Monthly Archives: May 2016

CES and the aging brain

There is a growing body of evidence suggesting that the aging brain undergoes neuroplastic changes to respond to functional declines and keep performance on the best level. During these changes, additional brain areas are recruited, such as the ipsilateral motor cortex. First proof of principle has been provided that CES might modulate cortical functions even in old subjects. Nevertheless, this exciting and progressing field is still at a starting point and more studies are needed to further substantiate the hypothesis that CES can be used to enhance functions that have declined with age. In comparison to pharmacological interventions, CES is applied focally and does not have systemic side effects, a crucial point to consider in this population. Moreover, these techniques are easy to apply and can be coupled with training protocols or rehabilitative programs, such as physio-, occupational, speech therapy, or gait training to enhance impaired functions with a consecutive improvement of quality of life.

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CES has been shown to reduce the levels of stress hormones

There are numerous CES studies in which CES has been shown to reduce the levels of stress hormones in the body. Usually this reduction is found to be in connection with a rebalanced relationship between stress related hormones and other hormones with which they are normally in balance in non stress states.

For example, Pozos and his team found that CES could bring back into homeostatic balance the neurotransmitter dopamine that had been deliberately thrown out of balance in an animal preparation, thus removing Parkinson like symptoms that he had induced with the imbalance earlier.

Gold and his coworkers found that CES could bring back into homeostatic balance the endorphin-norepinephrine system in the brains of withdrawing human addicts, thus eliminating the major stress of the drug abstinence syndrome.

Similar results were found in an animal preparation by Dougherty and his coworkers at the University of Texas.

Shealy studied stress hormones specifically in a group of 164 patients who were severely depressed and found abnormal levels of melatonin, norepinephrine, beta-endorphin, serotonin and cholinesterase ranging widely throughout the group.

Since similarly depressed patients had routinely responded well to CES in the past, he selected another group of 37 chronic pain patients whose pain was nonresponsive to usual treatments, and who were also depressed. He studied their stress hormone levels before and following CES treatment. He found pre-post changes in serotonin, beta-endorphin, norepinephrine and cholinesterase in the patients following stimulation with CES, 20 minutes a day for two weeks. Forty-four percent of the chronic pain patients reported significant improvement in their pain and required no additional treatment. The depressed patients reported 50% clinical improvement in their depression, often bringing them back within the normal range.

In searching for the mechanism with which CES induced these changes, Shealy studied the cerebral spinal fluid (CSF) vs. blood plasma in 10 normal subjects prior to and following 20 minutes of CES stimulation. He found changes in melatonin, serotonin, norepinephrine, beta-endorphin and cholinesterase in both the CSF and blood plasma, but with greater changes in the blood plasma, in each instance. He concluded that CES activated a hypothalamic response that resulted in a body-wide change in the levels of those stress realted biochemicals.

While inflammation was not measured in the above studies, in so far as stress hormones can engender the inflammation response CES could be inferred to be a significant treatment in reducing inflammation in the body, along with the myriad medical pathologies that accompany it.

As a typical follow on to stress engendered inflammation, Ware notes that psychological stress and depression have been established as important risk factors for coronary heart disease, while Cassels found that approximately 30% of adults with diabetes have comorbid depression, which is associated with poor metabolic control, more complications, increased healthcare use and costs, reduced quality of life, greater disability and lost productivity, and higher mortality rates.