Academy of Neurology Tobias Kurth, MD, ScD, of Brigham and Womens
Hospital, Harvard Medical School and INSERM, the French national research institute.
Nonetheless, more research is needed to determine how and why these differences
occur and whether preventing migraines could reduce the risk of stroke and heart problems.
Gastrin Plays Significant Role in
Helicobacter-Induced Stomach Cancer
A group led by Columbia University Medical Centers Timothy Wang, M.D., has studied
the role of Helicobacter infection in the development of stomach cancer and found that the
hormone gastrin, which stimulates secretion of gastric acid, plays a key role in the
development of Helicobacter-induced stomach cancer, and may have distinct effects on
carcinogenesis in different parts of the stomach.More than 50 percent of the worlds
population is infected with Helicobacter, which causes chronic inflammation of the stomach
lining and is strongly linked to the development of gastric ulcers and stomach cancer.
Stomach cancer is the second leading cause of cancer-related deaths worldwide.
Helicobacter infection results in increased expression of gastrin, although its role in
cancer development has been unclear. High levels of gastrin lead to the development of
stomach cancer, but absence of gastrin has been shown to increase the numbers of tumors in
the gastric antrum, the lower section of the stomach that empties into the small
intestine. To reconcile this apparent discrepancy, a group led by Dr. Wang studied
Helicobacter infection and stomach cancer in animal models with either high expression of
gastrin or no gastrin at all. They found that Helicobacter infection in mice with high
levels of gastrin resulted in cancer of the gastric corpus (main body of the stomach),
whereas infection in gastrin-deficient mice developed cancer in the gastric antrum.The
latest research by Dr. Wang and his colleagues appears in the July 2009 issue of The
American Journal of Pathology.
Laughter Differs in Children with
Autism
According to a recent paper entitled Laughter Differs in Children with Autism: An
Acoustic Analysis of Laughter Produced by Children with and without the Disorder,
children diagnosed with autism produce different laughs than their nonautistic peers.
We revealed that children with autism produce very engaging laughs that we call
voiced laughs, said William Hudenko, the lead author on the paper and
assistant professor of psychology at Ithaca College.The study recorded laughter during a
series of playful interactions with an examiner. The results showed that children with
autism exhibited only one type of laughter, compared to two types of laughter for
nonautistic children. There was no difference in laugh duration, frequency, change in or
number of laughs per interaction.We hypothesized that children with autism may be
expressing laughter primarily in response to positive internal states, rather than using
laughter to negotiate social interactions, said Hudenko. Hudenko specializes in
child and family clinical psychology. His clinical experience involves children who have
developmental disorders and disruptive behavior disorders.
Vitamin D Sufficiency Challenges
and Opportunities for the Food Industry
Scientific evidence shows vitamin D may go beyond its traditionally known role in
maintaining bone integrity, according to new research presented at the Institute of Food
Technologists Annual Meeting and Food Expo earlier this month. It may play a role in
preventing autoimmune diseases such as multiple sclerosis and rheumatoid arthritis, some
types of cancer (breast, ovarian, colorectal and prostate).
Anti-inflammatory drugs may defeat
a treatment-resistant type of cancer
Effective drugs for treating a chemotherapy-resistant form of lymphoma might already be on
the market according to a study that has pieced together a chemical pathway involved in
the disease. By following the trail of several molecular flags that mark this type of
cancer, a team from the University of California, San Diego, the Burnham Institute for
Medical Research and the University of Copenhagen Hospital have discovered that
anti-inflammatory drugs used to treat arthritis will shrink lymphoma tumors in mice. Their
report, published in the July issue of the journal EMBO Molecular Medicine, also
strengthens evidence for a link between inflammation and cancer. "If this shows
promise with early clinical experiments, the treatment would be immediately
available," said Michael David, a professor of biology who leads the group at UC San
Diego. The research focused on a type of non-Hodgkin lymphoma called diffuse large B-cell
lymphoma. In some patients with the disease, chemotherapy works well. In a recent study of
40 patients more than 75 percent of patients with one form of this type of lymphoma
survived five years or longer. But that study also identified a group of patients whose
cancer proved difficult to treat. Their tumors failed to respond to chemotherapy, and only
16 percent of patients with this form of lymphoma survived more than five years after they
were diagnosed. Several molecular flags mark this treatment-resistant lymphoma, but the
links between them were unknown until now. The new paper reports that tumor cells isolated
from these patients have depressed levels of a protein called SHIP1, which was known to
suppress tumors. In fact, patients with the lowest levels of SHIP1 are the least likely to
survive.
Gene predicts how brain responds to
fatigue, human study shows
New imaging research in the June 24 issue of The Journal of Neuroscience helps explain why
sleep deprivation affects some people more than others. After staying awake all night,
those who are genetically vulnerable to sleep loss showed reduced brain activity, while
those who are genetically resilient showed expanded brain activity, the study found. The
findings help explain individual differences in the ability to compensate for lack of
sleep. "The extent to which individuals are affected by sleep deprivation varies,
with some crashing out and others holding up well after a night without sleep," said
Michael Chee, MBBS, at the DukeNational University of Singapore Graduate Medical
School, an expert on sleep deprivation who was not affiliated with the study. However,
studying how the brain produces these behavioral differences is difficult: researchers
usually do not know whether their study participants will be vulnerable to sleep
deprivation until after a study is complete. Previous studies have shown conflicting
results, perhaps because the study subjects differed widely in vulnerability to sleep
deprivation. In the current study, the researchers, led by Pierre Maquet, MD, at the
University of Lìege in Belgium and Derk-Jan Dijk, PhD, at the University of Surrey in the
United Kingdom, avoided this problem by selecting study participants based on their genes.
Previous research showed that the PERIOD3 (PER3) gene predicts how people will respond to
sleep deprivation. People carry either long or short variants of the gene. Those with the
short PER3 variant are resilient to sleep loss they perform well on cognitive tasks
after sleep deprivation. However, those with the long PER3 variant are vulnerable
they show deficits in cognitive performance after sleep deprivation. Now the new study
explains why.
Smoking more than 5 cigarettes a
day provokes migraine attacks
Tobacco acts as a precipitating factor for headaches, specifically migraines. This is
indicated in a study which shows that smokers have more migraine attacks and that smoking
more than five cigarettes a day triggers this headache. The work has appeared in the
Journal of Headache and Pain. The influence of tobacco as a precipitating, non-causal
factor of migraine attacks has produced contradictory data in scientific literature. The
limited research prior to the work published in The Journal of Headache and Pain indicated
that smoking could improve migraines by reducing anxiety, one of the factors that triggers
an attack. "This study is groundbreaking in Spain as there are few studies on this
topic, and all are very biased. This is due to the complexity and need for prior training
of the participants", Julio Pascual, one of the authors of this research and doctor
at the Neurology Unit of Marqués de Valdecilla, University Hospital (Santander), explains
to SINC. One advantage of this study is that the sample used, 361 medicine students from
the University of Salamanca, were fully aware what a migraine was. The experts, who
enquired about the presence or absence of migraine (and its characteristics) and whether
or not they smoked, guaranteed the reliability of the results obtained, as most surveys
for this type of study are done over the phone, randomly and in people without knowledge
of the illness. The results show that 16% of students fulfilled migraine criteria, while
20% smoked. The percentage of smokers was higher (29%) in those who were also migraine
sufferers and migraine frequency in those students who were migraine sufferers and smokers
was clearly higher than in those who were non-smokers and migraine sufferers.
New mechanism for amyloid beta
protein's toxic impact on the Alzheimer's brain
Scientists have uncovered a novel mechanism linking soluble amyloid ? protein with the
synaptic injury and memory loss associated with Alzheimer's disease (AD). The research,
published by Cell Press in the June 25 issue of the journal Neuron, provides critical new
insight into disease pathogenesis and reveals signaling molecules that may serve as
potential additional therapeutic targets for AD. Amyloid ? protein (A?) plays a major
pathogenic role in AD, a devastating neurodegenerative disorder characterized by
progressive cognitive impairment and memory loss. "Given the mounting evidence that
small soluble A? assemblies mediate synaptic impairment in AD, elucidating the precise
molecular pathways by which this occurs has important implications for treating and
preventing the disease," explains senior study author, Dr. Dennis Selkoe from the
Center for Neurologic Diseases at Brigham and Women's Hospital and Harvard Medical School.
Dr. Selkoe, Dr. Shaomin Li, and colleagues examined regulation of a cellular communication
phenomenon known as long-term synaptic depression (LTD). LTD has been linked with neuronal
degeneration, but a role for A? in the regulation of LTD has not been clearly described.
The researchers found that soluble A? facilitated LTD in the hippocampus, a region of the
brain intimately associated with memory. The enhanced synaptic depression induced by
soluble A? was mediated through a decrease in glutamate recycling at hippocampal synapses.
Excess glutamate, the major excitatory neurotransmitter in the brain, is thought to
contribute to the progressive neuronal loss characteristic of AD. The researchers went on
to show that A?-enhanced LTD was mediated by glutamate receptor activity and that the LTD
could be prevented by an extracellular glutamate scavenger system. A very similar
enhancement of LTD could be induced by a pharmacological blocker of glutamate reuptake.
Importantly, soluble A? directly and significantly decreased glutamate uptake by isolated
synapses. "Our findings provide evidence that soluble A? from several sources
enhances synaptic depression through a novel mechanism involving altered glutamate uptake
at hippocampal synapses," concludes Dr. Selkoe. "These results have both
mechanistic and therapeutic implications for the initiation of hippocampal synaptic
failure in AD and in more subtle forms of age-related A? accumulation." Future
studies are needed to determine precisely how soluble A? protein physically interferes
with glutamate transporters at the synapse.
Study pinpoints novel cancer gene
and biomarker
ana-Farber Cancer Institute scientists' discovery of a cancer-causing gene the
first in its family to be linked to cancer demonstrates how the panoramic view of
genomics and the close-up perspective of molecular biology are needed to determine which
genes are involved in cancer and which are mere bystanders. The findings are reported in
the June 25 issue of the journal Nature. "In the coming years, we can expect genomic
studies [which chart the activity of thousands of cell genes] to generate hundreds or
thousands of genetic elements of interest in cancer research," says the study's
senior author, Lynda Chin, MD, of Dana-Farber. "To narrow that group to the genes
that actually drive cancer growth and metastasis, it's necessary to do functional studies,
which focus on what individual genes do to turn a cell cancerous, and mechanistic studies,
which examine how they turn cells cancerous and in what setting. It is a long and
intensive effort that will leverage knowledge from different fields and different model
systems."In the study, Chin, lead author Kenneth Scott, PhD, of Dana-Farber, and
their colleagues worked their way through a series of experiments -- in yeast cells,
multiple types of human cancer cells, laboratory cell cultures, and mouse models - to
demonstrate that a surplus of a gene known as GOLPH3 can spur cancer cell growth in a
variety of tissues. It is the first gene associated with the Golgi complex, a tiny
packaging plant that prepares proteins for their journey within and outside the cell,
which has been found to play a role in cancer. Chin's team also found that the protein
made from GOLPH3 may serve as a biomarker for tumors that can be effectively treated with
the chemotherapy drug rapamycin: tumors with a high level of the protein are more apt to
shrink in response to the drug than those with low levels. The study began with an
observation made years ago that a section of chromosome 5p13 is often duplicated, or
amplified, in cancers of the lung, ovary, breast, and prostate gland, as well as melanoma.
The presence of this abnormality in so many different types of cancer led Chin and her
associates to take a closer look at that stretch of chromosome to see what genes reside
there. Using a method called genomic qPCR that can pick out specific sequences of DNA,
they found four genes in the amplified region, two of which, GOLPH3 and SUB1, were
expressed at high levels, due to the increase in gene copy. To determine whether both, or
either, of these genes are involved in cancer, they conducted "loss of function"
tests, in which they lowered each gene's activity in a set of lab-grown tumor cells.
"When we 'knocked down' GOLPH3 expression [or activity] by 95 percent, it
significantly inhibited the ability of these cell lines to grow in a semi-solid condition,
a cancerous quality that normal cells do not typically share," Chin says.
"Knocking down SUB1 to a comparable level had only a minimal effect." Intriguing
as this finding was, it was hardly enough to prove that GOLPH3 is an oncogene -- a
contributor to cancer when overexpressed within a cell. Demonstrating that would require
several experiments to ensure that GOLPH3 itself, and not a nearby "shadow"
gene, is responsible for the effects. Next came gain-of-function studies to see whether
revving up GOLPH3 activity can turn a non-cancerous cell cancerous. It did in both mouse
and human cells. "All these results enabled us to build a case that GOLPH3 is an
oncogene," Chin states. But there was a problem. "This information wasn't very
helpful for achieving our ultimate goal, which is the translation of our findings into a
form that is clinically useful for patients."
Simple measures may prevent
transmission of stomach ulcer bacteria
The stomach ulcer bacterium Helicobacter pylori is not transmitted through drinking water
as previously thought, but rather through vomit and possibly faeces. This is shown in a
thesis at the Sahlgrenska Academy, University of Gothenburg, Sweden. It is therefore
possible to prevent the spread of the bacterium in developing countries through some
fairly simple measures. 'Taking some cheap but powerful measures may prevent the spread of
the bacterium. It could be enough to isolate vomiting patients especially from small
children for a short period of time, since Helicobacter pylori is not able to survive for
long outside the stomach. If isolation is not possible, it may suffice to pay extra
attention to good hygiene', says doctoral student Anders Janzon. The research team
analysed the drinking water, lake water and wastewater in an area in Dhaka in Bangladesh,
where the bacterium Helicobacter pylori is very common. The results show that while the
diarrhoea bacterium ETEC is often present in the drinking water, Helicobacter pylori is
not. Other studies have shown that new cases of Helicobacter pylori tend to pop up in
connection with various diarrhoea illnesses, and this pointed the research team in the
right direction.'We analysed vomit and diarrhoea from cholera patients, and found large
amounts of active Helicobacter pylori. We therefore conclude that vomit is a very likely
source of new infections', says Janzon.
Study Investigates DNA of Sleep
A new study at the University of Leicester aims to investigate the DNA of sleep. The
research in the renowned Department of Genetics at the University of Leicester is being
carried out by Ms Mobina Khericha and Dr Eran Tauber. It represents a new approach to
study the genetics of sleep. Using fruitflies as models the researchers aim at
understanding the genetics of sleep and identifying genes involved in this process. Ms
Khericha said Recent studies have revealed the presence of sleep-like state in the
fruit-fly Drosophila melanogaster that shares striking similarities with mammalian sleep.
For example, sleep in the fruit fly can be modulated by chemicals such as caffeine,
and is characterized by a reduced arousal following sleep deprivation. In older flies
sleep becomes shorter and fragmented. Fruit flies are a powerful model organism that has
been extensively used to understand the genetics of human development, behaviour and
disease. Sleep is ubiquitous in a diverse range of organisms including reptiles,
birds and mammals, and is widely accepted as critical for survival. However, despite
intensive research, the genetic and molecular mechanisms controlling sleep are largely
unknown.
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