Tag Archives: cranial electrical stimulation

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.

CES Ultra as a modern “electrosleep” device

Cranial Electrotherapy Stimulation (CES) is the American FDA’s term for what the rest of the world calls “electrosleep.” Modern electrosleep devices originated in Russia in 1953, and arrived in the U.S. ten years later, in 1963, when they began to be researched with patients complaining of insomnia.

Various uses of small to moderate electrical currents had been researched since the early 1900s in Europe, in an attempt to see exactly what current intensity and pulse rate were required to put a patient to sleep when applied to the head. By that, they meant what was required to knock him out or force him to lose consciousness and maintain the patient in that state for a period of time. Researchers finally gave up on finding a specific type of current that would reliably put most patients to sleep. Unlike those earlier models, modern CES devices are typically pocket sized, run off of a 9 volt battery, and pulse from 100 up to 15,000 times per second. The current intensity usually is at or just below 1 mAmp, but can go up to 4 mAmp with higher pulse rates. Most would just light a flashlight bulb at best, and in the majority of clinical studies, patients have not felt the stimulation at all during treatment.

In the early 1950s Russian medical researchers were working with these very low levels of current, which they applied via two electrodes attached to the closed eyelids and two attached behind the head at the base of the skull. They were attempting to find a psychiatrically useful current, and while the current level was much too low to force a person into a sleep state, they found to their great interest that patients were claiming vastly improved sleep during nights following sessions when these very minor amounts of stimulation passed across the head. They then began studying this effect specifically, and in 1953 finally came out with the Somniatron electrosleep device.

Several similar devices were later manufactured in the U.S. for research purposes, and their clinical use began among inpatient and outpatient psychiatric patients, usually in University Teaching Hospitals. Several other Universities began research with animals in an effort to see if CES really did change how the brain functioned, if it was safe to use, and what the mechanism of action might be.

They found that the current traveled throughout the brain, that it increased production and firing of neurotransmitters in neurons,3 and that when researchers deliberately threw neurotransmitters out of balance in the brain, electrosleep would put them back in balance. Other researchers found that electrosleep would apparently also put back into balance neurotransmitters in human patients whose neurotransmitters had been thrown out of balance by various addicting substances.

By Ray B. Smith, Ph.D

The Role of CES in Fighting Inflammation – Part 2

The role of CES in reducing the inflammatory response has been implicated more recently by Black who has shown that repeated acute or chronic psychological stress may also initiate the inflammatory response when the brain utilizes the same efferent pathways to respond to stress that it uses in the inflammatory response to fatty acids in the blood. The mediators are the major stress hormones norepinephrine, epinephrine, and cortisol together with components of the renin-angiotensin system, the proinflammatory cytokines.

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.4

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.5

Similar results were found in an animal preparation by Dougherty and his coworkers at the University of Texas.6,7

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.8

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.9

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.10

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.

To restate, we can assume that CES, by reducing depression and other signs of psychologically engendered chronic stress, may well play a significant role in reducing or eliminating psychogenic inflammation. That being the case, then another mechanism for the effectiveness of CES in reducing pain throughout the body, and engendering an overall return toward a state of wellness can be inferred. By reducing stress CES can rationally be implicated in assuaging or ameliorating all of the inflammation related medical conditions mentioned above, from diabetes to heart disease, stroke, and all of the various “itis” conditions, including pain.

By Ray B. Smith, Ph.D.

Presented by cesultra.com

Why You Shouldn’t Reach For a Sleeping Pill When You Can’t Sleep

Chronic lack of sleep has a cumulative effect when it comes to disrupting your health, so you can’t skimp on sleep on weekdays, thinking you’ll “catch up” over the weekend. You need consistency. Generally speaking, adults need between six and eight hours of sleep every night. There are plenty of exceptions though. Some people might need as little as five hours a night, while others cannot function optimally unless they get nine or 10 hours.

Find how Sleep Better With CES Ultra

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My strong recommendation and advice is quite simply to listen to your body. If you feel tired when you wake up, you probably need more sleep. Frequent yawning throughout the day is another dead giveaway that you need more shut-eye. Personally, I find that when I am reading during the day, if my eyes close and I tend to doze off, I know I did not get enough sleep the night before. However, above all, should insomnia strike, don’t make the mistake of reaching for a sleeping pill.

Not only do sleeping pills not address any of the underlying causes of insomnia, researchers have repeatedly shown that sleeping pills don’t work, but your brain is being tricked into thinking they do… One analysis found that, on average, sleeping pills help people fall asleep approximately 10 minutes sooner, and increase total sleep time by a mere 15-20 minutes. They also discovered that while most sleeping pills caused poor, fragmented sleep, they induced amnesia, so upon waking, the participants could not recall how poorly they’d actually slept!

In terms of health consequences, this could end up being worse than not sleeping and being aware of that fact. At least then you’d be encouraged to find and address the root cause of your sleeplessness. Besides not working as advertised, sleeping pills have also been linked to significant adverse health effects, including a nearly four-fold increase in the risk of death, and a 35 percent increased risk of cancer.