Posted on March 16th, 2011

Our basic neuroscience classes have long taught us that our brain communicates to our body through electrical impulses along our nervous system. We also understand the left and right hemispheres of our brain perform different functions and each side must also communicate to the opposite hemisphere.

Recent research has demonstrated that when the two sides of the brain mature at different rates, the electrical impulses go out of balance and communication is affected. Recent evidence this imbalance can lead to behavioral and learning disorders: autism, Asperger’s, ADHD, oppositional defiant disorder, anxiety, depression, and others. The name of this imbalance of electrical activity between the hemispheres of the brain is Functional Disconnection Syndrome (FDS).

Much of the research comes from leading functional neurologists and chiropractors Dr. Ted Carrick and Dr. Robert Melillo. in his book Disconnected Kids, Dr. Melillo states:

“in order for the brain to function normally, the activities in the right and left hemispheres must work in harmony, much like a concert orchestra. when a certain function can’t stay in rhythm, it can throw the entire hemisphere off key so the other side tries to tune it out. this can cause disharmony to such a degree that the two sides can no longer effectively share and integrate information. The brain becomes functionally disconnected.”

The symptoms of FDS depend on which hemisphere has the dysfunction. for example, a child with a slow-developing right brain may develop autism, ADHD, or Asperger’s syndrome. a left brain dysfunction may result in an inability to read words or stay focused on reading. this imbalance, if left untreated, will continue into adulthood and may progress to other disorders.

Just how does this imbalance occur? it is important to understand how the brain develops from birth to infancy and adulthood.

Though the brain is reliant on the left and right hemisphere balance to function optimally, it doesn’t grow or develop at a balanced rate. in the womb and during the first years of life, brain growth is primarily in the right hemisphere. The right brain drives big muscle tasks, such as moving arms, legs or head.

Around the age of two, growth switches primarily to the left brain. this is the hemisphere where the first words are generated. from then on, development switches back and forth between the left and right brain until approximately age ten, when the brain reaches adult size.

If a child isn’t exposed to the proper stimulation (not too much or too little) of the sensory pathway, the brain’s growth patterns can get out of sequence and cause a delay in a key growth area. Meanwhile, the opposite side stays on track, leaving the other behind.

This delay in development most often occurs during the most crucial times of right brain development: birth through the first two years of life. The consequence of a right brain delay shows up later as ADHD, autism, Asperger’s, or other disorders.

The symptoms differ according to when the delay in development occurred, but the result is the same: Functional Disconnection Syndrome.

You may be wondering what causes the delay, how do we measure it, how can it be corrected? these and other questions about FDS will be reviewed in future blogs. make sure you don’t miss them by signing up to receive our posts by e-mail in the “subscribe” section above.

* 19 January 2011 by AnilAnanthaswamy<newscientist.com/search?rbauthors=Anil+Ananthaswamy>* Magazine issue 2796 <newscientist.com/issue/2796> . 

Diabetes and even obesity, as well as Parkinson’s disease, might becured just by replacing the bacteria in your gut

A FEW years ago, John Gillies had trouble picking up his grandchild. Hewould stand frozen, waiting for his Parkinson’s disease to relinquishits hold and allow him to move. then in May 2008, Gillies was givenantibiotics to treat constipation, and astonishingly his Parkinson’ssymptoms abated. what on earth was going on?

Thomas Borody, a gastroenterologist at the Centre for Digestive Diseases<cdd.com.au/> in New South Wales, Australia, put Gillies onantibiotics because he had found that constipation can be caused by aninfection of the colon. “He has now been seen by two neurologists, whocannot detect classic Parkinson’s disease symptoms any more,” saysBorody.

Borody’s observations, together with others, suggest that manyconditions, from Parkinson’s to metabolic disorders such as obesity,might be caused by undesirable changes in the microbes of the gut. Ifthat is true, it might be possible to alleviate symptoms withantibiotics, or even faecal transplants<newscientist.com/article/mg20827911.100-taboo-transplant-how-new-poo-defeats-superbugs.html> using donor faeces to restore thebowel flora to a healthy state.

Borody uses faecal transplants to cure people infected by the superbugClostridium difficile, and to alleviate chronic constipation. over thepast decade, Borody has noticed that some of his patients also seeimprovements in symptoms of their other diseases, includingParkinson’s, multiple sclerosis (MS), chronic fatigue syndrome (CFS)and rheumatoid arthritis. “Some CFS patients, given a faecaltransplant, will regain their energy quite dramatically, and theirfoggy brains will get better,” says Borody.

To test a possible link between the gut and Parkinson’s disease, Borodyand neurologist David Rosen of the Prince of Wales Private Hospital inSydney are embarking on a pilot study, hoping to recruit people withboth constipation and Parkinson’s. The plan is first to treat them withantibiotics and eventually with faecal transplants. They hope bothfaecal transplants and antibiotics will treat gut infection and henceParkinson’s.

Rosen is cautious: “I wouldn’t for one minute be suggesting that thisis the next cure,” he says. But the idea that Parkinson’s could becaused by bacteria dovetails with work by neuroanatomists Heiko Braakand Kelly Del Tredici at the University of Ulm in Germany.

In 2003, Braak and Tredici showed that damage to the nervous system inParkinson’s progresses from the vagus nerve in the lower brain stem tothe higher regions of the brain and eventually to the cerebral cortex.They also found damage in the enteric nervous system, which controlsthe gastrointestinal (GI) tract and communicates with the brain via thevagus nerve. this discovery prompted them to suggest that Parkinson’smight be caused by a bug that breaks through the mucosal barrier of theGI tract and enters the central nervous system via the vagus nerve(Journal of Neural Transmission, DOI: 10.1007/s00702-002-0808-2<dx.doi.org/10.1007/s00702-002-0808-2> ).

So what about the dramatic improvements seen in people with autoimmunediseases, such as rheumatoid arthritis, after faecal transplant?Borody’s hypothesis is that an infection of the colon releases antigensinto the bloodstream, which trigger an immune response. Unlesssomething is done to completely clear the colon of the antigen, theimmune response is relentless, eventually leading to systemicinflammation that manifests itself as an autoimmune disease.

Interpreting Borody’s results requires extreme caution. However, thereis evidence from animal models that intestinal microbes can influenceautoimmunity. for instance, Alexander Chervonsky<biomed.uchicago.edu/common/faculty/chervonsky.html> of theUniversity of Chicago and colleagues have linked microbes in the gut totype 1 diabetes, an autoimmune disorder caused by the destruction ofinsulin-secreting pancreatic cells. over 80 per cent of a particularbreed of engineered mice that are kept germ-free develop type 1diabetes. When the same mice were dosed with a cocktail of bacteriasimilar to those present in the human gut, only 34 per cent of the micedeveloped type 1 diabetes, suggesting a connection between gut floraand autoimmune diabetes (Nature, DOI: 10.1038/nature07336<dx.doi.org/10.1038/nature07336> ).

Researchers are becoming increasingly aware of the link between gutflora and autoimmunity, says Arthur Kaser, an expert on inflammationand intestinal flora at the University of Cambridge. for instance, micedesigned to develop autoimmune diseases do so in some labs but not inothers. The discrepancy is down to differences in the intestinal floraof the mice. “Intestinal microbiota has a dramatic effect on [what] wecurrently consider as autoimmune disease,” says Kaser.

Evidence for such links in humans is also growing: Anne Vrieze of theAcademic Medical Center in Amsterdam, the Netherlands, and colleaguesstudied 18 obese men with metabolic syndrome, a collection of symptomsthat includes low insulin sensitivity. The group received faecaltransplants – either of their own stool or stool from lean, healthydonors.

The results of this first double-blind trial were presented at theannual meeting of the European Association for the Study of Diabetes inStockholm, Sweden, in September. The researchers found that, six weeksafter the infusions, insulin sensitivity improved significantly in thenine men who received donor stool.

Gut flora has also been linked to obesity. over the past five years,Jeffrey Gordon <gordonlab.wustl.edu/> of Washington Universityin St Louis, Missouri, and colleagues have shown that there are markeddifferences in the gut flora of obese and lean individuals. Theiranalysis suggested that the microbes in obese individuals are releasingnutrients from food that would have remained undigested in leanindividuals. Importantly, they showed that transferring the microbiotafrom obese mice into lean mice caused the lean mice to put on weight(Nature, DOI: 10.1038/nature05414<dx.doi.org/10.1038/nature05414> ).

So can you reverse obesity in humans by transferring gut microbes fromlean people into obese people? It’s a question that Alex Khoruts<med.umn.edu/gi/faculty/khoruts/home.html> , at theUniversity of Minnesota Medical School in Minneapolis, hopes to answer.He is planning a trial in which obese people will be given faecaltransplants, either of their own faeces or samples taken from lean,healthy donors. “The idea is to alter the composition of colon flora,and see whether it has an impact on obesity,” says Khoruts.

“This is absolutely exciting,” says Kaser. But he insists that we arefar from understanding the nature of the microbes that populate ourbody – after all, the colon alone contains nine times as many bacterialcells as there are human cells in the body. And we don’t yet know whatconstitutes “healthy” colon flora. this will make it difficult tojustify any large-scale adoption of faecal transplants, he adds. Ifintestinal bugs are indeed causing autoimmune diseases, “you don’t wantto treat one disease and introduce another”, says Kaser.

Nonetheless, he is convinced that human microbiota will becomeincreasingly important in our understanding of disease. “Textbooks willhave to be rewritten when we consider the contribution of intestinalmicrobiota,” he says. “We have an elephant in the room that has not yetbeen appreciated.”[Issue 2796 of New Scientist magazine] <newscientist.com/issue/2796>* from issue 2796 <newscientist.com/issue/2796> of NewScientist magazine, page 8-9.