Researchers have discovered a common denominator of low B 12 levels in brains of those afflicted with schizophrenia and autism.
Through the examination of brains of victims who have passed, ranging from birth up to 80 years of age, researchers found that B 12 levels were ten times lower in the oldest compared to the youngest samples. This indicates that levels decline continuously throughout the course of a lifetime.
B 12 levels naturally decline with age, protecting the brain by slowing cellular reactions and the production of chemicals that can severely damage DNA, known as free radicals. Abnormally low levels of the vitamin, however, can be detrimental. It causes a chain reaction in which an extreme decrease can cause a similar effect in metabolism, which in turn hinders the survival of cells.
In children under the age of 10, researchers discovered that those with autism had levels three times lower than other unaffected children of the same age have. The levels found in autistic children were considered normal in healthy adults in their 50s.
Similar results were found in the brains of adults with schizophrenia, with roughly a third of the levels that a normal, healthy individual has at the same age. Schizophrenic patients ranging from ages 36-49 were found to have similar B 12 levels to 72-year-olds. Their findings in both types of patients indicate a premature decline in the vitamin.
Some researchers suggest that a poor uptake of vitamin B 12 from the blood to the brain may create neurological conditions; the uptake is important because the amount of the vitamin detected in the blood does not always correlate with levels found in the brain. B 12 plays a vital role in building red blood cells and the functions of the central nervous system.
While there is no definitive link between B 12 deficiency and autism and schizophrenia, other studies have indicated that extreme vitamin and nutrition deprivation can create increased risk for heart disease, unstable pregnancies, depression, and memory loss.
There is an increasingly held belief that the human brain allocates extremely specific uses for vitamin B 12 that allow for the brain to control gene expression and trigger specific stages in neurological development at various periods throughout a person’s life. This includes fetal development, early childhood, the transition from adolescence to adulthood, and finally middle age to old age. Researchers assert that oxidative stress – which both disorders are linked to and cause premature aging – may cause decreased levels of B 12 in the brain.
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