As potential Autism causes go, Insulin Resistance (IR) doesn’t get much recognition from the established medical community. Swimming in a virtual sea of causation theories, IR’s cries for attention are drowned out by the frantic buzz around vaccinations, food allergies, and other, simpler concepts. Though the connection between IR and Autism PDD may be difficult to comprehend, similarities between the two conditions beg for further investigation.
Insulin Resistance is a metabolic disorder where cells in the body do not respond to insulin as quickly or efficiently as they should. Insulin is released into the blood stream when blood glucose levels rise. Its job is to alert certain receptor cells to accept glucose as nutrient from the blood, which will simultaneously feed muscles and organs while lowering blood glucose to acceptable levels.
When cells fail to respond to insulin, blood glucose remains elevated, resulting in the release of more insulin. As IR progresses, the receptor cells will more and more insulin to eventually respond. The physical consequences of IR, such as diabetes and obesity, are well documented. The neurological consequences of IR, however, remain largely unrecognized.
Individuals suffering from IR can experience a number of psychiatric and cognitive abnormalities. While research on neurological disruption is relatively limited compared to IR’s physical complications, what research exists consistently supports the existence of brain symptoms. These symptoms may include depression, psychosis, impaired brain development, and impaired social function.
In addition to sharing common symptoms, the neurological action caused by Insulin Resistance and associated with some cases of Autism PDD are strikingly similar. Individuals with IR and those with Autism may experience dysregulation of neurological processes which control mood and cognitive function. For instance, disturbance in dopaminergic, opioidergic, and serotonergic processes have been observed both in individuals with Autism and those with Insulin Resistance. The significance of these shared symptoms should not be discounted, particularly in light of another commonality between the disorders: GABAergic dysregulation.
GABA (gamma-aminobutyric acid) is an endogenous (produced naturally within the body) neurotransmitter that functions primarily to stop certain neurological and physiological processes. Its place in brain development, mood control, and physical health could not be more critical. It is GABA that enables us to be calmed when we are excited, to sleep when we are alert, and to reverse mood before it becomes hysterical.
Without GABA, joy would always lead to euphoria, anger would be experienced as rage, and energized agitation would prevent learning and development. Autistic children with severe behavioral and social impairment commonly experience a similar over-stimulated state on a daily basis. They also commonly experience GABA deficiency.
Disruption of the GABAergic process is common amongst individuals with Autism Spectrum Disorders. Research conducted by the Cohen Institute for Advanced GABA Studies (CIAGS) indicated that autistic boys typically have only 45.5% of a specific GABA enzyme (GABA-Transaminase) activity when compared to their neurotypical peers. The same study found high concentrations of GABA in blood plasma, indicating a disruption of the GABAergic process.
The link between GABA and a number of insulin-related disorders continues to be the subject of medical and scientific research. The theory of GABA-related Insulin Resistance was addressed in a medical hypothesis issued by experts Jeanrenaud and Di Blasi more than fifteen years ago. In a summary of their report, Insulin Resistance Syndrome: Defective GABA Neuromodulation as a Possible Hereditary Pathogenetic Factor (the ‘GABA hypothesis’), the pair state, “Alteration of the biochemical structure of GABA receptors is suggested as an interpretation of the origin of the syndrome.” Subsequent studies have yet to settle the ‘chicken-or-the-egg’ debate, but the likely connection between GABA and insulin disorders is widely accepted.
The occurrence of common symptoms and conditions in both individuals diagnosed with Autism and those diagnosed with Insulin Resistance does not prove a connection between the disorders, but it does provide good cause for further investigation. Some parents, having already subscribed to the IR theory, have implemented modified diets to minimize the damage IR can cause. Others have chosen to try GABA supplement therapy independently. Positive and negative results of varying degrees have been reported in both cases. Parents considering biomedical intervention in any form, even diet modification or supplementation, are urged to proceed only with qualified medical supervision.
Insulin Resistance Syndrome: Defective GABA Neuromodulation as a Possible Hereditary Pathogenetic Factor (the ‘GABA hypothesis’) available through http://www.PubMed.gov