The People's Perspective on Medicine

How Can You Stop Taking Klonopin for Insomnia?

Benzodiazepine drugs are frequently used to ease anxiety and sleep problems. It can be very challenging to stop a drug such as Klonopin for insomnia.

When you are feeling stressed and can’t seem to get to sleep, medicines can help. Many people have found, however, that it is too easy to rely on a sleep aid. Then, when you no longer feel you need the medication, you may find it a challenge to stop taking it. That is what happened to one reader who had been taking Klonopin for insomnia.

Getting Off Klonopin for Insomnia:

Q. I took Klonopin for insomnia for 20 years. To get off it, I tapered it slowly over two years.

Despite this effort, I had severe withdrawal symptoms: burning, stinging, muscle spasms, nerve pain, dizziness, memory problems, nausea, weight loss and others. It has been 19 months since the last dose and I am slowly recovering from this terrible ordeal. I take no prescriptions.

A specialist at a university teaching hospital said results of my genetic test explain why the drug withdrawal was so hard.

A. Doctors often prescribe clonazepam (Klonopin) and other benzodiazepines such as alprazolam and diazepam for anxiety and insomnia. Long-term use can indeed lead to dependence.

You are certainly not the only person who has found it difficult to quit taking a benzo such as Klonopin for insomnia. As you learned by sad experience, even gradual tapering can result in rebound insomnia and other withdrawal symptoms. In some instances, people who stop such a drug suddenly land in the emergency department of the nearest hospital (Santos & Olmedo, Emergency Medicine Practice, online March 1, 2017).

What Do Genes Have to Do with It?

A better understanding of the genes that control drug-metabolizing enzymes may explain why some people suffer especially prolonged withdrawal symptoms. Research shows that mice and men with an atypical gene for brain-specific angiogenesis inhibitor I-associated protein 3 (Baiap3) are more susceptible to benzodiazepine dependence (Wojcik et al, Molecular Medicine, July 24, 2013).

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About the Author
Terry Graedon, PhD, is a medical anthropologist and co-host of The People’s Pharmacy radio show, co-author of The People’s Pharmacy syndicated newspaper columns and numerous books, and co-founder of The People’s Pharmacy website. Terry taught in the Duke University School of Nursing and was an adjunct assistant professor in the Department of Anthropology. She is a Fellow of the Society of Applied Anthropology. Terry is one of the country's leading authorities on the science behind folk remedies. .
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The GABAergic system (GABA receptors) is an inhibitory system, counteracting the Glutamate system (Glutamate receptors), which is excitatory.

GABA and Glutamate regulate action potential traffic.

GABA, an inhibitory neurotransmitter, stops action potentials. (Rest and Digest)

Glutamate, an excitatory neurotransmitter, starts action potentials or keeps them going. (Fight or Flight)

Since GABA is inhibitory and Glutamate is excitatory, both neurotransmitters work together to control many processes, including the brain’s overall level of excitation. Under normal conditions these two system are in balance leaning this way or that based on external forces i.e. a bear attack (excitatory system takes over, adrenaline floods the system, muscles tighten, vision and hearing are heightened, mind races, anger takes over etc.) or i.e. bedding down for the night (Inhibitory system takes over, muscle tension decreases, cortisol levels drop, adrenaline levels drop, body prepares for digestion, sex and sleep.).

Benzodiazepines (as well as alcohol) attach to the GABA-A receptor site of the GABA receptors located on the dendrites of the cell neuron , imitating the natural GABA, signaling to allow a higher than normal flow of Negatively charged chloride Ions to pass though the GABA receptor gate depolarizing the neuron, super-activating the inhibitory system and overly suppressing the Excitatory system. Benzos also force natural GABA to bind tighter and longer to the cell dendrites signaling thru the GABA-A receptor site to also allow more Negatively charged chloride ions to pass though. Result = Very relaxed.

As a result the body up-regulates the Glutamate receptors (Excitatory system) and releases more Glutamate, which then attaches to the Glutamate receptors allowing more Positively changed Sodium and Potassium Ions through counteracting the Negatively changed Chloride Ions and bringing back the overall balance. If the body has more of a Negative charge it’s relaxed, if more of a Positive charge it’s more alert.

Where it all goes wrong is when the body and brain, due to being flooded with too many Negatively charged Chloride Ions, start to eliminate a minor yet significant percentage of the GABA receptors on each cell trying to hinder the Chloride ion flow. When this action fails to work the body and brain take further steps of producing new GABA receptors without the GABA-A Benzo/alcohol/GABA attachment site. All is well and good until such time as the newly produced GABA receptors now lacking the GABA-A attachment site outnumber the older receptors which have it. When this happens those prescribed benzos start to experience interdose withdrawal. Doctors will try to solve this issue by prescribing a higher dose, however, very quickly the body responds by producing more GABA receptors without the GABA-A attachment site, plus will continue to absorb older GABA receptors. Soon, Tolerance of the med hits. The meds poops out.

While the early days of the above disaster are unfolding the Limbic system of the brain, thyroid, pituitary gland, etc. which are directly attached to the GABAergic system start to misfire and odd states of reality, emotion, fear, anxiety, paranoia, memory, balance, aggression states, sexual arousal etc. become more and more pronounced. Moreso once tapering begins and worse still once off the meds. Here are the parts of the Limbic system which start to misfire.

Amygdala – The Aggression/Emotional Center. Responsible for detecting fear and preparing for emergency events. Fight or flight. Stimulated, it produces feeling of anger, violence, fear, anxiety. Damaged, or medicated, can result in a very mellow state of being, hyperorality, hyper sexuality, disinhibited behavior – ignoring social conventions and engaging in dangerous, reckless behavior. Responsible for fear conditioning, the “associative learning process” where we learn to fear some thing, some place, someone, and/or a social circumstance.

Hippocampus – Memory and spatial navigation. Forming new and storing memories. Coverts short term memory to long term memory. Responsible for emotional reactions to past memories and events.

Thalamus – Regulates the body’s voluntary motor control, consciousness and its sleep/wake cycle. It also regulates the senses of sight, sound, taste, touch and the sense of where the person’s body is in space.

Hypothalamus – Produces hormones which control the production of hormones in the pituitary gland. Hypothalamus function is directly related to overall hormone health. Fight or Flight/Rest and Digest plus body temperature regulation. Responsible for the release of adrenaline via the autonomic nervous system. Hunger, thirst, sleep, sex.

Cingulate Gyrus – processing emotions and behavior regulation. It also helps to regulate autonomic motor function. Emotional Memory. Regulates pain and emotion. Is particularly involved in driving the body’s conscious response to unpleasant experiences, therefore the avoidance of negative consequences.

The end result of this, in part, is the Excitatory Glutamate system is no longer being kept in check by the GABAergic system so it’s running wild. This causes overblown and confused states of mind, body malfunctions and pain becomes the norm. To add insult to injury now the patient has to come off the meds, the only substance slowing down the Excitatory system and giving it even more freedom. Unfortunately glutamatergic receptors are not homeostatic like GABA receptors, changes to glutamatergic receptors stick around. Since GABAergic medications or substances no longer work to offset the now raging Excitatory system all one can do is endure it (survive) until such time as new GABA receptors are being created with the GABA-A receptor site. This is what happens during the healing process (Benzodiazepine Withdrawal Syndrome) and is entirely dictated by the level of damage done by the medications and the genetics of the individual which allow how fast the body and brain grow new GABA receptors with the GABA-A attachment site restoring the broken and off balance systems.

In the meantime, any substances, or states of mind (Stress), which irritates, or boosts the Excitatory Glutamate system must be avoided. Items such as sugar, MSG, caffeine, any GABAergic agent (alcohol, St. John’s Wort, Camomile, 5HTP, KAVA, Z-drugs [Ambien], etc) and everyday chemicals and foods become landmines as each can cause horrific increases in withdrawal symptoms for the individual, again based on genetics and sensitivities, and since GABA is directly responsible for muscle tone and mass we also experience a wasting, withering physical state. We lose muscle mass, gain (or massively lose) weight and have an immune system which is barely there all while the body and brain are malfunctioning on a level never imagined possible.

Are there recommendations on what the maximum amount of Tumeric a day should be?
I take 500 mg. BID BUT could use more pain relief from OA,
especially in my finger joints.
THANK YOU for all the information I have learned from the newsletters.

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