Brain

Plants Won’t Grow Near Wi-Fi Routers

Posted on Dec 16, 2013

It’s not difficult to understand the appeal of Wi-Fi.  This revolutionary technology, which has been commercially available since 1999, eliminates cabling and wiring for computers, reduces cellular usage charges and allows us to connect to the Internet from anywhere with a signal.  Despite these benefits, however, studies continue to show that the radiation generated by wireless routers is negatively affecting our health.  In fact, the British activist website Stop Smart Meters recently published a list of 34 scientific studies demonstrating the adverse biological effects of Wi-Fi exposure, including studies linking it to headaches, reduced sperm count and oxidative stress. The latest research into the dangers of Wi-Fi, though, comes from a surprisingly humble source: Five ninth grade female students from Denmark, whose science experiment revealed that wireless radiation is equally as devastating to plants. Undeniable results The experiment began when the five students realized that they had difficulty concentrating in school if they slept near their mobile phones the previous night. Intrigued by this phenomenon, the students endeavored to study the effects of cellphone radiation on humans. Unfortunately, their school prevented them from pursuing this experiment due to a lack of resources, so the students decided to test the effects of Wi-Fi radiation (comparable in strength to cellphone radiation) on a plant instead. The girls placed six trays of Lepidium sativum seeds (a garden cress grown commercially throughout Europe) in a room without radiation, and an equal amount in a room next to two Wi-Fi routers. Over a 12-day period, they observed, measured, weighed and photographed the results. Even before the 12th day arrived, however, the end results were obvious: The cress seeds placed near the routers either hadn’t grown or were completely dead, while the seeds placed in the radiation-free room had blossomed into healthy plants. The experiment earned the five students top honors in a regional science competition. Moreover, according to a teacher at their school, Kim Horsevad, a professor of neuroscience at the Karolinska Institute in Sweden was so impressed with the experiment that he is interested in repeating it in a controlled scientific environment. READ...

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Is Alzheimer’s Caused by an Infection?

Posted on Dec 7, 2013

Is Alzheimer’s Caused by an Infection?

Research has shown that some common bacteria are consistently detected in the central nervous system of Alzheimer’s patients.1 Doctors from the International Alzheimer Research Center in Switzerland published a study indicating a high probability of a causal relationship, not just an association, between spirochete infections and Alzheimer’s disease. What they discovered was pretty amazing. They found spirochetes in about 90% of Alzheimer’s patients, while the bacteria were virtually absent in healthy age-matched controls.1 Could Alzheimer’s disease be caused by this infection? Let’s explore. Spirochetes Form Brain Plaques Much insight about what could happen in the brain during this process comes from studies on a spirochete, Borrelia burgdorferi, which is the cause of Lyme disease. Spirochete infection begins with the bacteria entering the brain. Once within the brain tissue, they cause disease by forming plaques or masses along the cerebral cortex — the surface of the brain. Agglutination in the center of the plaque results in a homogeneous central core, which attracts brain macrophages, called microglial cells. The macrophages are responsible for recognizing foreign invaders, engulfing them and presenting them to bacteria fighting immune cells. The macrophages become trapped within the core of the spirochete plaque. Once trapped, they are vulnerable to attack by the spirochetes. This results in their dysfunction and diminished capacity for fighting the infection. The infection spreads and begins to damage and kill brain cells.2 Damaged brain cells produce the characteristic amyloid-beta protein seen in Alzheimer’s patients. Now here’s where it gets really interesting… Amyloid-beta Protein has Antibacterial Properties Scientists have discovered that amyloid-beta protein has anti-bacterial properties, indicating that its production may be an adaptive response to infectious organisms, like invading spirochetes.3,4 The whole process may work something like this: Spirochetes invade and infect the brain. The brain’s normal defenses become dysfunctional as the macrophages (microglia) become trapped and then attacked within the core of the spirochete plaque. With immune dysfunction setting in, the spirochete infection intensifies involving more and more brain cells. Damaged brain cells produce amyloid-beta protein as an adaptive response to the infection. Amyloid-beta deposits grow and begin to affect brain cell connections and communication highways. With damaged connections and communication highways, dementia symptoms begin and gradually worsen. Early Intervention with Antibacterials These findings have led some researchers to hypothesize that “…early intervention against infection may delay or even prevent the future development of Alzheimer’s disease.”3 Early intervention might include preventative antibacterial remedies in people at high risk of developing Alzheimer’s — a person with a strong family history or the presence of the Apo-E4 allele (a lipoprotein used for fat and cholesterol transport).5 Antibacterial herbs and other remedies could also be used as part of the early treatment regimen in patients diagnosed with Alzheimer’s disease. Reversing Macrophage Dysfunction with Curcumin Here’s something amazing: Curcumin helps enhance the engulfing properties of brain macrophages — the same macrophages that are damaged and dysfunctional by the spirochetes. As it turns out, curcumin can bind to amyloid-beta plaques, allowing the brain macrophages to “latch on” and engulf the plaques. The clearing of the plaques can help resolve the infection and reestablish normal brain cell connections and communication highways.6 Could antibacterial remedies and curcumin make up an early Alzheimer’s prevention and treatment regimen in the future? It sure is looking possible. References: J Neuroinflammation. 2011 Aug 4;8:90. Neurobiol Aging.2006;27:228–236. Alzheimers Dement. 2009 Jul;5(4):348-60. PLoS One. 2010 Mar 3;5(3):e9505. N Engl J Med. 1995 Nov 9;333(19):1242-7. J Biol Chem. 2005 Feb 18;280(7):5892-901. Based on an article by Michael A. Smith MD for the Life Extension Blog. READ...

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AUTISM: Bad air, genetics add up to higher risk

Posted on Dec 7, 2013

AUTISM: Bad air, genetics add up to higher risk

Air pollution and a common genetic makeup may interact to significantly increase a baby’s risk for autism, USC scientists found. The researchers at USC’s Keck School of Medicine cautioned in an interview that they need to do more studies to replicate their findings. The study, to be published in the January 2014 edition of the journal Epidemiology, found that children with the specific gene who spent their in-utero months and their first year after birth in polluted areas of California had three-fold higher risks for autism disorders. “We need to do more studies, but the genetic disposition and air pollution appear to work together to increase the risk of autism more than the risk of each one alone,” said the study’s lead author, Heather E. Volk, an assistant professor of research in preventive medicine at the medical school. Volk’s earlier work found that children had twice the risk of developing autism if their mothers lived within 1,000 feet of a busy freeway during pregnancy. For this research, Volk collaborated with genetics expert Daniel B. Campbell, an assistant professor in psychiatry and behavioral science at the USC medical school. Campbell explained by telephone that roughly half the population has what geneticists call the “MET receptor tyrosine kinase gene.” The gene is found in about 60 percent of people who have autism, indicating that those with the gene have a higher risk, he said. THE CHILDREN To probe the potential interplay between the gene and air quality, Volk, Campbell and their colleagues analyzed the genetics and air pollution exposures of 408 children in the Sacramento, San Francisco and Los Angeles areas; the children’s cases already were being tracked for research purposes. Of those children, 252 met the diagnostic criteria for the spectrum of autism disorders. Using regional air quality readings and traffic proximity data, the research team determined each child’s air pollution exposure while they were fetuses and in their first year after birth — a critical period in the development of the brain and other organs. The scientists used a blood test to determine each child’s genetics. The team found no increase in the autism risk among the children who had the gene but breathed relatively clean air. But those who had the gene and were exposed to air pollution were three times more likely to have the disease, Volk said. Beth Burt, president of the Autism Society Inland Empire, said she appreciates the research. “It is fascinating and important work,” said Burt, a Corona resident who has an autistic son who is 20. “It is not an either/or situation — genetics or the environment,” she said. “But it may be the combination of a genetic predisposition with an environmental trigger.” Lillian Vasquez, who also has a 20-year-old son with autism, said she was not surprised by USC’s findings. She said she has always thought autism was the result of genetics and some sort of trigger, such as a vaccination or an artificial sweetener. “Air pollution as a trigger seems quite plausible,” she said. Vasquez, vice president of the Inland autism society, has lived in Colton since before her pregnancy. Colton, like most of the Inland area, has long had unhealthful levels of air pollution. OTHER RESEARCH Autism disorders are incurable, lifelong brain disabilities characterized by problems with social interaction, communication and repetitive behaviors. The Centers for Disease Control and Prevention estimates that one in 88 children in the United States has an autism disorder. Thousands of studies have linked air pollution to lung, heart and circulatory disorders. The work by Volk and her colleagues, however, is part of a...

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Toxin-Emitting Bacteria May Be Environmental Trigger for MS

Posted on Nov 15, 2013

Toxin-Emitting Bacteria May Be Environmental Trigger for MS

Could eating meat from animals infected with one type of Clostridia bacteria be the MS ‘smoking gun?’ Researchers may have unearthed a trigger for multiple sclerosis (MS) that’s been hiding in plain sight. Scientists from Weill Cornell Medical College and Rockefeller University have identified a bacterium they believe can trigger MS—and it’s found just about everywhere, including dirt. Their study, published in PLOS ONE, is the first to identify the bacterium, Clostridium (C.) perfringens type B, in humans. They first identified it in the blood of a 21-year-old woman with MS who was having a relapse. She was part of the Harboring the Initial Trigger for MS (HITMS) observational study launched by Timothy Vartanian, a professor of neurology and neuroscience at Weill Cornell Medical College and director of the Judith Jaffe Multiple Sclerosis Center at New York-Presbyterian Hospital and Weill Cornell, and Kareem Rashid Rumah, an MD/PhD student at Weill Cornell and lead investigator. See 13 Early Signs of MS » Getting the Dirt on C. perfringens C. perfringens, found in soil, is one of the most common types of bacteria in the world. It has five subsets, A through D. Type A commonly occurs in the human gastrointestinal tract and is thought to be harmless. Types B and D, however, can emit a harmful substance called epsilon toxin when eaten by grazing livestock. The substance travels through the bloodstream, crossing the blood-brain barrier and destroying myelin, causing MS-like symptoms in the animals. Vartanian, Rashid, and their team wondered if C. perfringens types B or D could be identified in humans. They tested the blood of both MS patients and healthy control subjects. In samples from MS patients, the levels of antibodies to the toxins were 10 times higher than in the healthy controls. They also noted that only one sample in 100 from the healthy controls showed any sign of exposure to the bacteria. Researchers hypothesize that eating grazing animals who are infected with the bacteria could be the way C. perfringens Type B is introduced into the human digestive system. The human gut plays host to many types of bacteria, not all of them bad. Some are actually necessary for maintaining good health. Researchers suppose that the reason one person reacts to the toxin emitted by the bacteria while another does not may depend on the natural balance of bacteria in a person’s gut. Learn 6 Surprising Facts About the Microbes Living in Your Gut » “We believe the toxin enters the blood from the gut,” said Vartanian in an interview with Healthline. “Once in the blood, the toxin binds to a specific receptor present on the [lining of] the brain blood vessels, resulting in injury to the blood brain barrier (BBB). The toxin in the blood can then enter the brain at focal sites of BBB injury and bind to the same receptor on oligodendrocytes, the myelin forming cells of the central nervous system, resulting in oligodendrocyte death.” Bacterial “Relapses” The type B bacteria, once settled in the gut, goes through growth cycles followed by periods of dormancy. Since the toxin is only emitted during active periods, it is not always present in the bloodstream. Researchers are intrigued by this cyclical activity and hope to investigate whether these growth cycles coincide with relapses in people with relapsing-remitting forms of MS. “We are working on that now and need funding to push this project faster,” said Vartanian. The findings of this small study are exciting, but must be replicated by other researchers. Could the immune response seen in MS patients in fact be caused by the body’s attempt to fight the toxin? According to the researchers, it’s possible....

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Research finds brain scans may aid in diagnosis of autism

Posted on Nov 6, 2013

Research finds brain scans may aid in diagnosis of autism

Joint research from the University of Alabama at Birmingham Department of Psychology and Auburn University indicates that brain scans show signs of autism that could eventually support behavior-based diagnosis of autism and effective early intervention therapies. The findings appear online today in Frontiers in Human Neuroscience as part of a special issue on brain connectivity in autism. “This research suggests brain connectivity as a neural signature of autism and may eventually support clinical testing for autism,” said Rajesh Kana, Ph.D., associate professor of psychology and the project’s senior researcher. “We found the information transfer between brain areas, causal influence of one brain area on another, to be weaker in autism.” The investigators found that brain connectivity data from 19 paths in brain scans predicted whether the participants had autism, with an accuracy rate of 95.9 percent. Kana, working with a team including Gopikrishna Deshpande, Ph.D., from Auburn University’s MRI Research Center, studied 15 high-functioning adolescents and adults with autism, as well as 15 typically developing control participants ages 16-34 years. Kana’s team collected all data in his autism lab at UAB that was then analyzed using a novel connectivity method at Auburn. The current study showed that adults with autism spectrum disorders processed social cues differently than typical controls. It also revealed the disrupted brain connectivity that explains their difficulty in understanding social processes. “We can see that there are consistently weaker brain regions due to the disrupted brain connectivity,” Kana said. “There’s a very clear difference.” Participants in this study were asked to choose the most logical of three possible endings as they watched a series of comic strip vignettes while a functional MRI scanner measured brain activity. The scenes included a glass about to fall off a table and a man enjoying the music of a street violinist and giving him a cash tip. Most participants in the autism group had difficulty in finding a logical end to the violinist scenario, which required an understanding of emotional and mental states. The current study showed that adults with autism spectrum disorders struggle to process subtle social cues, and altered brain connectivity may underlie their difficulty in understanding social processes. “We can see that the weaker connectivity hinders the cross-talk among brain regions in autism,” Kana said. Kana plans to continue his research on autism. “Over the next five to 10 years, our research is going in the direction of finding objective ways to supplement the diagnosis of autism with medical testing and testing the effectiveness of intervention in improving brain connectivity,” Kana said. Autism is currently diagnosed through interviews and behavioral observation. Although autism can be diagnosed by 18 months, in reality, earliest diagnoses occur around ages 4-6 as children face challenges in school or social settings. “Parents usually have a longer road before getting a firm diagnosis for their child now,” Kana said. “You lose a lot of intervention time, which is so critical. Brain imaging may not be able to replace the current diagnostic measures; but if it can supplement them at an earlier age, that’s going to be really helpful.” The findings of this study build on Kana’s research collaborations with Auburn that began in 2010. Lauren Libero, a graduate student in the UAB Department of Psychology, assisted in the research. READ...

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